dihydroergotoxine and Bradycardia

Topics: Adrenergic alpha-Antagonists; Aminophylline; Angina Pectoris; Bradycardia; Bronchial Diseases; Cerebrovascular Disorders; Coronary Circulation; Coronary Disease; Dementia; Dihydroergotoxine; Ethylamines; Furans; Humans; Hypotension; Injections, Intramuscular; Injections, Intravenous; Moxisylyte; Naphthalenes; Nitrates; Oxprenolol; Phenoxybenzamine; Practolol; Propionates; Propranolol; Vasodilator Agents

Dihydroergotoxine (0.01-0.3 mg kg-1 i.v.) decreased heart rate in pentobarbitone-anaesthetized rats. The bradycardia was reduced but not blocked by pre-treatment with guanethidine, yohimbine, propranolol or pithing. It was not prevented by bivagotomy, atropine, sulpiride or haloperidol. Dihydroergotoxine failed to affect, either the bradycardia produced by electrical stimulation of the vagus, or the cardioacceleration induced by i.v. isoprenaline. The increase in heart rate elicited in pithed rats by electrical stimulation of the spinal cord was reduced by dihydroergotoxine; this effect being inhibited by yohimbine but not by sulpiride. In conclusion, the main mechanism by which dihydroergotoxine (i.v.) induces bradycardia in the rat involves stimulation of alpha 2-adrenoceptors located predominantly at the cardiac sympathetic nerve endings.

Topics: Animals; Bradycardia; Decerebrate State; Dihydroergotoxine; Electric Stimulation; Heart Rate; Male; Rats; Rats, Inbred Strains; Spinal Cord; Vagus Nerve

The alpha-adrenergic blocking drugs, phentolamine and Hydergine, both act centrally at different sites to depress and enhance the pressor and sympathetic nerve response to decreased baroreceptor afferent input in anesthetized cats. Depression of the rise in blood pressure and sympathetic nerve discharge during bilateral carotid occlusion (BCO) followed injection of the agents into the 4th cerebral ventricle when the brain was intact but not when connections were interrupted at the midcollicular level by transection or lesion. Enhancement of responses occurred when drug distribution was confined to the brain rostral to the midcollicular level via injection into the 3rd cerebral ventricle with the cerebral aqueduct cannulated. Both agents decreased resting blood pressure and Hydergine decreased heart rate in intact and decerebrate preparations but not in 3rd ventricle-cerebral aqueduct experiments. We found that pretreatment with the noradrenergic precursor. L-dopa consistently prevented depression by phentolamine but was less effective against Hydergine. The results indicate that mechanisms which enhance and suppress the baroreceptor pressor response are normally operative in anesthetized cats and, furthermore, that neural pathways mediating the effects are ones connecting the caudal brainstem with supracollicular levels of the brain. It is further suggested that the pathways may be noradrenergic.

Topics: Animals; Arterial Occlusive Diseases; Bradycardia; Carotid Artery Diseases; Cats; Decerebrate State; Depression, Chemical; Dihydroergotoxine; Dose-Response Relationship, Drug; Hemodynamics; Injections, Intraventricular; Levodopa; Norepinephrine; Phentolamine; Phenylephrine; Pressoreceptors; Stimulation, Chemical; Superior Colliculi; Sympathetic Nervous System

Topics: Aged; Bradycardia; Cerebrovascular Disorders; Dementia; Dihydroergotoxine; Ergoloid Mesylates; Female; Humans; Male

Topics: Aged; Bradycardia; Dihydroergotoxine; Ergoloid Mesylates; Humans

Topics: Acetates; Adrenalectomy; Animals; Atropine; Bis-Trimethylammonium Compounds; Bradycardia; Carotid Sinus; Chlorpromazine; Cold Temperature; Decerebrate State; Dihydroergotoxine; Ergot Alkaloids; Heart Function Tests; Hexobarbital; Mice; Pharmacology; Procaine; Rats; Research; Vagotomy