Biomedical subjects

I Cavero

Publications and source records attributed to I Cavero.

At least 127 records · Page 7Linked to original sources

PubMed1976

Analysis of cardiac chronotropic responses to some autonomic blocking agents in conscious trained dogs.

The changes of heart rate in response to i.v. administration of methylatropine (0.5 mg/kg) and/or propranolol (2 mg/Kg) or practolol (2.5 mg/Kg) were studied in conscious trained dogs. Cholinergic blockade alone or combined blockade of sympathetic and parasympathetic effector systems resulted in cardiac acceleration. Conversely, beta-adrenoceptor antagonism with either propranolol or practolol reduced heart rate. The data were analysed by means of a new method, whereby the heart (HRN) of the dog is considered to be the product of the intrinsic heart rate (HR0) and 3 further factors: HRN-HR0 times S times V times W (Multiplicative model). 2 of these factors represent the tonic sympathetic (S) and parasympathetic (V) influences, whereas the third (W) represents the sympathetic-parasympathetic interaction. This type of analysis reveals that W was approximately 1, i.e., the sympathetic-parasympathetic interaction did not play any significant role in determining the heart rate of conscious resting dogs (HRN = HRO-S-V-W = HRO-S-V). The change of heart rate due to the action of parasympathetic system (-53% of the intrinsic heart rate) was more important than the change caused by the action of the sympathetic system (26% of the intrinsic heart rate).

Animals↗

PubMed1976

Analysis of cardiac chronotropic responses to diazepam and bromazepam in conscious trained dogs.

In conscious trained dogs, administration of bromazepam (0.3 mg/kg p.o.) or diazepam (0.3 and 1.0 mg/kg p.o.) had no influence on heart rate. A higher dose (10 mg/kg p.o.) of two benzodiazepines elicited a positive chronotropic effect which was rapid in onset and of long duration. The beta-adrenoceptor blocking agent practolol (2.5 mg/kg i.v.) did not revert heart rate after the benzodiazepines to the same level as in controls, indicating that the tachycardia was not produced by an increase in sympathetic outflow to the heart. For diazepam, a sympathetic--parasympathetic interaction cannot be excluded. However, diazepam and bromazepam significantly reduced the tachycardia which is normally observed after administration of methylatropine (0.5 mg/kg i.v.) alone or in combination with practolol. In anaesthetized dogs, bromazepam failed to modify the heart rate responses to electrical stimulation of cardiac vagal or sympathetic nerves, excluding an action on this compound on ganglionic transmission and cardiac cholinoceptors and adrenoceptors. It is concluded that high doses of diazepam and bromazepam influence the heart rate of conscious dogs in a biphasic way. Firstly, they cause a central reduction of vagal tone to the heart resulting in tachycardia. Secondly, the two drugs decrease the cardiac pacemaker rate directly. Since the overall effect is tachycardia, the central action is more pronounced.

Administration, Oral↗

PubMed1976

Time-course effects of oral guanethidine administration on cardiovascular and autonomic effects on dogs.

The time-course effects of guanethidine (2.5 mb/kg/day, p.o.) administered for 2 days, 7 days and 7-8 months were investigated in dogs. Guanethidine treatment for 2 days failed to produce any significant alterations in sympathetic neuronal activity to the myocardium, resting neurogenic tone in the perfused hind limb vasculature and lumbar sympathetic neuronal transmission. Following guanethidine administration for a peroid of 7 days both cardiac and lumbar sympathetic neuronal activity was markedly and significantly depressed with concomitant reduction in heart rate and resting neurogenic tone to the hind limb. However, continued treatment with guanethidine for a period of 7-8 months resulted in complete restoration of cardiac as well as lumbar sympathetic neuronal activity. Both heart rate and resting neurogenic tone were also returned to placebo levels. The development of tolerance of these sympathetic nerves to guanethidine treatment was not associated with any alterations in the activity of adrenergic receptors. Further, there was a significant and time-dependent increase in cholinergic vasocilator activity in the lumbar sympathetic chain which could account for the exertional hypotension noted in the patients receiving guanethidine treatment.

Administration, Oral↗

PubMed1976

Cardiovascular effects of prazosin in dogs.

1. In pentobarbitone-anaesthetized dogs, prazosin (2 x 1-3 micronmol day-1 kg-1; 2 x 0-5 mg day-1 kg-1) administered orally for 3 days reduced resting aortic blood pressure as well as the pressor response to bilateral carotid occlusion. Prazosin neither affected resting heart rate nor the tachycardia induced by intravenous isoprenaline, noradrenaline and electrical stimulation of preganglionic and postganglionic sympathetic nerve fibres. Prazosin significantly attenuated the fall in perfusion pressure in a perfused hind leg resulting from the section of the ipsilateral sympathetic lumbar chain. Furthermore, the drug inhibited by about 50% the hind-leg pressor responses elicited by intra-arterial administration of alpha-adrenoreceptor agonists and by stimulation of the lumbar sympathetic chain, without altering the effects of angiotension II. 2. Acute administration of prazosin into the innervated hind leg provoked a dose-related reduction in vascular resistance. However, after spinal anaesthesia no such an effect was observed even when vascular tone was increased by infusion of vasopressin. Under the same experimental conditions administration of papaverine induced a vasodilatation. 3. This study confirms that prazosin impairs the function of vascular alpha-adrenoreceptors, and strongly challenges the claim that this compound produces a directly mediated vasodilatation of the leg vascular bed.

Animals↗

PubMed1975

Effects of chronic guanethidine administration on cardiovascular function of dogs.

Chronic guanethidine administration 2.5 mg/kg/day for 7 to 8 months did not produce any essential changes in blood pressure and heart rate of the anesthetized dogs while there was a significant elevation of stroke volume and stroke work. There was a reduction in total peripheral resistance and an increase in cardiac output in the treated dogs in comparison with the placebo group. Ventricular function curves obtained in both the treated and placebo group were virtually identical. The data suggested that chronic guanethidine administration did not induce any adverse effect on myocardial functions.

Animals↗

PubMed1974