Objective: To study influence of acute hypoxia on the current of voltage-gated potassium channel (IK) in pulmonary artery smooth muscle cells (PASMC) of rats. Methods: A total of 20 male SD rats were randomly and equally divided into normoxic control group and acute hypoxia group. The rats in acute hypoxia group were kept in hypoxic chamber for 8 h before experiment. Whole cell patch-clamp technique was used to record IK in PASMC. Results: Acute hypoxia significantly decreased the IK density in PASMC of rats. During -60mV to -10mV of resting membrane potential（RMP）, acute hypoxia did not significantly decrease peak IK density in PASMC of rats, P>0.05; At 0 mV, acute hypoxia significantly decreased the peak IK density in PASMC [from（38.1 ± 5.2） pA / pF decreased to（9.82 ± 2.1） pA / pF ,P<0.05], then along with RMP increase in PASMC, the decreasing amplitude of peak IK density in PASMC gradually increased（P<0.05）; From + 30 mV to+ 60 mV, the decreasing amplitude of peak IK density in PASMC further significantly increased（P<0.01）; At + 60 mV the peak IK density decreased from（38.1 ± 5.2） pA / pF to（9.82 ± 2.1） pA / pF , and the decreasing amplitude reached (46.8±3.3)%. Conclusion: Acute hypoxia can decrease Kv current in PASMC of rats, leading to hypoxic pulmonary vasoconstriction.

OBJECTIVE: Hemorrhoidal disease (HD) is the most common proctological disease, with an estimated prevalence rate of 4.4%, and a peak in individuals between 45 and 65 years of age. This study was done to evaluate whether Lian-Zhi-San (LZS), a clinically used anti-hemorrhoidal ointment could alleviate the inflammatory injury, with its associated changes of inflammatory cytokines and morphology of anorectal tissues, in an experimental model of HD in rats. METHODS: HD was induced by croton oil preparation (COP) applied to the anorectal region. Rats were then treated with cotton swabs soaked in LZS ointment, water or white vaseline, twice a day for 7 d. At the end of the experiment, HD was evaluated by measuring hemorrhoidal and biochemical parameters along with histopathological observations. RESULTS: In this study, COP induced a significant increase in the macroscopic severity score, anorectal coefficient and Evans blue extravasation, compared to normal rats. Additionally, it greatly enhanced the expression and secretion levels of some important inflammation-related cytokines along with marked histological damage, compared to normal rats. Rats treated with LZS ointment experienced significantly ameliorated Evans blue extravasation (P < 0.05), decreased macroscopic severity score (0.86 ± 0.14 vs. 1.65 ± 0.16) and the anorectal coefficient (P < 0.01); its use also attenuated tissue damage and inhibited the expression and secretion levels of inflammation-related cytokines (interleukin-1β, interleukin-6 and tumor necrosis factor-α). CONCLUSION This study validates a preliminary understanding of the use of LZS ointment to treat inflammatory factors and tissue damage in an experimental model of HD in rats.

Objective     To investigate the effect of ginkgolide B (GB) on cysteinyl aspartate specific proteinase-3 (Caspase-3)/chromosome 10 deletion phosphatase-tension protein homologue (PTEN)/protein kinase B (Akt) pathway and cell proliferation and apoptosis in hypoxia/reoxygenation cardiomyocytes. Methods     H9C2 cells were cultured in vitro. A control group was cultured in serum-free DMEM high glucose medium at 37°C and 5% CO2 for 28 hours. The remaining groups were prepared with hypoxia/reoxygenation models. A GB low-dose group and a GB high-dose group were treated with GB pretreatment with final concentration of 50 μmol/L and 200 μmol/L respectively at 1 h before hypoxia/reoxygenation. A carvedilol group was treated with carvedilol of a final concentration of 10 μmol/L at 1 h before hypoxia/reoxygenation. The proliferation and apoptosis of H9C2 cells were detected, and the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), reactive oxygen species (ROS), PTEN, Akt, phosphorylated Akt (p-Akt) and Caspase-3 in H9C2 cells were also detected. Results     Compared with the control group, the proliferation rate of H9C2 cell, and the levels of PTEN, Akt and p-Akt in other groups decreased, and the apoptosis rate, and the levels of LDH, MDA, ROS and Caspase-3 increased (P<0.05). Compared with the hypoxia/reoxygenation group, the proliferation rate of H9C2 cell, and the levels of PTEN, Akt and p-Akt in all GB dose groups and the carvedilol group increased; the apoptosis rate, and the levels of LDH, MDA, ROS and Caspase-3 decreased, and the effect of GB was in a dose dependent manner; however, the effect of GB was not as strong as carvedilol (P<0.05). Conclusion     GB can inhibit H9C2 cell apoptosis and promote H9C2 cell proliferation by activating Caspase-3/PTEN/Akt pathway.