جستجوی مقالات مرتبط با کلیدواژه "پست کاندیشنینگ" در نشریات گروه "پزشکی"

Ischemic heart diseases are the leading cause of mortality in modern society and postconditioning is considered as a new therapeutic strategy in cardioprotection against ischemic insults. The purpose of this study was to investigate the effect of ischemic postconditioning on inflammation caused by ischemia-reperfusion myocardium injury in rat.

In this experimental study, 21 male Wistar rats were used and divided into three groups: control, ischemia-reperfusion and postconditioning. After surgery, the hearts of rats were isolated and mounted on a Langendorff apparatus with a constant pressure. In second and third groups, after 15-minutes stabilization period of cardiac function‚ the hearts were exposed to 30-minutes regional ischemia by occlusion of left anterior descending coronary artery and followed by 60-minutes reperfusion. In third group (postconditioning), postconditioning was exerted at the start of reperfusion by applying 3 alternative cycles of 30 seconds reperfusion and ischemia. The resulting supernatants of samples from ischemic zone of left ventricle were used to measure creatine kinase (CK) enzyme as in indicator of damage and inflammatory factors interlukin-6 (IL-6) and tumor necrosis factor (TNF-α) using laboratory kits via ELISA assay.

Ischemia-reperfusion significantly increased the level of myocardial CK enzyme as compared with control group (27±3 vs. 12±4 U/l) (p<0.05). In addition, the levels of inflammatory agents IL-6 and TNF-α were significantly increased in I/R group (p<0.05). Induction of postconditioning significantly reduced the CK level to about 17±3 U/l in third group and significantly decreased the levels of IL-6 and TNF-α as compared with those of I/R group (p<0.05).

Postconditioning can protect the heart by preventing the production of inflammatory agents in myocardium, and thereby reduce the reperfusion injury.

This study was aimed to investigate the effects of postconditioning by natural honey on cardiac arrhythmias in the ischemic isolated rat heart. Male Wistar rats were divided into four groups then anesthetized by sodium pentobarbital. The animal hearts were removed and quickly mounted on a Langendorff apparatus and perfused under constant pressure by a modified Krebs-Henseleit (K/H) solution that was previously equilibrated with 95% O2–5% CO2. The hearts were subjected to 30 min regional ischemia followed by 30 min reperfusion. In the control group, the hearts perfused by normal K/H solution, however in the postconditioning groups, they were perfused with natural honey (0.25, 0.5 and 1%) enriched K/H solution from 10 min before to 10 min after reperfusion. The ECGs were analyzed to determine the total number of ventricular ectopic beats (VEBs), ventricular tachycardia (VT), the incidence and duration of VT and ventricular fibrillation (VF) during last 10 min of ischemia and the first 30 min of reperfusion. During ischemia, honey (0.25, 0.5 and 1%) produced significant reduction in the number of VEBs and number, duration and incidence of VT (P<0.01). The incidence and time spent in VF were lowered by honey compared to the control group (P<0.05). During reperfusion time, all used concentrations of honey significantly reduced the number of VEBs (P<0.05). In addition, honey (0.5 and 1%) decreased the number and duration of VT (P<0.01 and P<0.05, respectively). Moreover, VF duration was lowered by perfusion of honey (0.25 and 0.5 %) versus the control group (P<0.05). The results showed protective effects of postconditioning by honey against ischemia-reperfusion injuries as anti-arrhythmic activities. Probably, antioxidant activity of honey, by scavenging of free radicals, and the presence of important energy sources such as glucose and fructose by improvement of cardiac function may involve in these protective effects.

In this study, effects of ischemic postconditioning (IPC) and pharmacologic postconditioning (PPC) by using L-Carnitine (L-Car) on infarct size in the ischemic-reperfused isolated rat heart were investigated and compared.

Male rats were divided in five groups (control, IPC, and three PPC groups treated by L-Car) and were anesthetized by sodium pentobarbital (50 mg/kg-ip). Heart was removed and quickly mounted on a Langendorff apparatus and perfused by a modified Krebs-Henseleit (K/H) solution that was previously equilibrated with 95% O2–5% CO2. The hearts were subjected to 30 min regional ischemia followed by 120 min reperfusion. In the control and IPC groups, the hearts were perfused by normal K/H solution at stabilization, 30 min regional ischemia and 120 min reperfusion, while PPC groups were perfused by 0., 2.5 and 5mM of L-Car enriched K/H solution 10 min before and after reperfusion. At the end of reperfusion, infarct size was determined by triphenyltetrazolium chloride method and computerized planimetry.

Infarct size was decreased significantly in both IPC and PPC groups versus control. In control group, infarct size was 46.3±2.9 %, however, IPC reduced it to 22.6±1.5 % (p<0.001). Application of 0.5, 2.5 and 5mM of Car-enriched K/H solution 10 min before and after reperfusion in the PPC groups, reduced the infarct size from control group value to 41.8±4.0 (not significant), 28.1±2.0 (p<0.001) and 25.4±. % (p<0.001), respectively. Except the effects of 0.5 mM L-Car, there was no significant difference between IPC and PPC groups on infarct size reduction.

Considering the results, it may be concluded that IPC and PPC (by L-Car) have protective effects against cardiac I/R injuries by reduction of infarct size.