Biomedical subjects

S Ellis

Publications and source records attributed to S Ellis.

At least 145 records · Page 8Linked to original sources

PubMed1985

Brevetoxins: chemistry and pharmacology of 'red tide' toxins from Ptychodiscus brevis (formerly Gymnodinium breve).

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Animals↗

PubMed1985

Cardiovascular effects of brevetoxins in dogs.

In anesthetized spontaneously breathing dogs, brevetoxin caused dose-dependent periods of apnea and, at high doses, respiratory arrest. In artificially ventilated dogs, i.v. brevetoxin caused complex dose-related cardiovascular changes consisting of: (1) bradycardia; (2) triphasic blood pressure changes, sequentially characterized by depressor/pressor/depressor phases; (3) cardiac arrhythmias including ventricular fibrillation; (4) muscle fasciculations. Prevention of bradycardia by atropine, vagotomy or ganglionic blockage unmasked a tachycardic action of the toxin. Ganglionic blockade, but not atropine or vagotomy, reduced the initial depressor effect of toxin. Phentolamine prevented the toxin-induced initial hypotension and secondary hypertension. Propranolol prevented the tachycardic and late depressor effects of toxin. In reserpinized dogs, low doses of toxin caused muscle fasciculations but none of the above cardiovascular effects; large doses caused bradycardia preventable by atropine, but not by vagotomy or chlorisondamine. These results suggest that brevetoxin: elicits the Bezold-Jarisch effect, i.e. initial hypotension, bradycardia and apnea; releases catecholamines, probably adrenal epinephrine, causing tachycardic, secondary pressor and late depressor effects; in large doses, releases vagal acetylcholine; -induced catecholamine and acetylcholine release is not nicotinic; produces effects, like those reported for veratridine, attributable to a common action on excitable membranes.

Animals↗

PubMed1985

Neurological analysis of respiratory, cardiovascular and neuromuscular effects of brevetoxin in cats.

Effects of brevetoxin were evaluated in cats anesthetized with pentobarbital under conditions of controlled end-expiratory pCO2 and constant body temperature. Recordings were made of arterial blood pressure, heart rate, respiratory pattern, diaphragm EMG, evoked tibialis muscle twitch and evoked contraction of the nictitating membrane. Electrical stimulation was employed for periodic excitation of the medullary respiratory center, the phrenic nerve, the peroneal nerve and the cervical sympathetic nerve. Brevetoxin was prepared at a concentration of 1.0 mg/ml in an aqueous medium of 2.5% ethanol plus 2.5% Emulphor 620 (General Aniline and Film Corp., New York). Small i.v. bolus injections of the toxin (40 micrograms/kg) evoked, without tachyphylaxis, the Bezold-Jarisch reflex triad of bradycardia, hypotension and bradypnea. This effect was essentially abolished by vagotomy. Continued injections then resulted in pressor reactions and tachycardia, along with the development of respiratory dysrhythmia. Large doses of brevetoxin (160 micrograms/kg i.v.) caused somatomotor seizures accompanied by severe hypertension, that occurred even after decerebration and cervical spinal cord transection. Cranial intra-arterial and intra-cerebroventricular injections of brevetoxin produced hypertension and respiratory depression more effectively than did i.v. injections. Systemic cumulation of the toxin, with the respiration supported artificially, caused death from cardiovascular collapse, without significant blockade of neuromuscular and ganglionic transmission. It is concluded that brevetoxin exerts its major toxic effects on the circulation and respiration through reflex and central actions, largely sparing peripheral motor mechanisms.

Animals↗

PubMed1985

Specific antagonism by RO 15-1788 of benzodiazepine-induced increases in food intake in rhesus monkeys.

Food intake of rhesus monkeys was limited to a single daily 2 hr session of banana flavored pellet availability, seven days a week. Following stabilization of intake, the effects of intragastric bromazepam, diazepam and pentobarbital, when given alone, were determined by delivering a dose twice weekly, 60 min before the session. Dose-dependent increases in food intake were observed with the following descending order of potencies: bromazepam, diazepam and pentobarbital. RO 15-1788 (0.5-1.0 mg/kg, IM), when given alone, five min before the session had no effect on food intake. When given in combination with bromazepam and diazepam, RO 15-1788 completely blocked the increases in food intake observed when the benzodiazepines were given alone. The specificity of this antagonism was shown by the failure of RO 15-1788 to alter the food intake increases induced by pentobarbital. These results confirm and extend previous reports of the specific antagonism of benzodiazepine behavioral effects by RO 15-1788 to an additional species and another behavioral effect of benzodiazepines.

Animals↗

PubMed1985