Abstract
This investigation is aimed at examining the effects of pharmacological PostC with potassium cyanide (KCN) on functional recovery, gene expression, cytochrome c expression, and redox status of isolated rat hearts. Rats were divided into the control and KCN groups. The hearts of male Wistar albino rats were retrogradely perfused according to the Langendorff technique at a constant perfusion pressure of 70 cmH2O. After stabilisation, control hearts were subjected to global ischemia (5 minutes), followed by reperfusion (5 minutes), while experimental hearts underwent global ischemia (5 minutes) followed by 5 minutes of reperfusion with 10 μmol/L KCN. The following parameters of heart function were measured: maximum and minimum rates of pressure development, systolic and diastolic left ventricular pressure, heart rate, and coronary flow. Levels of superoxide anion radical, hydrogen peroxide, nitrites, and index of lipid peroxidation (measured as thiobarbituric acid-reactive substances) were measured in coronary venous effluent, and activity of catalase was determined in heart tissue. Expression of Bax, Bcl-2, SOD-1, SOD-2, and cytochrome c was studied as well. It was shown that expression of Bax, Bcl-2, and SOD-2 genes did not significantly differ between groups, while expression of SOD-1 gene and cytochrome c was lower in the KCN group. Our results demonstrated that KCN improved the recovery of myocardial contractility and systolic and diastolic function, enhanced catalase activity, and diminished generation of prooxidants. However, all possible mechanisms and potential adverse effects of KCN should be further examined in the future.
Highlights
The leading causes of morbidity and mortality nowadays are cardiovascular diseases
Ischemic PostC is an adaptive response induced by short periods of ischemia alternating with short periods of reperfusion applied at onset of reperfusion after continuous ischemia; the similar effects can be caused by pharmacological agents as well [9]
In the KCN group, dp/dt max values at S (2657.08 ± 252.2) and R1 (2645.56 ± 220.2) were similar; a statistically significant increase was noticed at R2 (3370.32 ± 210.3)
Summary
The leading causes of morbidity and mortality nowadays are cardiovascular diseases. Acute myocardial infarction probably represents the most often variety within this pathophysiological entity due to reduction of coronary blood flow and myocardial ischemia. Reperfusion strategies can be used for rescuing the myocardium, but immediate reperfusion of ischemic myocardial tissue can paradoxically induce further damage known as the phenomenon of “reperfusion injury.”. The beneficial effect of ischemic PostC involves postponed reversal of acidosis, activation of protein kinase C (PKC), formation of autacoids, such as adenosine and bradykinin, and release of endogenous opioids [5]. Ischemic PostC may diminish the harmful effects of reactive oxygen species (ROS), bearing in mind that oxidative burst during reperfusion remains one of the major factors responsible for reperfusion injury [8]. Ischemic PostC is an adaptive response induced by short periods of ischemia alternating with short periods of reperfusion applied at onset of reperfusion after continuous ischemia; the similar effects can be caused by pharmacological agents as well [9]
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