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Pulmonary vasoconstriction

Kuriyama H, Kitamura K, Itoh T, Inoue R 1998 Physiological features of visceral smooth muscle cells, with special reference to receptors and ion channels. Physiol Rev 78 811—920 McDaniel SS, Platoshyn O, Wang J et al 2001 Capacitative Ca2+ entry in agonist-induced pulmonary vasoconstriction. Am J Physiol 280 L870-L880 Montell C 2001 Physiology, phylogeny, and functions of the TRP superfamily of cation channels. In Science s STKE, July, pi—17... [Pg.89]

Wilson HL, Dipp M, Thomas JM, Lad C, Galione A, Evans AM 2001 ADP-ribosyl cyclase and cyclic ADP-ribose hydrolase act as a redox sensor. A primary role for cyclic ADP-ribose in hypoxic pulmonary vasoconstriction. J Biol Chem 276 11180-11188... [Pg.253]

Frostell, D., Fratacci, M. D., Wain, J. C., Jones, R., and Zapol, W. M. (1991). Inhaled nitric oxide. A selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction. Circulation 83, 2038-2047. [Pg.73]

Cyanide toxicity, overshoot hypotension, and myocardial ischaemia. Hypoxia caused by increased ventilation-perfusion mismatch due to pulmonary vasodilatation and inhibition of hypoxic pulmonary vasoconstriction. Rebound hypertension after discontinuation of SNP infusion. [Pg.147]

When given rapidly, protamine causes hypotension due to a decrease in vascular resistance, possibly linked to the release of nitric oxide from endothelium. Flypotension can be minimised by slow administration over 10-15 minutes. Protamine does not affect myocardial contractility. In some patients, systemic hypotension occurs in conjunction with pulmonary hypertension and, in severe cases, right ventricular failure. The mechanism is activation of the complement pathways by the heparin-protamine complex leading to release of thromboxane A2, which mediates pulmonary vasoconstriction. Unlike in anaphylaxis, plasma histamine concentrations are not increased. When this syndrome develops protamine administration should be stopped, and some have recommended giving heparin in an attempt to reduce the size of the heparin-protamine complex. [Pg.259]

Calcium channel blockers with vasodilator effects, such as nifedipine, nicardipine, and nimodipine, will potentiate the effect of vasodilator effects of, e.g. halothane or isoflurane, potentiating any hypotension. This is especially obvious in hypertensive patients and when combined with similarly acting agents, such as sodium nitroprusside or nitroglycerin. Similarly, they also enhance the tendency of volatile anaesthetics to reduce hypoxic pulmonary vasoconstriction, which might exacerbate ventilation/perfusion mismatching during anaesthesia. [Pg.276]

In rats, acted as vasodilator, weakening hypoxic pulmonary vasoconstriction 641... [Pg.201]

VEGF is a major regulator of vascular growth and is likely to be involved in the pulmonary vascular remodeling that occurs as a result of hypoxic pulmonary vasoconstriction in... [Pg.2310]

Hypoxaemia (Pa02 < 70 mm Hg) is observed in 45-69% of patients suffering from cirrhosis or liver insufficiency. Only rarely has severe hypoxaemia been demonstrated (Pa02 < 50 mm Hg). (6, 32, 51, 52, 56) Intrapulmonary vasodilations could be ascertained in 13-47% of liver transplant candidates. (27) In about 50% of all cirrhotic patients, a decline in the diffusion capacity for carbon monoxide was detected. (24) About 30% of cirrhotic patients showed no (physiological) reduction in pulmonary vasoconstriction under conditions of hypoxia. The prevalence of HPS in cirrhotic patients varies between 4% and 19%. It occurs more... [Pg.334]

In poorly ventilated lung areas, perfusion is diminished (= von Euler-Liljestrand reflex). This reflex is impaired in liver cirrhosis. The decrease in or loss of hypoxia-induced pulmonary vasoconstriction leads to the greater perfusion of poorly ventilated lung areas this results in an increase in the intrapulmonary shunt volume and... [Pg.335]

Fischer, S.R. Bone, H.G. Powell, W.C. McGuire, R. Traber, L.D. Traber, D.L. Pyridoxalated hemoglobin polyoxyethylene conjugate does not restore hypoxic pulmonary vasoconstriction in ovine sepsis. Crit. Care Med. 1997, 25 (9), 1551-1559. [Pg.374]

Weir EK, Reeve HL, Huang JM, Michelakis E, Nelson DP, Hampl V, Archer SL. Anorexic agents aminorex, fenfluramine, and dexfenfluramine inhibit potassium current in rat pulmonary vascular smooth muscle and cause pulmonary vasoconstriction. Circulation 1996 94(9) 2216-20. [Pg.137]

Hoit B, Gregoratos G, Shabetai R. Paradoxical pulmonary vasoconstriction induced by nitroglycerin in idiopathic pulmonary hypertension. J Am Coll Cardiol 1985 6(2) 490-2. [Pg.2537]

Severe acute pulmonary vasoconstriction with cardiovascular collapse was identified in 1983 and subsequent studies showed that the incidence of protamine-induced pulmonary artery vasoconstriction was about 1.5% after cardiac surgery (3). Protamine-induced pulmonary artery vasoconstriction is accompanied by generation of large quantities of thromboxane A2, a potent vasoconstrictor (3). [Pg.2964]

There is very limited information on the mechanisms of toxicity of MEK. Relatively high inhaled concentrations of 1475-29 500 mg m (500-10 000 ppm) caused pulmonary vasoconstriction and hypertension... [Pg.1661]

NO acts as a sympathoinhibitory substance within the central nervous system [44], Using SIN-1 (32), central NO administration has been shown to enhance acute hypoxic pulmonary vasoconstriction (HPV) [45], and accentuation of the HPV by NO is exacerbated in spontaneously hypertensive rats (SHR) compared with Wister-Kyoto (WKY) rats [46]. [Pg.143]

Dopamine often is recommended as the initial catecholamine in sepsis because it increases blood pressure by increasing myocardial contractility and vasoconstriction. Dopamine has been described to have dose-related receptor activity at DAj-, DA2-, fi -, and i-receptors. Unfortunately, this dose-response relationship has not been confirmed in critically ill patients. In patients with septic shock, there is a great overlap of hemodynamic effects even at doses as low as 3 mcg/kg per minute. Tachydysrhythmias are common owing to the release of endogenous norepinephrine by dopamine entering the sympathetic nerve terminal. Dopamine may increase the PAOP through pulmonary vasoconstriction. This drug also may depress ventilation and worsen hypoxemia in patients dependent on the hypoxic ventilatory drive. [Pg.467]

Weissmann N, Sommer N, Schermuly RT, et al. Oxygen sensors in hypoxic pulmonary vasoconstriction. Cardiovasc Res 2006 71(4) 620-9. [Pg.160]


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Hypoxic pulmonary vasoconstriction

Protamine pulmonary vasoconstriction

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