Ischemic-reperfusion injury of myocardium: from calcium paradox to free radicals
|Type:||Article in Proceedings|
|Keywords:||ischemia; reperfusion; myocardium; calcium paradox; free radicals|
Cardiac ischemia has been extensively studied for last several decades. This adverse state of myocardium is very important clinically as numerous patients in developed countries suffer from ischemic heart disease with all its consequences (e.g. myocardial infarction). Later, the crucial role of reperfusion – the period following the successful blood flow recovery, often caused by therapeutic interventions – has been widely investigated. Still, two mainstreams can be traced in the literature concerning ischemic-reperfusion injury of myocardium. One group of researchers focuses on the calcium overload phenomenon, the others study the role of reactive oxygen species (ROS) during ischemia and reperfusion. More recently, the terms preconditioning and postconditioning have been introduced and these events are intensely studied. The methods used for studying both electrical and mechanical events on the heart are of various origin and elaborateness. In our laboratory, the registration of monophasic action potential by means of voltage-sensitive dye di-4-ANEPPS is employed. However, very little is known about the direct effect of this compound on the heart muscle. Thus, the changes in electrogram, coronary flow and production of ROS measured by HPLC were followed. These parameters were studied in two animal models – the isolated heart of guinea pig and of rabbit. We may conclude that rabbit heart is a suitable model for studying ischemia-reperfusion injury at the organ level by voltage-sensitive dyes.