Significant age-related peculiarities in the dynamics of stroke volume and parameters of variational pulsogram are revealed in bilaterally vagotomized in rats. Asymmetry in vagal influences on cardiac function appear during puberty. Right-sided vagotomy predominantly affects variability of the cardiac rhythm, while left-sided vagotomy mostly affects the force of heart contractions.

Selective blocker of α(1A)-adrenoceptors WB4101 induced changes in heart rate in rats: it caused bradycardia in 3-, 6-, or 20-week-old rats (severity of bradycardia increased with increasing animal age) and increased heart rate in newborn rat pups.

Obsidan induced age-dependent bradycardia in intact rats and in rats with chemical sympathetic denervation. Subsequent vagal stimulation produced further decrease in heart rate. Administration of atropine to obsidan-treated rats increased heart rate. Key Words: rat; vagus; chemical sympathetic denervation; cardiac rhythm; obsidanThe degree of postvagotomy tachycardia varies in different species [7]. In small rodents the vagal tone is the lowest [5]. Inhibition of cardiotropic adrenergic influences produces only minor changes in heart rate in humans [9] and dogs [10]. The release of norepinephrine is regulated by adrenoreceptors of various types. Down-regulation of this release is mediated by ot-adrenoreceptors, while up-regulation is activated by stimulation of 13-adrenoreceptors [6]. However, the direct effect of catecholamines on postsynaptic 13-adrenoreceptors in the pacemakers cannot be ruled out [8]. Different effects of vagotomy on the dynamics of variational pulsogram were revealed in rats of different ages subjected to sympathetic denervation (SD) [2]. At the same time, electrical stimulation of the vagi resulted in proIound tachycardia both in intact and SD-animals [3].Our aim was to study the dynamics of cardiac variational pulsogram parameters in rats of different ages with SD produced by pharmacological means during vagal stimulation after blockade of cardiac [3-adrenoreceptors by obsidan. MATERIALS AND METHODSThe study was carried out on 4, 6, 8, and 20-week-old random-bred albino rats. The test group consisted of Department of Anatomy, Physiology and Human Health Protection, State Pedagogical University, Kazan SD rats. Chemical SD was pertbrmed in neonatal rats by daily subcutaneous injections of guanethidine sulfate (10 ml/kg body weight) during a 28-day period. The control group consisted of rats of the same age which were kept under identical conditions.Both the vagi and the right femoral vein were dissected in narcotized rats (urethane 800 mg/kg) under a microscope. Obsidan (0.8 mg/kg) and atropine (0.6 mg/kg) were injected intravenously.Vagal electrical stimulation was performed with 5-V pulses generated by an ESL-2 stimulator. Repetition rate, duration, and delay of the pulses were chosen individually tor every rat.The signals from an EKSP-02 electrocardiograph were fed into a C1-83 oscilloscope via an original interface and into a microcomputer via an F707732 digitizer. This computer was also used to control the set-up.The ECG was recorded and processed on-line [l ]. The original software calculated 13 parameters of the variational pulsogram from the arrays of the cardiointervals [4]. Six parameters were analyzed statistically: mean cardiointerval (Xmean), mode, amplitude of the mode, variation range (AX), standard deviation (8), and tension index (TI). RESULTSIntravenous injection of obsidan produced pronounced bradycardia in all age groups of intact and SD-ani-0007-4888/98/0012-l 184520.00 ~

Experiments on rats showed that blockade of hyperpolarization-activated currents moderates tachycardia induced by beta-adrenoceptor agonist isoproterenol and potentiates the increase in stroke volume produced by this agonist. Electrical stimulation of the vagus nerve against the background of isoproterenol treatment augmented bradycardia and increased stroke volume. Blockade of hyperpolarization-activated currents followed by application of isoproterenol moderated vagus-induced bradycardia and had no effect on the dynamics of stroke volume.