Alterations in cardiac function in response to epinephrine in rats with hereditary hypertension (An ECG study)

Abstract

A comparative electrocardiographic evaluation of changes in cardiac function in rats with hereditary arterial hypertension (NISAG strain) and normotensive (Wistar) rats in response to a single epinephrine injection revealed much more pronounced changes in NISAG rats, including an unfavorable time course of electrocardiographic waves (left ventricle overload) and impaired conduction (blockade) and excitability (extrasystoles). The results indicate that the myocardium of NISAG rats is much more responsive to the acute stimulation of adrenergic receptors by epinephrine than is the myocardium of normotensive rats. Key Words: hereditary arterial hypertension; heart; epinephrine; electrocardiographyThe strong reaction of the cardiovascular system to hormones, including epinephrine, that are secreted during stress is held to be one of the important mechanisms responsible for the development of arterial hypertension and associated complications such as myocardial infarction and stroke [1,6]. For this reason, adrenergic receptor blockers are used as agents to lower arterial pressure and protect the heart [8].A hypertensive rat strain, NISAG, was recently developed at the Institute of Cytology and Genetics of the Siberian Division of the Russian Academy of Sciences. The hypertensive status of these rats and the condition of their cardiovascular system can be judged by evaluating their responsiveness to epinephrine. Such an evaluation is of particular interest because arterial hypertension in this strain is established as a stress-dependent phenomenon [3, 4]. In the present electrocardiographic study we compared changes in cardiac function brought about by a single epinephrine injection in MATERIALS AND METHODSSix-month-old male Wistar and NISAG rats were used, 60 animals of each population. For the recording of the electrocardiogram (ECG), they were anesthetized with ether (etherrausch) and placed supine in a screened box. Needle electrodes were inserted under the skin of all four limbs and also in the chest region in three positions: one electrode along the midstemal line at the level of the apex beat and the other two 1 cm to the left and 1 cm to the fight of this line, which corresponds to the standard positions of the chest leads V~, V:, and V 3. The ECG was thus recorded in 3 standard leads, 3 augmented limb leads, and 3 unipolar chest leads. The recording was done on a Mingograph 34 cardiograph at a paper speed of 100 mm/sec and a channel sensitivity of 20 mm/mV. After the background ECG was recorded, each rat received a subcutaneous injection of epinephrine in a dose of 0.2 mg/100 g body weight. A second ECG was recorded ten minutes postinjection. The data were evaluated

State of the myocardium in rats of a new hypertensive strain

“…A parallel and more pronounced decrease in the Na content indicates, on the one hand, impaired ion transport and Na,K-ATPase function, and, on the other, can be considered as a compensatory reaction aimed at maintaining the myocardial contractile function [13]. However, these changes are unlikely to be adaptive and adequate, since each of them modulates the levels of all the cations and gives rise to pathogenetic changes in electrophysiological and structural parameters of the myocardium [6]. However, these changes are unlikely to be adaptive and adequate, since each of them modulates the levels of all the cations and gives rise to pathogenetic changes in electrophysiological and structural parameters of the myocardium [6].…”