Vascular Protection with Less Activation Evoked by Progressive Thermal Preconditioning in Adrenergic Receptor-Mediated Hypertension and Tachycardia

10.4077/CJP.2009.AMH048

Shih-Chung Huang；Yi-Fen Tsai；Yu-Shuan Cheng；Ko-Hua Liu；Ping-Chia Li；Chiang-Ting Chien

progressive thermal preconditioning ； FeCl3 ； heat shock protein ； adrenergic receptor ； thrombosis

The Chinese Journal of Physiology

52卷6期（2009 / 12 / 01）

419 - 425

英文

Thermal preconditioning may afford cardiovascular protection against oxidative injuries. However, hypertension and taychardia by sympathetic stimulation frequently occur during 42°C whole body thermal preconditioning (TP). We aimed to develop a modified TP to achieve cardiovascular protection with to reduced cardiovascular stimulation in the rat. We used a progressive thermal preconditioning (PTP) with three-step 5-min immersion of male Wistar rats in 42℃ bath water. Treatment with phentolamine (α-adrenergic blocker), propranolol (β-adrenergic blocker) and atropine (muscarinic cholinergic blocker) was used to evaluate the effect and mechanism of PTP on systemic hemodynamics. Protective function was evaluated by FeCl3-induced acute femoral arterial occlusion (TTO) and heat shock protein 70 expression. Our results show that TP enhanced body temperature, hypertension and tachycardia. However, PTP produced a similar increase in body temperature with significantly less enhancement of hypertension and tachycardia when compared with the TP group. TP-or PTP-induced increase of blood pressure and heart rate was inhibited by phentolamine and propranolol, respectively. PTPinduced attenuation of changes in hemodynamic parameters was via α- and β-adrenergic inhibition. FeCl3 induced femoral arterial injury indicated by TTO at 416±51 sec in the control rats. After 24 h of TP or PTP treatment with or without adrenergic blocker treatment, TP or PTP upregulated similar femoral arterial heat shock protein 70 expression and significantly (P＜0.05) delayed FeCl3-induced femoral TTO to a similar degree. PTP may provide vascular protection against oxidative injuries with less activation in α-adrenergic receptor-mediated hypertension and β-adrenergic receptor-mediated tachycardia.

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