Calcium-activated chloride channels are involved in two-phase hypoxic pulmonary vasoconstriction in rat pulmonary arteries / 生理学报

The aim of the present study was to investigate the roles of calcium-activated chloride channels (Cl(Ca)) in the two-phase hypoxic pulmonary vasoconstriction (HPV). The second pulmonary artery branches were dissected from male Sprague-Dawley rats, and the changes in vascular tone were measured by using routine blood vascular perfusion in vitro. The result showed that, under normoxic conditions, Cl(Ca) inhibitors (NFA and IAA-94) significantly relaxed second pulmonary artery contracted by norepinephrine (P < 0.01), but merely had effects on KCl-induced second pulmonary artery contractions. A biphasic contraction response was induced in second pulmonary artery ring pre-contracted with norepinephrine exposed to hypoxic conditions for at least one hour, but no biphasic contraction was observed in pulmonary rings pre-contracted with KCl. NFA and IAA-94 significantly attenuated phase II sustained hypoxic contraction (P < 0.01), and also attenuated phase I vasodilation, but had little effect on phase I contraction. These results suggest that Cl(Ca) is an important component forming phase II contraction in secondary pulmonary artery, but not involved in phase I contraction.

Effects of shenmai injection on pulmonary aquaporin 1 in rats following traumatic brain injury / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Aquaporin-1 (AQP1) has involved in fluid transport in diverse pulmonary edema diseases. Our study aimed to explore the dynamic changes of AQP1 in pulmonary water metabolism in rats following traumatic brain injury (TBI) and the protective effect provided by shenmai injection.</p><p><b>METHODS</b>Sixty male Sprague Dawley rats weighting 280 - 300 g were randomly divided into three groups: the normal control group, the model group and the shenmai injection (SMI) group. One piece skull was taken away without injuring cerebral tissue in normal control group, while rats in model group and SMI group were subject to free fall injury in the cerebral hemisphere. Rats in model group received intraperitoneal normal sodium (15 ml/kg) at one hour post-injury and the same dose of shenmai injection instead in SMI group, respectively. The expression of AQP1 was detected by immunohistochemical analysis and semi-quantitative RT-PCR at 0 hour, 10 hours, 72 hours and 120 hours after TBI. Arterial blood gas analysis and lung wet to dry were also measured.</p><p><b>RESULTS</b>AQP1 was mainly presented in the capillary endothelium and slightly alveolar epithelial cells in three groups, but the expression of AQP1 in the normal control group was positive and tenuous, weakly positive in the model and SMI groups, respectively. Compared with normal control group, AQP1 mRNA levels were down regulated in the model and SMI groups at 10 hours, 72 hours and 120 hours (P < 0.05). While AQP1 mRNA levels in the SMI group was up-regulated than that in the model group (P < 0.05). Lung wet to dry weight ratio (W/D) in the model and SMI groups at 10 hours were higher than that in normal control group (P < 0.05). Compared with normal control group, PaO2 was markedly lower in the model and SMI groups (P < 0.05), but there were no statistically significant differences between model and SMI groups (P > 0.05).</p><p><b>CONCLUSIONS</b>The decreased AQP1 expression may be involved in the increased lung water content and dysfunction of pulmonary water metabolism following TBI. The treatment with SMI could improve water metabolism by promoting AQP1 expression.</p>