In rabbits under nembutal anesthesia delta sleep-inducing peptide injected intravenously or directly into a ventricle of the brain raised the threshold for ventricular fibrillation. Its effect on the electrical stability of the heart after central administration developed later than after systemic administration. Bilateral vagotomy did not alter the central effects of this peptide.Key Words: electrical stability of the heart; delta sleep-inducing peptide; systemic and intraventricular administration An important development in research on the physiological activity of delta sleep-inducing peptide (DSIP) was the discovery of its ability to alleviate stress. DSIP was found to make animals more resistant to emotional stress and to prevent their death from cardiovascular disorders [4]. Studies into the mechanisms of the antistress effect revealed that the peptide produces this effect primarily by acting on the brain [6]. When injected into a brain ventricle, it blocks the behavioral and autonomic manifestations of negative emotional reactions in various animals [2,6].It has been established that the increased stability of cardiovascular functions shown by stressed animals administered DSIP is determined not only by its central action but also by its direct influence on the heart. For example, DSIP raises the thresholds for the elicitation of ventricular arrhythmias in intact animals, prolongs the effects of the vagus nerves on the heart and suppresses those of sympathetic nerves, and enhances or weak- ens, respectively, the effects of cholinergic and adrenergic transmitters [8]. Systemically administered DSIP normalizes the electrical stability of the heart and exhibits an antiarrhythmJc effect in emotional stress [1,8].Studies on the mechanisms of action of DSIP have thus demonstrated that central and peripheral effects can be produced by this peptide following its intracentral as well as intravenous administration. In view of the conflicting evidence regarding the permeability of the blood-brain barrier to DSIP [3,9,11] we compared in the present study the effects of DSIP on the electrical stability of the heart m rabbits after its intravenous injection with the effects after its injection directly into a brain ventricle. This work was undertaken to gain insight into the relationship between the central and peripheral mechanisms of DSIP action on the heart. MATERIALS AND METHODSAcute experiments were carried out on 28 male Chinchilla rabbits (body weight 2.0-2.5 kg) under Nembutal anesthesia (40 mg/kg). In 15 of the rabbits, the effect of DSIP on myocardial electri-
It is demonstrated that immobilization stress against the background of lowered catalase activity impairs the function of the sarcoplasmic reticulum Ca pump, particularly at high Ca 2+ levels. The membranes of intraceltular Ca 2+ depots are destroyed much more rapidly than in the control, which results in Ca 2 § release. Administration of delta sleep-inducing peptide to control animals results in a 30% increase in catalase activity for an unchanged level of superoxide dismutase and markedly improves the function of the Ca-transporting system at elevated levels of free Ca 2 § A long-term stress after administration of the peptide not only causes no damage to the Ca-transporting system but actually increases its efficiency (compared with the control) at a high catalase level.Key Words: delta sleep-inducing peptide; Ca pump; sarcoplasmic reticulum; superoxide dismutase; myocardium Stress-induced damage to myocardial ion-transporting systems: sarcolemmal Na,K-ATPase [6] and sarcoplasmic reticulum Ca-ATPase [13] resulting from the activation of lipid peroxidation (LPO) can be prevented by central and peripheral stress-limiting systems of the organism [5]. Adaptation to a short-term stress, which can prevent disturbances of the electrical stability of the heart and arrhythmias in stress, ischemia, reperfusion, myocardial infarction, and postinfarction cardiosclerosis [14], is an example of combined activation of the central and peripheral stresslimiting systems of the organism. Adaptation to stress also prevents stress-induced damage to the Na,K pump [6] and optimizes the function of the Ca pump [13], i.e., it triggers a mechanism that operates at the level of the heart, limits arrhythmias, and protects against alterations in Ca homeostasis.An important role of delta sleep-inducing peptide (DSIP) in adaptation has recently been recognized. It has been shown that, in addition to normalizing sleep, this peptide activates the monoaminergic transmitter and serotoninergic systems and, being an opiate receptor agonist, displays antidepressant and analgetic activities [3,11]. DSIP raises the resistance of animals to emotional stress [7], prevents their death from cardiovascular disorders [4], and elicits an antiarrhythmic effect in emotional stress [8]. Moreover, it prevents stress-induced sleep disorders in rabbits [15]. Administration of DSIP and its analogs forestalls activation of LPO in acute pancreatitis and cold stress and stabilizes tysosomal membranes [10]. Thus, DSIP elicits both central and peripheral effects, regardless of the route of administration. However, its effect on the electrical stability of the heart devel-
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