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Vasodilation increases pulse pressure variation, mimicking hypovolemic status in rabbits

WESTPHAL, Glauco A; GONÇALVES, Anderson Roman; BEDIN, Antônio; STEGLICH, Raquel Bissacotti; SILVA, Eliezer; POLI-DE-FIGUEIREDO, Luiz Francisco
Fonte: Faculdade de Medicina / USP Publicador: Faculdade de Medicina / USP
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
37.009607%
OBJECTIVE: To test the hypothesis that pulse pressure respiratory variation (PPV) amplification, observed in hypovolemia, can also be observed during sodium nitroprusside (SNP)-induced vasodilation. INTRODUCTION: PPV is largely used for early identification of cardiac responsiveness, especially when hypovolemia is suspected. PPV results from respiratory variation in transpulmonary blood flow and reflects the left ventricular preload variations during respiratory cycles. Any factor that decreases left ventricular preload can be associated with PPV amplification, as seen in hypovolemia. METHODS: Ten anesthetized and mechanically ventilated rabbits underwent progressive hypotension by either controlled hemorrhage (Group 1) or intravenous SNP infusion (Group 2). Animals in Group 1 (n = 5) had graded hemorrhage induced at 10% steps until 50% of the total volume was bled. Mean arterial pressure (MAP) steps were registered and assumed as pressure targets to be reached in Group 2. Group 2 (n = 5) was subjected to a progressive SNP infusion to reach similar pressure targets as those defined in Group 1. Heart rate (HR), systolic pressure variation (SPV) and PPV were measured at each MAP step, and the values were compared between the groups. RESULTS: SPV and PPV were similar between the experimental models in all steps (p > 0.16). SPV increased earlier in Group 2. CONCLUSION: Both pharmacologic vasodilation and graded hemorrhage induced PPV amplification similar to that observed in hypovolemia...

Efeito do exercício físico aeróbio no relaxamento aórtico de ratos e no controle da biodisponibilidade do óxido nítrico; Effects of acute aerobic exercise on vasodilation response of rat aorta and regulation of nitric oxide biovalability

Tanaka, Leonardo Yuji
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 29/08/2008 Português
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O presente estudo avaliou o efeito do exercício físico aeróbico na função vasomotora dependente do endotélio em aorta de ratos bem como os mecanismos envolvidos na regulação da biodisponibilidade do NO. Para tanto, um grupo de animais foi submetido a uma sessão de exercício (EX, n=17) enquanto o outro grupo permaneceu em repouso (CT, n=18). Imediatamente após o exercício, os ratos de ambos os grupos foram eutanasiados para a retirada da aorta torácica para análises funcionais e bioquímicas. Resultados: observamos que o grupo exercitado apresentou uma melhora no relaxamento dependente do endotélio com um efeito máximo de 12%, sendo esse efeito relacionado a um aumento na ativação da eNOS. Apesar de aumentar o NO, os animais do grupo EX apresentaram níveis aumentados de superóxido (28%), efeito que foi associado à maior ativação do complexo enzimático NAD(P)H oxidase. Além do superóxido, o peróxido de hidrogênio também foi aumentado nos animais exercitados porém a maior produção de espécies reativas de oxigênio não foi suficiente para causar um estresse oxidativo vascular. Esses resultados demonstram que uma única sessão de exercício físico aeróbico é capaz de melhorar a vasodilatação dependente do endotélio por aumentar a biodisponibilidade de NO e que a produção de espécies reativas oxigênio também aumenta porém em níveis controlados .; The present study evaluated the effect of aerobic physical exercise on endothelium-dependent vasomotor function of rat aorta as well the mechanisms involved in nitric oxide bioavalability control. One group of rats was submitted to one bout of exercise (EX...

Vasodilatação induzida pelo calor através de dispositivo portátil no leito na insuficiência cardíaca descompensada; Thermal vasodilation using a portable infrared thermal blanket in decompensated heart failure

Lima, Marcelo Villaça
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 24/03/2014 Português
Relevância na Pesquisa
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Fundamento: medidas adjuvantes têm sido propostas para o tratamento de pacientes com insuficiência cardíaca, algumas não farmacológicas, como o uso do calor. Apesar dos resultados positivos para pacientes clinicamente estáveis, não existem trabalhos relacionados ao tratamento com calor na fase descompensada da insuficiência cardíaca em pacientes em uso de drogas vasoativas. Objetivos: avaliar os efeitos hemodinâmicos agudos do calor aplicado através da manta térmica em pacientes com insuficiência cardíaca descompensada (ICD) refratária. Para isso foi estabelecido como desfechos o aumento do índice cardíaco e a redução da resistência vascular sistêmica no primeiro dia de seguimento. Como objetivo secundário, avaliar se sessões repetidas de calor por cinco dias consecutivos promoveria ou sustentaria os efeitos hemodinâmicos obtidos agudamente e, se reduziria os níveis de BNP ao longo do seguimento. Métodos: ensaio clínico randomizado aberto, prospectivo, com grupo controle em pacientes portadores de ICD. O estudo foi dividido em duas fases. Na primeira fase foram estudados pacientes em um único dia e foi avaliado o efeito agudo do calor antes e após a intervenção. Na segunda fase o calor foi avaliado através de sessões diárias por cinco dias consecutivos. Foi utilizada a manta térmica por radiação infravermelha para o aquecimento dos pacientes. As medidas hemodinâmicas foram avaliadas por método invasivo através do cateter de Swan-Ganz e de maneira não invasiva pelo método de modelflow. Os pacientes estavam em uso de inotrópico endovenoso contínuo...

Avaliação dos mecanismos envolvidos na vasodilatação dependente do endotélio em aorta de camundongos tratados com isoproterenol.; Evaluation of the mechanisms involved on the endothelium-dependent vasodilation in aorta of isoproterenol-treated mice.

Oliveira, Angelo Bernak de
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 20/02/2014 Português
Relevância na Pesquisa
37.009607%
Esta dissertação investigou os mecanismos envolvidos na vasodilatação focando no papel das cavéolas e na possível interação com a isoforma endotelial da sintase de óxido nítrico (eNOS)/ óxido nítrico e neuronal (nNOS)/ peróxido de hidrogênio (H2O2) em aorta de camundongos tratados com isoproterenol (ISO). Anéis de aorta foram montados em banho de órgãos para medida de tensão isométrica. A expressão das proteínas foi avaliada a partir da técnica de Western blot. Os resultados demonstraram que o tratamento com ISO: 1) não modifica nem a vasodilatação à acetilcolina (ACh) nem ao nitroprussiato de sódio; 2) aumenta a dependência das cavéolas na resposta vasodilatadora à ACh e ao ionóforo de cálcio e a expressão proteica da caveolina-1, mas não da caveolina-3; 3) aumenta a modulação das NOS, principalmente a nNOS, à ACh; 4) aumenta a participação do H2O2 na vasodilatação à ACh e 5) aumenta a expressão de proteínas da defesa antioxidante. Conclui-se que a hiperativação β-AR com ISO ativa mecanismos vasodilatadores compensatórios em resposta à ACh nas aortas de camundongos.; The aim of this thesis was to investigate the mechanisms involved on the endothelium-dependent vasodilation focusing on the role of caveolae and the possible interaction between endothelial nitric synthase (eNOS)/ nitric oxide and neuronal (nNOS)/ hydrogen peroxide (H2O2) in aorta of ISO-treated mice. Aortic rings were mounted in an organ bath for measurement of isometric tension. The expression of proteins was evaluated using Western blot. The results demonstrated that ISO treatment: 1) did not change acetylcholine (ACh) or NO donor-induced relaxation; 2) increases the caveolae participation in ACh and calcium ionophore-induced relaxation and caveolin-1 protein expression...

Central nitric oxide modulates hindquarter vasodilation elicited by AMPA receptor stimulation in the NTS of conscious rats

Dias, Ana Carolina Rodrigues; Colombari, Eduardo
Fonte: Universidade Estadual Paulista Publicador: Universidade Estadual Paulista
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
37.009607%
Microinjection of S-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) in the nucleus of the solitary tract (NTS) of conscious rats causes hypertension, bradycardia, and vasoconstriction in the renal, mesenteric, and hindquarter vascular beds. In the hindquarter, the initial vasoconstriction is followed by vasodilation with AMPA doses >5 pmol/100 nl. To test the hypothesis that this vasodilation is caused by activation of a nitroxidergic pathway in the NTS, we examined the effect of pretreatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10 nmol/100 nl, microinjected into the NTS) on changes in mean arterial pressure, heart rate, and regional vascular conductance (VC) induced by microinjection of AMPA (10 pmol/100 nl in the NTS) in conscious rats. AMPA increased hindquarter VC by 18 ± 4%, but after pretreatment with L-NAME, AMPA reduced hindquarter VC by 16 ± 7% and 17 ± 9% (5 and 15 min after pretreatment, P < 0.05 compared with before pretreatment). Pretreatment with L-NAME reduced AMPA-induced bradycardia from 122 ± 40 to 92 ± 32 beats/min but did not alter the hypertension induced by AMPA (35 ± 5 mmHg before pretreatment, 43 ± 6 mmHg after pretreatment). Control injections with D-NAME did not affect resting values or the response to AMPA. The present study shows that stimulation of AMPA receptors in the NTS activates both vasodilatatory and vasoconstrictor mechanisms and that the vasodilatatory mechanism depends on production of nitric oxide in the NTS. Copyright © 2006 the American Physiological Society.

Evidence for a role of nitric oxide in hindlimb vasodilation induced by hypothalamic stimulation in anesthetized rats

Ferreira-Neto,Marcos L.; Possas,Olga S.; Lopes,Oswaldo U.; Cravo,Sérgio L.
Fonte: Academia Brasileira de Ciências Publicador: Academia Brasileira de Ciências
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/06/2005 Português
Relevância na Pesquisa
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Electrical stimulation of the hypothalamus produces cardiovascular adjustments consisting of hypertension, tachycardia, visceral vasoconstriction and hindlimb vasodilation. Previous studies have demonstrated that hindlimb vasodilation is due a reduction of sympathetic vasoconstrictor tone and to activation of beta2-adrenergic receptors by catecholamine release. However, the existence of a yet unidentified vasodilator mechanism has also been proposed. Recent studies have suggested that nitric oxide (NO) may be involved. The aim of the present study was to investigate the role of NO in the hindquarter vasodilation in response to hypothalamic stimulation. In pentobarbital-anesthetized rats hypothalamic stimulation (100 Hz, 150µA, 6 s) produced hypertension, tachycardia, hindquarter vasodilation and mesenteric vasoconstriction. Alpha-adrenoceptor blockade with phentolamine (1.5 mg/kg, iv) plus bilateral adrenalectomy did not modify hypertension, tachycardia or mesenteric vasoconstriction induced by hypothalamic stimulation. Hindquarter vasodilation was strongly reduced but not abolished. The remaining vasodilation was completely abolished after iv injection of the NOS inhibitor L-NAME (20 mg/kg, iv). To properly evaluate the role of the mechanism of NO in hindquarter vasodilation...

Dissociation between vasodilation and Leishmania infection-enhancing effects of sand fly saliva and maxadilan

Castro-Sousa,Fábio; Paranhos-Silva,Moacir; Sherlock,Ítalo; Paixão,Mariza S; Pontes-de-Carvalho,Lain C; dos-Santos,Washington LC
Fonte: Instituto Oswaldo Cruz, Ministério da Saúde Publicador: Instituto Oswaldo Cruz, Ministério da Saúde
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/10/2001 Português
Relevância na Pesquisa
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In this study, the ability of maxadilan and Lutzomyia longipalpis salivary gland lysate to enhance the infection of CBA mice by Leishmania major and of BALB/c mice by L. braziliensis was tested. No difference was observed between sizes of lesion in CBA mice infected with L. major and treated or not with salivary gland lysate or maxadilan, although they were injected in concentrations that induced cutaneous vasodilation. Although parasites were more frequently observed in foot pads and spleens of animals treated with maxadilan than in the animals treated with salivary gland lysate or saline, the differences were small and not statistically significant. The lesions in BALB/c mice infected with L. braziliensis and treated with maxadilan were slightly larger than in animals that received Leishmania alone. Such differences disappeared 14 weeks after infection, and were statistically significant only in one of two experiments.

Role of non-nitric oxide non-prostaglandin endothelium-derived relaxing factor(s) in bradykinin vasodilation

Resende,A.C.; Ballejo,G.; Salgado,M.C.O.
Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/09/1998 Português
Relevância na Pesquisa
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The most conspicuous effect of bradykinin following its administration into the systemic circulation is a transient hypotension due to vasodilation. In the present study most of the available evidence regarding the mechanisms involved in bradykinin-induced arterial vasodilation is reviewed. It has become firmly established that in most species vasodilation in response to bradykinin is mediated by the release of endothelial relaxing factors following the activation of B2-receptors. Although in some cases the action of bradykinin is entirely mediated by the endothelial release of nitric oxide (NO) and/or prostacyclin (PGI2), a large amount of evidence has been accumulated during the last 10 years indicating that a non-NO/PGI2 factor accounts for bradykinin-induced vasodilation in a wide variety of perfused vascular beds and isolated small arteries from several species including humans. Since the effect of the non-NO/PGI2 endothelium-derived relaxing factor is practically abolished by disrupting the K+ electrochemical gradient together with the fact that bradykinin causes endothelium-dependent hyperpolarization of vascular smooth muscle cells, the action of such factor has been attributed to the opening of K+ channels in these cells. The pharmacological characteristics of these channels are not uniform among the different blood vessels in which they have been examined. Although there is some evidence indicating a role for KCa or KV channels...

Ionic radiocontrast inhibits endothelium-dependent vasodilation of the canine renal artery in vitro: possible mechanism of renal failure following contrast medium infusion

Discigil,B.; Evora,P.R.B.; Pearson,P.J.; Viaro,F.; Rodrigues,A.J.; Schaff,H.V.
Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/02/2004 Português
Relevância na Pesquisa
37.009607%
To determine if radiocontrast impairs vascular relaxation of the renal artery, segments (4-5 mm in length) of canine renal artery were suspended in vitro in organ chambers to measure isometric force (95% O2/5% CO2, at 37ºC). Arterial segments with and without endothelium were placed at the optimal point of their length-tension relation and incubated with 10 µM indomethacin to prevent synthesis of endogenous prostanoids. The presence of nonionic radiocontrast (iohexol, Omnipaque 350, 1 ml in 25 ml control solution, 4% (v/v)) did not alter endothelium-dependent relaxation to acetylcholine in rings precontracted with both norepinephrine and prostaglandin F2alpha (N = 6). When the rings were precontracted with prostaglandin F2alpha, the presence of ionic contrast did not inhibit the relaxation of the arteries. However, in canine renal arteries contracted with norepinephrine, the presence of ionic radiocontrast (diatrizoate meglumine and diatrizoate sodium, MD-76, 1 ml in 25 ml control solution, 4% (v/v)) inhibited relaxation in response to acetylcholine, sodium nitroprusside (N = 6 in each group), and isoproterenol (N = 5; P < 0.05). Rings were relaxed less than 50% of norepinephrine contraction. Following removal of the contrast, vascular relaxation in response to the agonists returned to normal. These results indicate that ionic radiocontrast nonspecifically inhibits vasodilation (both cAMP-mediated and cGMP-mediated) of canine renal arteries contracted with norepinephrine. This reversible impairment of vasodilation could inhibit normal renal perfusion and act as a mechanism of renal failure following radiocontrast infusion. In the adopted experimental protocol the isoproterenol-induced relaxation of renal arteries precontracted with norepinephrine was more affected...

Vasodilation increases pulse pressure variation, mimicking hypovolemic status in rabbits

Westphal,Glauco A; Gonçalves,Anderson Roman; Bedin,Antônio; Steglich,Raquel Bissacotti; Silva,Eliezer; Poli-de-Figueiredo,Luiz Francisco
Fonte: Faculdade de Medicina / USP Publicador: Faculdade de Medicina / USP
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/01/2010 Português
Relevância na Pesquisa
37.009607%
OBJECTIVE: To test the hypothesis that pulse pressure respiratory variation (PPV) amplification, observed in hypovolemia, can also be observed during sodium nitroprusside (SNP)-induced vasodilation. INTRODUCTION: PPV is largely used for early identification of cardiac responsiveness, especially when hypovolemia is suspected. PPV results from respiratory variation in transpulmonary blood flow and reflects the left ventricular preload variations during respiratory cycles. Any factor that decreases left ventricular preload can be associated with PPV amplification, as seen in hypovolemia. METHODS: Ten anesthetized and mechanically ventilated rabbits underwent progressive hypotension by either controlled hemorrhage (Group 1) or intravenous SNP infusion (Group 2). Animals in Group 1 (n = 5) had graded hemorrhage induced at 10% steps until 50% of the total volume was bled. Mean arterial pressure (MAP) steps were registered and assumed as pressure targets to be reached in Group 2. Group 2 (n = 5) was subjected to a progressive SNP infusion to reach similar pressure targets as those defined in Group 1. Heart rate (HR), systolic pressure variation (SPV) and PPV were measured at each MAP step, and the values were compared between the groups. RESULTS: SPV and PPV were similar between the experimental models in all steps (p > 0.16). SPV increased earlier in Group 2. CONCLUSION: Both pharmacologic vasodilation and graded hemorrhage induced PPV amplification similar to that observed in hypovolemia...

Vasoactive intestinal polypeptide in cholinergic neurons of exocrine glands: Functional significance of coexisting transmitters for vasodilation and secretion

Lundberg, Jan M.; Änggärd, Anders; Fahrenkrug, Jan; Hökfelt, Tomas; Mutt, Viktor
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1980 Português
Relevância na Pesquisa
27.33258%
By a combination of the indirect immunofluorescence technique with acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.1.1.7) staining, it was shown that vasoactive intestinal polypeptide (VIP) is present in cholinergic (acetylcholinesterase-rich) neurons involved in control of secretion and vasodilation in exocrine glands of cat. The submandibular salivary gland was used as a functional model. Preganglionic nerve stimulation induced an atropine-resistant, hexamethonium-sensitive vasodilation and release of VIP into the venous outflow from the gland and an atropine- and hexamethonium-sensitive secretion. Infusion of VIP antiserum reduced both the vasodilation and secretion. Infusion of VIP caused vasodilation only, whereas acetylcholine caused both vasodilation and secretion. Simultaneous infusion of VIP and acetylcholine in low doses resulted in a marked potentiation of both vasodilation and secretion. The present morphological and functional data support the following hypothesis for regulation of vasodilation and secretion in exocrine glands. Preganglionic cholinergic nerves activate, via nicotinic receptors, postganglionic neurons, causing concomitant release from the same nerve endings of two coexisting putative transmitters...

Hypoxia Impairs Vasodilation in the Lung

Voelkel, Norbert F.; McMurtry, Ivan F.; Reeves, John T.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /01/1981 Português
Relevância na Pesquisa
27.391716%
Alveolar hypoxia causes pulmonary vasoconstriction; we investigated whether hypoxia could also impair pulmonary vasodilation. We found in the isolated perfused rat lung a delay in vasodilation following agonist-induced vasoconstriction. The delay was not due to erythrocyte or plasma factors, or to alterations in base-line lung perfusion pressure. Pretreating lungs with arachidonic acid abolished hypoxic vasoconstriction, but did not influence the hypoxia-induced impairment of vasodilation after angiotensin II, bradykinin, or serotonin pressor responses. Progressive slowing of vasodilation followed angiotensin II-induced constriction as the lung oxygen tension fell progressively below 60 Torr. KCl, which is not metabolized by the lung, caused vasoconstriction; the subsequent vasodilation time was delayed during hypoxia. However, catecholamine depletion in the lungs abolished this hypoxic vasodilation delay after KCl-induced vasoconstriction. In lungs from high altitude rats, the hypoxia-induced vasodilation impairment after an angiotensin II pressor response was markedly less than it was in lungs from low altitude rats. We conclude from these studies that (a) hypoxia impairs vasodilation of rat lung vessels following constriction induced by angiotensin II...

Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans

Cheng, Kang; Wu, Tsuei-Ju; Wu, Kenneth K.; Sturino, Claudio; Metters, Kathleen; Gottesdiener, Keith; Wright, Samuel D.; Wang, Zhaoyin; O’Neill, Gary; Lai, Eseng; Waters, M. Gerard
Fonte: National Academy of Sciences Publicador: National Academy of Sciences
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
27.355522%
Nicotinic acid (NA) is commonly used to treat dyslipidemia, but it elicits an adverse effect, termed flushing, which consists of cutaneous vasodilation with associated discomfort. An animal model of NA-induced flushing has been established in mice. As in humans, NA stimulated vasodilation in a dose-dependent manner, was associated with an increase of the vasodilatory prostaglandin (PG) D2 in plasma and could be blocked by pretreatment with aspirin. Two PGD2 receptors have been identified: PGD2 receptor 1 (DP1, also called DP) and PGD2 receptor 2 (DP2, sometimes termed CRTH2). DP2 does not mediate NA-induced vasodilation; the DP2-specific agonist DK-PGD2 (13,14-dihydro-15-keto-PGD2) did not induce cutaneous vasodilation, and DP2−/− mice had a normal vasodilatory response to NA. By contrast, BW245C, a DP1-selective agonist, induced vasodilation in mice, and MK-0524, a DP1-selective antagonist, blocked both PGD2- and NA-induced vasodilation. NA-induced vasodilation was also studied in DP1+/+, DP1+/−, and DP1−/− mice; although NA-induced vasodilation depended almost completely on DP1 in female mice, it depended only partially on DP1 in male mice. The residual NA-induced vasodilation in male DP−/− mice was aspirin-sensitive. Thus...

Developmental changes in endothelium-dependent vasodilation and the influence of superoxide anions in perinatal rabbit pulmonary arteries

Morecroft, Ian; MacLean, Margaret R
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /12/1998 Português
Relevância na Pesquisa
27.33258%
ACh-induced vasodilation was investigated in pulmonary arteries from 8 and 2 day pre-term foetal, neonatal (0–12 h and 4 day old) and adult rabbits. The effects of superoxide anion generation [with hypoxanthine (HX, 0.1 mM)/xanthine oxidase (XO, 15 mu ml−1)], endogenous superoxide dismutase (SOD) inhibition [with the Cu-Zn SOD inhibitor triethylenetetramine (TETA, 1 mM)], endogenous superoxide anion scavenging [by superoxide dismutase (SOD, 50 u ml−1)] and inhibition of endothelial nitric oxide synthase (eNOS) [with, Nω-nitro-L-arginine methylester (L-NAME, 0.1 mM)], on basal and ACh-induced NO activity were studied by examining phenylephrine-induced contraction and ACh-induced vasodilation respectively.L-NAME and endothelium removal abolished all ACh-induced vasodilation and 1 μM sodium nitroprusside fully dilated all vessels. ACh-induced vasodilation was absent in the 8 day pre-term foetus and 0–12 h neonate but present at all other ages. L-NAME itself contracted 2 day pre-term foetal vessels. At 0–12 h, SOD, but not the phosphodiesterase 5 inhibitor zaprinast (1 μM), uncovered ACh-induced vasodilation. At this age SOD reduced phenylephrine-induced contraction which was not influenced by TETA...

Intravascular ATP and coronary vasodilation in the isolated working rat heart

Korchazhkina, Olga; Wright, Gordon; Exley, Christopher
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /06/1999 Português
Relevância na Pesquisa
27.391716%
Adenosine-5′-triphosphate (ATP) is a potent coronary vasodilator. Because of the efficient hydrolysis of ATP, adenosine-5′-diphosphate (ADP) and adenosine-5′-monophosphate (AMP) by ectonucleotidases located in the coronary endothelium ATP-induced vasodilation may be mediated via both P1 (AMP and adenosine) and P2Y (ATP and ADP) receptors. We have used the change in total coronary resistance (TCR) induced by intravascular ATP in the isolated working rat heart to determine both the component of the vasodilation mediated via P2Y receptors and the identity of the subclass of receptor involved.The dose response for ATP revealed a half maximal effect at an apparent ATP concentration of 0.08±0.009 μM. The response was saturated at apparent ATP concentrations greater than 0.23 μM. Contrary to much of the current literature, the perfusion of a 0.25 μM concentration of adenosine resulted in the identical response to an equimolar concentration of ATP suggesting a significant role for adenosine in coronary vasodilation.The non-selective P1 receptor antagonist 8-(p-Sulfophenyl)theophylline (8-SPT) was used to show that the response to ATP was mediated via both P1 and P2Y receptors. Whilst 8-SPT abolished the effect of adenosine it reduced the effect of ATP by only 50%. Thus...

Age impairs Flk-1 signaling and NO-mediated vasodilation in coronary arterioles

LeBlanc, Amanda J.; Shipley, Robert D.; Kang, Lori S.; Muller-Delp, Judy M.
Fonte: American Physiological Society Publicador: American Physiological Society
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
27.33258%
Impairment of flow-induced vasodilation in coronary resistance arterioles may contribute to the decline in coronary vasodilatory reserve that occurs with advancing age. This study investigated the effects of age on flow-induced signaling and activation of nitric oxide (NO)-mediated vasodilation in coronary resistance arterioles. Coronary arterioles were isolated from young (∼6 mo) and old (∼24 mo) male Fischer-344 rats to assess vasodilation to flow, vascular endothelial growth factor (VEGF), and ACh. Flow- and VEGF-induced vasodilation of coronary arterioles was impaired with age (P ≤ 0.05); however, ACh-induced vasodilation was preserved with age. NG-nitro-l-arginine methyl ester (l-NAME) (1 × 10−5 M) eliminated vasodilation to flow, VEGF, and ACh, indicating dependence of these responses on NO. SU-1498, an inhibitor of vascular endothelial growth factor receptor 2 (VEGFR, also known as Flk-1), abolished age-related differences in flow-induced vasodilation. Flow-stimulated phosphorylation of Flk-1 in coronary arterioles from young but not old rats and Flk-1 protein was reduced in coronary arterioles from old rats compared with those from young rats. Flow stimulated phosphorylation of endothelial nitric oxide synthase (eNOS) in coronary arterioles from both young and old rats. VEGF induced phosphorylation of both protein kinase B (Akt) and eNOS in coronary arterioles. VEGF-induced phosphorylation of Akt...

Improved functional vasodilation in obese Zucker rats following exercise training

Sebai, Mohamad; Lu, Silu; Xiang, Lusha; Hester, Robert L.
Fonte: American Physiological Society Publicador: American Physiological Society
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
27.37499%
Obese individuals exhibit impaired functional vasodilation and exercise performance. We have demonstrated in obese Zucker rats (OZ), a model of morbid obesity, that insulin resistance impairs functional vasodilation via an increased thromboxane receptor (TP)-mediated vasoconstriction. Chronic treadmill exercise training improves functional vasodilation in the spinotrapezius muscle of the OZ, but the mechanisms responsible for the improvement in functional vasodilation are not clear. Based on evidence that exercise training improves insulin resistance, we hypothesized that, in the OZ, exercise training increases functional vasodilation and exercise capability due to decreases TP-mediated vasoconstriction associated with improved insulin sensitivity. Six-week-old lean Zucker rats (LZ) and OZ were exercised on a treadmill (24 m/min, 30 min/day, 5 days/wk) for 6 wk. An oral glucose tolerance test was performed at the end of the training period. We measured functional vasodilation in both exercise trained (spinotrapezius) and nonexercise trained (cremaster) muscles to determine whether the improved functional vasodilation following exercise training in OZ is due to a systemic improved insulin resistance. Compared with LZ, the sedentary OZ exhibited impairments in glucose tolerance and functional vasodilation in both muscles. The TP antagonist SQ-29548 improved the vasodilator responses in the sedentary OZ with no effect in the LZ. Exercising training of the LZ increased the functional vasodilation in spinotrapezius muscle...

Cyclooxygenase-derived vasoconstriction restrains hypoxia-mediated cerebral vasodilation in young adults with metabolic syndrome

Harrell, John W.; Schrage, William G.
Fonte: American Physiological Society Publicador: American Physiological Society
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
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Poor cerebrovascular function in metabolic syndrome (MetSyn) likely contributes to elevated risk of cerebrovascular disease in this growing clinical population. Younger MetSyn adults without clinical evidence of cerebrovascular disease exhibit preserved hypercapnic vasodilation yet markedly impaired hypoxic vasodilation, but the mechanisms behind reduced hypoxic vasodilation are unknown. Based on data from rats, we tested the hypothesis that younger adults with MetSyn exhibit reduced cerebral hypoxic vasodilation due to loss of vasodilating prostaglandins. Middle cerebral artery velocity (MCAv) was measured with transcranial Doppler ultrasound in adults with MetSyn (n = 13, 33 ± 3 yr) and healthy controls (n = 15, 31 ± 2 yr). Isocapnic hypoxia was induced by titrating inspired oxygen to lower arterial saturation to 90% and 80% for 5 min each. Separately, hypercapnia was induced by increasing end-tidal CO2 10 mmHg above baseline levels. Cyclooxygenase inhibition (100 mg indomethacin) was conducted in a randomized double-blind, placebo controlled design. MCAv was normalized for group differences in blood pressure (healthy: 89 ± 2 mmHg vs. MetSyn: 102 ± 2 mmHg) as cerebrovascular conductance index (CVCi), and used to assess cerebral vasodilation. Hypoxia increased CVCi in both groups; however...

Corticotropin-Releasing Hormone Causes Vasodilation in Human Skin via Mast Cell-Dependent Pathways

Crompton, R.; Clifton, V.; Bisits, A.; Read, M.; Smith, R.; Wright, I.
Fonte: Endocrine Society Publicador: Endocrine Society
Tipo: Artigo de Revista Científica
Publicado em //2003 Português
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CRH plays a central role as a mediator of the hypothalamic-pituitary-adrenal axis and stress response and is a potent vasodilator. Previously, we have shown that CRH causes a gender-specific vasodilation in human skin, although the mechanism by which CRH operates is unclear. CRH causes mast cell degranulation in rat skin. As such, histamine and other mast cell-derived factors may be indirectly responsible for the vasodilatory effects of CRH, although CRH is also known to act directly on the vasculature. CRH-induced vasodilation in human skin was examined using laser Doppler flowmetry and iontophoresis in adult females. CRH (1 nM) was administered iontophoretically to the forearm, and blood flow was measured simultaneously in the same area by laser Doppler. CRH-induced dilation of the skin microvasculature was significantly reduced in the presence of the mast cell degranulation inhibitor, sodium cromoglycate, the histamine H1-antagonist, promethazine, or the H2-antagonist, ranitidine. CRH-induced dilation was also significantly reduced in the presence of the nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester, or the cyclooxygenase inhibitor, piroxicam. These findings provide novel evidence that CRH-induced vasodilation in human skin occurs via mast cell degranulation and is principally mediated by histamine and...

Vasodilation increases pulse pressure variation, mimicking hypovolemic status in rabbits

Westphal, Glauco A; Gonçalves, Anderson Roman; Bedin, Antônio; Steglich, Raquel Bissacotti; Silva, Eliezer; Poli-de-Figueiredo, Luiz Francisco
Fonte: Universidade de São Paulo. Faculdade de Medicina Publicador: Universidade de São Paulo. Faculdade de Medicina
Tipo: info:eu-repo/semantics/article; info:eu-repo/semantics/publishedVersion; ; ; ; ; Formato: application/pdf
Publicado em 01/01/2010 Português
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OBJECTIVE: To test the hypothesis that pulse pressure respiratory variation (PPV) amplification, observed in hypovolemia, can also be observed during sodium nitroprusside (SNP)-induced vasodilation. INTRODUCTION: PPV is largely used for early identification of cardiac responsiveness, especially when hypovolemia is suspected. PPV results from respiratory variation in transpulmonary blood flow and reflects the left ventricular preload variations during respiratory cycles. Any factor that decreases left ventricular preload can be associated with PPV amplification, as seen in hypovolemia. METHODS: Ten anesthetized and mechanically ventilated rabbits underwent progressive hypotension by either controlled hemorrhage (Group 1) or intravenous SNP infusion (Group 2). Animals in Group 1 (n = 5) had graded hemorrhage induced at 10% steps until 50% of the total volume was bled. Mean arterial pressure (MAP) steps were registered and assumed as pressure targets to be reached in Group 2. Group 2 (n = 5) was subjected to a progressive SNP infusion to reach similar pressure targets as those defined in Group 1. Heart rate (HR), systolic pressure variation (SPV) and PPV were measured at each MAP step, and the values were compared between the groups. RESULTS: SPV and PPV were similar between the experimental models in all steps (p >; 0.16). SPV increased earlier in Group 2. CONCLUSION: Both pharmacologic vasodilation and graded hemorrhage induced PPV amplification similar to that observed in hypovolemia...