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Biomedical subjects

M D Thames

Publications and source records attributed to M D Thames.

At least 109 records · Page 6Linked to original sources

Reflex inhibition of renal sympathetic nerve activity during myocardial ischemia mediated by left ventricular receptors with vagal afferents in dogs.

The major goal of this investigation was to determine if activation of cardiac receptors during coronary artery occlusion could inhibit efferent renal sympathetic nerve activity. In nine chloralose anesthetized dogs with only carotid (n = 3) or with sinoaortic (n = 6) baroreceptors operative, anterior descending coronary artery (LAD) occlusion resulted in a small decrease in mean arterial pressure (-9.8+/-5.1 mm Hg, NS) and in a significant (P < 0.05) increase in renal nerve activity (24.0+/-4.1%). In these dogs, circumflex coronary artery (Cx) occlusion resulted in greater hypotension (-18.4+/-4.0 mm Hg), and yet no change (1.1+/-9%) in renal nerve activity was noted. Changes in left atrial pressure during LAD and Cx occlusion were not different. In seven dogs with carotid sinus denervation, coronary occlusions resulted in decreases both in arterial pressure and in renal nerve activity which were consistently greater during Cx occlusion. The responses to coronary occlusion in six dogs after sinoaortic deafferentation were similar to those observed with only carotid sinuses denervated. In all experiments, vagotomy abolished the difference in the blood pressure responses and the decreases in renal sympathetic nerve activity during Cx occlusion. Vagotomy also abolished the decrease in nerve activity during LAD occlusion in dogs with carotid or sinoaortic denervation. These data show that Cx occlusion and, to a lesser degree, LAD occlusion resulted in reflex withdrawal of renal sympathetic nerve activity mediated by left ventricular receptors with vagal afferents. The reflex withdrawal of renal nerve activity during Cx occlusion occurred in spite of hypotension and the presence of functioning sinoaortic baroreceptors.

Animals↗

Preferential distribution of inhbititory cardiac receptors in left ventricle of the dog.

The purpose of this study was to determine the relative magnitudes of the reflex effects mediated by sensory endings in the left ventricle activated by intracoronary injection of nicotine or veratridine into left anterior descending (LAD) or circumflex (Cx) coronary arteries in the dog. Injection of nicotine or veratridine into the Cx consistently resulted in larger decreases in heart rate, arterial pressure, and in gracilis perfusion pressure than were observed following injection of the same dose into the LAD. Vagotomy abolished the cardioinhibitory and vasodepressor responses to intracoronary nicotine or veratridine. The weight of left ventricle perfused by LAD or Cx was not different (43.5 +/- 1.65 and 44.5 +/- 2.2 g, respectively. These data indicate that chemical activation of sensory endings with vagal afferents in the inferoposterior left ventricle of the dog results in larger cardionhibitor and vasodepressor responses than result from activation of respects in the anterior left ventricle. Further, these data provide strong evidence that these sensory endings which are chemically activated are preferentially distributed to the inferoposterior left ventricle.

Afferent Pathways↗

Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog.

The purpose of this study was to determine the relative magnitudes of the reflex effects mediated by cardiac receptors during anterior as opposed to inferoposterior ischemia of the left ventricle of the dog. Cessation of perfusion (coronary "occlusion") of the circumflex coronary artery (Cx) in 29 chloralose-anesthetized dogs with common carotids ligated (group I) resulted in significant bradycardia and hypotension, but in no significant change in perfusion pressure in the gracilis muscle perfused at constant flow. Occlusion of the left anterior descending coronary artery (LAD) produced less hypotension, no change in heart rate, and vasoconstriction in the gracilis. After vagotomy and aortic nerve section, no significant change in heart rate or gracilis perfusion pressure was observed during lad or Cx occlusion, and the blood pressure responses to LAD and Cx occlusion were not different. In nine dogs with sinoaortic denervation (group II), brief Cx occlusion resulted in bradycardia, hypotension, and vasodilation in the gracilis muscle. LAD occlusion in group II dogs caused less hypotension and no change in heart rate or gracilis perfusion pressure. After vagotomy, the bradycardia and vasodilation resulting from Cx occlusion were abolished and the blood pressure responses to LAD and Cx occlusion were not different. The weights of left ventricle perfused by each occluded vessel were not different. These data show that left ventricular receptors with vagal afferents which are activated during coronary occlusion and which mediate cardioinhibitory and vasodepressor responses are located mainly in the inferoposterior left ventricle of the dog heart.

Animals↗

Contribution of cardiopulmonary baroreceptors to the control of the kidney.

The role of cardiopulmonary receptors in the control of renal sympathetic nerve activity and of renin release is reviewed. The evidence indicates that cardiopulmonary receptors with vagal afferents exert a tonic inhibition on both renal nerve activity and on renin release. The magnitude of this inhibition appears directly related to changes in blood volume. Atrial as well as ventricular receptors can influence the secretion of renin. Cardiopulmonary receptors with vagal afferents may also reflexly modulate renal prostaglandin secretion. There is preliminary evidence to suggest that cardiopulmonary receptors with sympathetic afferents can influence renal nerve activity. The limitations of previous studies are outlined and a direction for future studies is suggested. It is concluded that alterations in cardiopulmonary vagal afferent input and the resulting changes in renal nerve activity and in renin release are appropriate for the maintenance of blood volume homeostasis.

Animals↗

Syncope in patients with pulmonary embolism.

A review of 132 consecutive cases of acute pulmonary embolism (PE) documented by pulmonary angiography indicated that syncope was the initial or predominant clinical feature in 17 (13%). When massive PE causes syncope in a nonhospitalized patient, the diagnosis of PE is frequently overlooked. Hypotension after PE may resolve spontaneously after a short interval. In this circumstance, the syncopal episode might easily be attributed to another cause. The appropriate diagnosis can be established only if other clues, suggestive of PE, are sought. Both arterial blood gas determinations and pulmonary scintigraphy are helpful in making this diagnosis.

Adult↗

Reflex suppression of renin release by ventricular receptors with vagal afferents.

Intracoronary injection of veratrum alkaloids is known to stimulate ventricular receptors with vagal afferents resulting in bradycardia and hypotension. This study examined the role of veratrum-sensitive ventricular receptors in the control of renin secretion in eight chloralose-anesthetized dogs. Hemorrhage of 10% caused renin release to increase significantly from a control of 778 to 1,971 ng/min. Arterial pressure and renal blood flow did not change significantly. The augmented release of renin during volume depletion was virtually abolished by injection of cryptenamine (2 microgram/kg) into the main left coronary artery, falling from 1,971 to 269 ng/min by 4 min after the cryptenamine injection. Blood pressure decreased significantly from 130 mmHg before to 111 mmHg after injection. Renal blood flow did not change significantly. This reflex suppression of renin release by excitation of ventricular receptors was abolished by vagotomy. These data indicate that ventricular receptors with vagal afferents participate in the reflex control of renin release.

Afferent Pathways↗

Behavior of cardiac receptors with nonmyelinated vagal afferents during spontaneous respiration in cats.

Activity from left atrial and left ventricular receptors with nonmyelinated vagal afferents (mean conduction velocity, 1.2 m/sec) was recorded in 13 closed-chest spontaneously breathing cats anesthetized with alpha-chloralose. The anatomic position of each receptor was determined by probing the opened heart at the conclusion of the experiment. Three of eight left atrial receptors and four of five left ventricular receptors were silent under resting conditions. The mean discharge frequency under resting conditons for the six receptors displaying spontaneous activity was 1.0 +/- 0.15 impulse/sec. Thus cardiac receptors with vagal nonmyelinated afferent have a low resting discharge in spontaneously breathing cats. The frequency and pattern of discharge of atrial but not of ventricular receptors was altered during spontaneous respiration. The atrial receptors discharged with cardiac rhythmicity during end inspiration and early expiration when transmural pressure was greatest and were silent for the remainder of the respiratory cycle. Whe respiration was augmented by CO2 breathing or blood volume was increased, the rate of discharge was a linear function of atrial transmural pressure. Eleven ventricular receptors with nonmyelinated afferents (mean conduction velocity, 1.0 m/sec) were exposed to graded volume expansion and phenylephrine infusion in eight open-chest and three spontaneously breathing cats. Raising left ventricular end-diastolic pressure alone increased the frequency of discharge, and a concomitant increase in systolic pressure caused a further increase in firing.

Animals↗

Ionic strength and the contraction kinetics of skinned muscle fibers.

The influence of KCl concentration on the contraction kinetics of skinned frog muscle fibers at 5-7 degrees C was studied at various calcium levels. The magnitude of the calcium-activated force decreased continuously as the KCl concentration of the bathing solution was increased from 0 to 280 mM. The shortening velocity at a given relative load was unaffected by the level of calcium activation at 140 mM KCl, as has been previously reported by Podolsky and Teichholz (1970. J. Physiol. [Lond.]. 211: 19), and was independent of ionic strength when the KCl concentration was increased from 140 to 280 mM. In contrast, the shortening velocity decreased as the KCl concentration was reduced below 140 mM; the decrease in velocity was enhanced when the fibers were only partially activated. In the low KCl range, the resting tension of the fibers increased after the first contraction cycle. The results suggest that in fibers activated at low ionic strength some of the cross bridges that are formed are abnormal in the sense that they retard shortening and persist in relaxing solution.

Adenosine Triphosphate↗