| Objective: In recent years, intermittent hypoxia (IH) had been proved to have protective effects on the heart. Our previous work showed that rats given 28 days of IH treatment, mimicking 5000m altitude, 6h/day, displayed a obvious cardiac protection, including prevention of arrhythmia induced by ischemia/reperfusion, increasing of antioxidant, reducing infarct size and limiting the contractile falling in ischemia/reperfusion rat heart.It is known that chronic intermittent hypercapnic hypoxia caused pulmonary hypertension, but effects of intermittent hypoxia on the systemic arterial blood pressure (SABP) are diverse. Different protocols cause different results. For instance, Fu Q reported 4 wk of intermittent hypobaric hypoxia exposure (3h/d, 5d/wk, and altitude of 4000-5000m) did not cause sustained alterations in autonomic control of blood pressure in young athletes. While systemic arterial pressure is frequently elevated in patients with obstructive sleep apnea syndrome (OSAS). Our previous study showed that the IH protocol we applied (5000m, 6h/day) could not alter SABP under normal condition, but availably prevented the decrease in SABP exposing to acute hypoxia. However the mechanism was not clear.As we all know, carotid sinus baroreflex (CSB) plays a key role in the rapid regulation of SABP. It is not known whether the CSB involves the protective effect of IH on SABP or the effects of IH on carotid sinus.Methods: Male Sprague-Dawley rats were randomly divided into three groups: control group (Con), 14-day IH treating group (IH14) and 28-day IH treating group (IH28). The IH rats were exposed to simulated high-altitude hypoxia in a hypobaric chamber mimicking 5000m altitude (O2:11.1%) 6h per day for 14 and 28d, respectively. The control animal lived in the same environment as the IH animals with free access to food and water, except that they breathed normal room air. So, the purpose of present study is to investigate effects of IH on CSB using perfusion of isolated carotid sinus area and to explore the underlying mechanism.Results1 Effects of intermittent hypoxia on carotid sinus baroreflexIH treatment (IH14 day, IH28 day) facilitated the CSB, shifting the functional curve of the baroreflex downward and leftward in a time-dependent manner. Peak slope (PS) markedly increased form 0.38±0.02 to 0.44±0.01 (P<0.01) and 0.57±0.02 mmHg/mmHg (P<0.01), respectively, and reflex decrease (RD) in blood pressure also markedly increased form 37.95±4.95 to 44.77±1.97 mmHg (P<0.01) and 57.30±2.47 mmHg (P<0.01), respectively. Meanwhile the threshold pressure (TP) was significantly decreased from 66.83±2.89 to 52.76±1.52 (P<0.01) and 47.36±1.93 mmHg (P<0.01), the equilibrium pressure (EP) decreased from 94.57±3.05 mmHg to 88.53±1.49 (P<0.01) and 84.52±1.65 mmHg (P<0.01), the saturation pressure (SP) decreased from 177.60±4.05 to 164.32±2.42(P<0.01) and 51.88±2.60 mmHg (P<0.01), respectively.2 Effects of glibenclamide on carotid sinus baroreflexAfter perfusing the isolated carotid sinus with K-H solution containing glibenclamide (Gli, 10μmol/L), there were no changes of functional parameters of CSB in Con and IH14 groups before and after Gli applying. But in IH28 group, peak slope (PS) decreased from 0.58±0.02 to 0.54±0.02 mmHg/mmHg (P<0.05); RD decreased from 58.96±2.51 to 54.35±2.85 mmHg (P<0.05);TP increased from 47.47±2.26 to 52.83±1.64 mmHg (P<0.01). While the facilitatory effect induced by IH was abolished partly in IH28 rats.3 Effects of L-NAME (100μmol/L) on carotid sinus baroreflex There were no changes of the facilitatory effects of carotid sinus baroreflex induced by intermittent hypoxia while L-NAME (100μmol/L) applying.Conclusion: Taken together, intermittent hypoxia facilitated carotid sinus baroreflex through opening KATP channels in anesthetized rats. |
PDF Full Text Request