TXB2 and 6-keto-PGF1 alpha levels in arterial and venous plasma of Wistar and Hilltop rats during hypoxia were measured to investigate the roles of TXA2 and PGI2 in hypoxic pulmonary vasoconstriction (HPV) and responsiveness difference of pulmonary vessels to hypoxia between different strains of rats. The results showed that PGI2 might play an important role in maintaining the low resistance in pulmonary circulation of these two strains of rats. Increased TXA2 during hypoxia may partially mediate HPV in Wistar rats, while augmented PGI2 during hypoxia may modulate HPV in Wistar rats. This might be the important mechanism responsible for more intensive responsiveness of pulmonary vessels to hypoxia in Hilltop rats than in Wistar rats.
The difference in pulmonary vascular response to hypoxia between Hilltop Sprague-Dawley (HT) rats and Wistar (W) rats was studied. Effects of inhibitor of leukotriene (LT) synthesis or prostaglandin (PG) synthesis on hypoxic pulmonary vasoconstriction (HPV) and chronic pulmonary hypertension were observed, and variations in plasma TXB2 and 6-keto-PGF1 alpha during hypoxia were determined. The results showed that in rats of both strains LTs are the major mediator of HPV, which is also mediated by vasoconstrictive PGs in HT rats, while modulated by vasodilative PGs in W rats. This might be the crucial mechanism responsible for the higher pulmonary vascular responsiveness in HT rats. Differences in the modulating effect of histamine and in the structural feature of pulmonary arteriole might be contributing factors as well.
The effects of acute and chronic cigarette smoking on the metabolism of exogenous arachidonic acid (AA) and angiotensin I (AI) in perfused isolated rat lungs were studied. The results showed that acute cigarette smoking did not alter the contents of 6-keto-PGF1 alpha (the stable metabolite of PGI2) and TXB2 (the stable metabolite of TXA2) in the effluent and the increment of pulmonary artery pressure (delta Ppa) caused by AA. The conversion of A I into A II was significantly increased (P < 0.01), while the delta Ppa induced by A I injection was obviously decreased as compared with controls (P < 0.05). After cigarette smoke exposure for 30 days, the delta Ppa caused by AA or A I did not differ from that of controls, but the contents of 6-keto-PGF1 alpha and A II increased more markedly than those in non-smoking rats (P < 0.05). It is suggested that acute and chronic cigarette smoking in rats can promote the lung function of converting A I into A II, chronic smoking can increase the lung function of metabolizing AA into PGI2.
The roles of sympathicus, sensory neuropeptides (SNP), cyclooxygenase metabolites (COX-M), lipoxygenase metabolites (LOX-M), endothelium derived relaxing factor (EDRF), reactive oxygen (ROS) and potassium channels (PC) in the hypoxic pulmonary vasoconstriction (HPV) and hypoxic cerebral vasodilation (HCVD) were investigated in intact rats, rabbits and dogs. The results showed that during hypoxia, the excitation of sympathicus caused a constriction of both pulmonary and cerebral vessels, while SNP, EDRF and the opening of voltage sensitive PC caused the dilation of both of them; LOX-M mediated HPV and HCVD, COX-M might serve as their modulators; the blockade of ATP sensitive PC induced by hypoxia mediated HPV, but had no effect on HCVD; the reduction of O2-. in the lung might potentiate HPV, however, O2-. remained unchanged in brain during hypoxia. It is suggested that the alterations of LOX-M, ROS and the ATP sensitive PC are the factors accounting for the difference in the response of pulmonary and cerebral vessels to hypoxia.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.