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Biomedical subjects

M C Koss

Publications and source records attributed to M C Koss.

106 records · Page 6Linked to original sources
PubMed1976

Inhibition of prostaglandin F2alpha-induced reflex bradycardia and hypotension by meclofenamic acid.

Intravenous injection of prostaglandin F2alpha (4-15 mug/kg, i.v.) produces an increase in pulmonary arterial pressure in conjunction with reflex bradycardia and hypotension in the anesthetized cat. Meclofenamic acid (30 mg/kg, i.v.) inhibited the bradycardia and the reflex contribution to the systemic hypotension. Neither the PGF2alpha-induced pulmonary vasoconstriction nor the direct systemic vasodilator actions of PGF2alpha were blocked by meclofenamate. In addition, the reflex responses caused by i.v. veratrine and 5-HT were not inhibited by meclofenamate. These results suggest that meclofenamic acid selectively blocks the afferent mechanism by which PGF2alpha induces reflex bradycardia and hypotension in the cat.

Animals↗
PubMed1976

Cardiovascular actions of prostaglanding F2alpha; 15-me-F2alpha; F1alpha; F2beta and F1beta in the cat.

Prostaglandin F2alpha (5mug/kg, i.v.) causes an increase in pulmonary arterial pressure, decrease in systemic arterial pressure, and reflex bradycardia in the anesthetized cat. The same dose of the 15-methyl analogue of PGF2alpha produces the same triad of effects but of greater magnitude and duration. Although prostaglandins F1alpha, F2beta and F1beta also cause the same cardiovascular effects as F2alpha, there is a decrease in potency for all parameters measured, with PGF2alpha greater than PGF1alpha greater than PGF2beta greater than PGF 1beta. When compared to the actions of PGF2alpha in producing an increase in pulmonary arterial pressure, PGs F1alpha, F2beta and F1beta were less potent by approximately 10, 100, and 1000 fold respectively.

Animals↗
PubMed1976

Reflex bradycardia and hypotension produced by prostaglandin F2alpha in the cat.

1 Intravenous administration of prostaglandin F2alpha results in a dose-dependent increase in pulmonary arterial pressure, decrease in systemic arterial pressure and a delayed bradycardia. Pulmonary vasoconstriction was observed at doses as low as 0.1 and 0.3 mug/kg. The systemic depressor and heart rate lowering effects were observed at 1 mug/kg doses and above. 2 A moderate bradycardia was still observed after atropine blockade but was abolished following bilateral vagotomy. Neither of these procedures affected the pulmonary vascular response. 3 Injections of submaximal doses of prostaglandin F2alpha (1--4 mug/kg) produced a greater and longer lasting bradycardia when injected into the left atrium than was observed following intravenous administration. In addition the latency of onset was much shorter following left atrial injection. These doses resulted in no change in heart rate and a minimal hypotension when injected into the brachiocephalic artery or into the aortic arch. 4 Small doses of prostaglandin F2alpha administered at the level of the origin of the coronary arteries produced marked decreases in heart rate and blood pressure whereas no change occurred following injection of the same amount into the ascending aorta at more distal sites. 5 These results suggest that prostaglandin F2alpha produces bradycardia and hypotension in the cat by activating 'receptors' located in the left heart or by acting on structures perfused by means of the coronary arteries.

Animals↗
PubMed1976

Differential transmission in the superior cervical ganglion of the cat.

Mechanisms in the superior cervical ganglion resulting in contraction of the nictitating membrane (NM) and dilation of the parasympathectimized pupil were studies in anesthetized cats. Frequency-response curves were obtained following pregangionic stimulation with NM and pupillary responses recorded simultaneously in the same preparations.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1976

Analysis of clonidine-induced mydriasis.

In addition to its centrally mediated hypotensive action, clonidine causes a decrease in intraocular pressure associated with a long-lasting mydriasis. The present study was conducted to determine to what extent this drug-induced pupillary dilation is of central or peripheral origin. Pupil size was observed in cats anesthetized with pentobarbital. Clonidine (1 to 100 mug per kilogram, intravenously) resulted in a dose-dependent increase in pupillary diameter in intact as well as sympathectomized preparations. These same doses of clonidine produce no effect on the eserinized, parasympathectomized iris. Epinephrine administration (0.1 to 30 mug, intra-arterially) produced an equivalent pupillary dilation in all preparations. In addition, clonidine caused a dramatic decrease in postganglionic ciliary nerve activity and both the decreased nerve activity and pupillary dilation were reversed by intravenous administration of yohimbine hydrochloride. These results suggest that the inhibition of parasympathetic tone by clonidine may involve a central adrenergic inhibitory mechanism.

Animals↗
PubMed1975

Brainstem loci for activation of electrodermal response in the cat.

Brainstem loci from which electrodermal responses could be elicited were systematically explored by direct-stimulation techniques in chloralose-anesthetized and decerebrate cats. Reactive sites of the greatest amplitude were found to extend from the rostral border of the posterior hypothalamus, through the ventrolateral reticular formation of the pons and the medulla, to the cervical cord. Stimulation of these sites elicited stable, reproducible electrodermal responses of 10-30 mV in amplitude. In addition, it was found that stimulation of the ventrolateral extent of the lower brainstem evoked similar responses in the decerebrate preparation. Electrodermal responses could not be elicited from the dorsal medulla, the posterior commissure, or the midline region. The electrodermal response could be elicited from an apparently hypothalamus through the ventrolateral brainstem.

Animals↗
PubMedDate not supplied

Some physiologic characteristics of the electrodermal reflex in the cat.

The amplitudes of electrodermal reflexes evoked in intact cats were compared under a variety of anesthetic conditions. Electrodermal reflexes were elicited in both decerebrate and spinal preparations with and without anesthesia. Reflex amplitude was significantly depressed in the anesthetized preparation after decerebration or spinal transection. In contrast, spinal transection performed after decerebration in unanesthetized preparations significantly increased the amplitude of the reflex. The evidence presented in this study supports the concept of a primarily inhibitory lower brainstem system with regard to this reflex. The relative stability of the reflex amplitude in the anesthetized cat suggests that this reflex system could be useful in the analysis of the effects of drugs acting on the central nervous system.

Anesthesia↗