ABSTRACT
Aim To observe the cardioprotection of chronic intermittent hypobaric hypoxia (CIHH) against ischemia/reperfusion injury in adult and young rats.Methods Adult and postnatal male Sprague-Dawley rats were divided randomly into four groups:control 28-day group (CON28),control 42-day group (CON42), CIHH 28-day treatment group (CIHH28), and CIHH 42-day treatment group (CIHH42). CIHH animals with maternal rats were put into a hypobaric chamber 2 days before birth to get 28 days and 42 days CIHH mimicking 3000 m altitude (P_B=525 mmHg,P_(O_2)=108.8 mmHg), 5 h daily, respectively.The control animals were kept in the same environment as CIHH rats with free access to water and food except hypoxic exposure. The isolated hearts were perfused in the Langendorff apparatus, undergoing 30 min global ischemia and 60 min reperfusion.Cardiac function was recorded continuously during the whole experiment. Parameters of left ventricular function included left ventricular developing pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), maximal positive (+LVdp/dt) and negative (-LVdp/dt) velocity of left ventricular pressure, coronary flow (CF) and heart rate(HR).Results ① For adult rats, there was no significant difference in the parameters of left ventricular function between CIHH28 and CON28 groups. However, the recovery of cardiac function in CIHH42 rats was much better than that in CON42, including LVDP, LVEDP, ±LVdp/dt and CF (P<0.05). ② For young rats, the basic coronary flow (CF) in CIHH rats was significant higher than that in CON rats, while other parameters of cardiac function didn't change. The recovery of cardiac function in CIHH rats was much better than that in CON rats, including LVDP, LVEDP,±LVdp/dt and CF (P<0.05).Conclusion CIHH confers cardioprotection against ischemia/reperfusion injury in rat cardiomyocytes, which is predominant in CIHH42 group and significantly affected by the age of animals. Cardioprotective effects produce more easily in young rats by CIHH.
ABSTRACT
AIM To study the relationship between cardioprotective effects of resveratrol and carotid sinus baroreflex (CSB). METHODS The functional curve of the CSB was measured by recording changes in arterial pressure in anesthetized male rats with perfused isolated carotid sinus. RESULTS Resveratrol (30, 60 and 120 μmol·L-1) inhibited the CSB, which shifted the functional curve of the baroreflex to the right and upward. There were a marked decrease in peak slope and a reflex decrease of blood pressure, and also an increase in threshold pressure. Changes of these parameters showed a concentration-dependent manner. Pretreatment with Nω-nitro-L-arginine methylester (100 μmol·L-1), an inhibitor of nitric oxide synthase, and pretreatment with Bay K8644 (500 nmol·L-1), an agonist of L-type calcium channel, could both eliminate the inhibitory effect of resveratrol on CSB. A potent inhibitor of tyrosine phosphatase sodium orthovanadate (1 mmol·L-1) did not influence the effect of resveratrol on CSB. CONCLUSION Resveratrol inhibits carotid baroreflex, which may be mediated by the locally released NO and decreased calcium influx.
ABSTRACT
This study is to evaluate the effect of resveratrol on carotid baroreceptor activity (CBA). The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus. Resveratrol (30, 60 and 120 μmol·L-1) inhibited CBA, which shifted FCCB to the right and downward. There was a marked decrease in peak slope (PS) and peak integral value (PIV) of carotid sinus nerve charge in a concentration-dependent manner. Pretreatment with Nω-nitro-L-arginine methyl ester (L-NAME, 100 μmol·L-1), an inhibitor of nitric oxide synthase (NOS), eliminated the inhibitory effect of resveratrol. Pretreatment with Bay K8644 (an agonist of L-type calcium channel, 500 nmol·L-1) abolished the effect of resveratrol on CBA. A potent inhibitor of tyrosine phosphatase (sodium orthovanadate, 1 mmol·L-1) did not influence the effect of resveratrol on CBA. Resveratrol inhibits carotid baroreceptor activity, which may be mediated by the locally released NO and decreased calcium influx. Several studies have showed a cardioprotective effect of resveratrol, with the penetrating study of resveratrol, it may show a potential value in the clinical treatment of cardiovascular disease as an alternative medicine.
ABSTRACT
AIM In order to investigate whether resveratrol can be used as a kind of antiarrhythmic drug, the electrophysiological effect of resveratrol on pacemaker cells in sinoatrial node was studied. METHODS Using intracellular microelectrode technique to record the action potential of pacemaker cells in sinoatrial node of rabbits. RESULTS Resveratrol (30-120 μmol·L-1) significantly decreased amplitude of action potential, maximal rate of depolarization (Vmax), velocity of diastolic (phase 4) depolarization and rate of pacemaker firing, but did not affect maximal diastolic potential and duration of 90% repolarization of action potential. Pretreatment with L-type calcium channel agonist Bay-K-8644 (0.5 μmol·L-1) 10 min antagonized the effect of resveratrol (60 μmol·L-1). While applying cesium chloride (2 mmol·L-1), a hyperpolarization-activated current blocker, adding tetraethylammonium chloride (20 mmol·L-1), a potassium channel antagonist, or applying L-NAME (0.5 mmol·L-1), a NO synthase inhibitor, had no significantly influence on the electrophysiological effects of resveratrol. CONCLUSION Resveratrol exerts inhibitory electrophysiological effects on pacemaker cells in sinoatrial node of rabbits, which may be due to reduction in calcium influx via a NO-independent manner.