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Biomedical subjects

F M Abboud

Publications and source records attributed to F M Abboud.

At least 127 records · Page 7Linked to original sources
PubMed1979

Interaction of somatic and cardiopulmonary receptors in control of renal circulation.

The purpose of this study was to determine if there is an important interaction between somatic and cardipulmonary receptors in the control of vasomotor outflow to the kidney. This interaction was examined by determining the renal vasoconstrictor responses to afferent electrical stimulation (30 V, 1 ms, 20--40 Hz) of the sectioned sciatic nerve in 8 chloralose-anesthetized dogs with sinoaortic deafferentation. During isovolemia, sciatic stimulation resulted in significant increases in arterial pressure and heart rate, and in renal vasoconstriction. Volume expansion significantly attenuated and vagotomy significantly augmented the renal vasoconstrictor responses to sciatic stimulation. These interventions did not significantly influence the arterial pressure or heart rate responses to sciatic stimulation. In 4 dogs with aortic nerves sectioned and carotid sinuses isolated and perfused at constant pressure (135 mmHg), the renal vasoconstrictor responses to stimulation were attenuated by volume expansion and augmented by vagotomy. These data show that in the absence of the arterial baroreceptors or with intermediate levels of carotid baroreceptor activation, volume expansion and, thus, augementation of discharge of cardiopulmonary receptors (vagal afferents) markedly attenuated the renal vasoconstrictor responses to somatic afferent stimulation.

Animals↗
PubMed1979

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↗
PubMed1978

Influence of low- and high-pressure baroreceptors on plasma renin activity in humans.

We evaluated effects of the low- and high-pressure baroreceptors on plasma renin activity (immunoassay) using graded lower body suction (LBS) in six healthy men. LBS at -10 and -20 mmHg for 10 min decreased central venous pressure without changing arterial pressure and thereby presumably reduced low- but not high-pressure baroreceptor inhibition of renin release. LBS at these levels produced forearm vasoconstriction, but did not increase renin. LBS at -40 mmHg decreased central venous and arterial pulse pressure and thus reduced both low- and high-pressure baroreceptor inhibition. LBS at this level produced forearm vasoconstriction and tachycardia and increased renin from 2.1 +/- 0.4 (mean +/- SE to 7.4 +/- 1.4 ng.ml-1.h-1 (P less than 0.05). In summary, reduction in low-pressure baroreceptor inhibition in humans did not increase renin in the presence of physiological tonic inhibition from high-pressure baroreceptors. Increases in renin did not occur until there was combined reduction of high- and low-pressure baroreceptor inhibition on plasma renin activity.

Adult↗
PubMed1978

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↗
PubMed1978

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↗
PubMed1978

Depression of ventilation by dopamine in man. Evidence for an effect on the chemoreceptor reflex.

Dopamine is present in the carotid body and has been postulated to be an inhibitory neurotransmitter. The purpose of this study was to determine the effects of dopamine on ventilation in man and to examine its mechanism of action. Dopamine (0.5-10 mug/kg per min) was infused in eight normal men at different levels of arterial chemoreceptor activity, produced by varying the inspired Po(2). During normoxia dopamine produced a small decrease in minute ventilation (Ve) and an increase in arterial Pco(2). When arterial chemoreceptors were stimulated by hypoxia, infusion of dopamine produced a marked initial depression of Ve followed by a sustained although less pronounced decrease in Ve. An increase in Pa(co) (2) and a decrease in Pao(2) were also observed. When arterial chemoreceptor activity was suppressed by hyperoxia, infusion of dopamine did not affect ventilation. Subjects also breathed a hypercarbic, hyperoxic gas mixture. The hypercarbia produces hyperventilation by stimulating central chemoreceptors, whereas the hyperoxia suppresses peripheral chemoreceptors. Dopamine did not alter ventilation while the subjects were breathing this gas mixture. These studies suggest that dopamine suppresses ventilation in man through an action on the arterial chemoreceptor reflex. These findings support the hypothesis that dopamine is an inhibitory neurotransmitter in the carotid body, and that release of dopamine may modulate the sensitivity of peripheral arterial chemoreceptors.

Adult↗
PubMed1978

Regulation of blood flow to the aortic media in dogs.

Morphologic observations suggest that the inner layers of the thoracic aorta in man and dog are avascular and the outer layers have vasa vasorum. It appears that vasa vasorum are essential in the thoracic aorta because their interruption produces medial necrosis. These experiments provide the first measurements of blood flow through aortic vasa vasorum and examine physiologic regulation of that flow. During control conditions the outer two-thirds of the media of the thoracic aorta received 10 ml/min per 100 g blood flow through vasa vasorum. Flow to the inner third of the aorta was 1 ml/min per 100 g. Flow to both the inner and outer media of the abdominal aorta was less than 1 ml/min per 100 g. Adenosine increased blood flow to vasa vasorum in the outer media of the thoracic aorta from 7 to 18 ml/min per 100 g, but did not increase flow to the inner layers of the aorta. Hemorrhagic hypotension decreased flow in the outer media of the thoracic aorta from 14 to 2 ml/min per 100 g. Acute hypertension failed to increase blood flow through vasa vasorum, as conductance decreased significantly. These studies indicate that vasa vasorum provide a considerable amount of blood flow to the outer layers of the thoracic aorta. The vessels are responsive to physiologic stimuli because they dilate during infusion of adenosine and constrict during both hemorrhagic hypotension and acute hypertension. We speculate that the failure of blood flow to the aortic wall to increase during acute hypertension might, if it were sustained, contribute to aortic medial necrosis.

Adenosine↗
PubMed1978

Role of large arteries in regulation of cerebral blood flow in dogs.

Previous studies have demonstrated a significant pressure gradient from carotid artery to pial or middle cerebral arteries. This pressure gradient suggests that large cerebral arteries contribute to cerebral resistance. We have tested the hypothesis that large cerebral arteries contribute to regulation of cerebral blood flow during changes in blood gases and arterial pressure. Microspheres were used to measure brain blood flow in anesthetized dogs. Resistance of large cerebral arteries was estimated by determining the pressure gradient between common carotid and wedged vertebral artery catheters. Systemic hypercapnia and hypoxia dilated large cerebral arteries, and hypocapnia constricted large cerebral arteries. Resistance of large arteries was 0.6+/-0.1 (mean +/- SE) mm Hg per ml/min per 100 g during normocapnia. During hypercapnia and hypoxia, large artery resistance decreased significantly to 0.2 +/- 0.03 and 0.3 +/- 0.05, respectively. During hypocapnia large artery resistance increased significantly to 1.0 +/- 0.1. In other experiments, we found that large cerebral arteries participate in auto-regulatory responses to hemorrhagic hypotension. When arterial pressure was reduced from 110 to 58 mm Hg, autoregulation maintained cerebral blood flow constant, and resistance of large cerebral arteries decreased significantly from 1.0 +/- 0.2 to 0.6 +/- 0.1 mm Hg per ml/min per 100 g. In absolute terms, we calculated that 20-45% of the change in total cerebral resistance during these interventions was accounted for by changes in large artery resistance. These studies indicate that large cerebral arteries, as well as arterioles, participate actively in regulation of cerebral blood flow during changes in arterial blood gases and during autoregulatory responses to hemorrhagic hypotension.

Animals↗
PubMed1977

Echocardiography in experimentally-induced myocardial ischemia.

Using an experimental canine model, we have employed echocardiography to study segmental dyskinesis produced by acute coronary occlusion. Characteristic alterations in posterior wall and septal motion occur after acute coronary ligation; these resemble clinical abnormalities described in acute and old myocardial infarction. The degree of dyskinesis produced is directly related to the severity of the perfusion deficit. Coronary reperfusion had variable effects on dyskinesis; most animals showed improvement but in some the myocardial contraction abnormalities became more severe. A vaviety of interventions were undertaken during ischemia. The elevated level of arterial pressure induced by the administration of methoxamine increased ventricular diameter and presumably oxygen requirements, and was deleterious to ischemic wall motion whereas the administration of norpinephrine reduced ventricular diameter and improved function. Intra-aortic balloon counterpulsation had little effect on either ischemic motion or perfusion. These experimental studies generally support conclusions drawn from clinical echocardiograms about the relationship of abnormalities of wall motion to coronary artery lesions and myocardial ischemia, and suggest further clinical uses for echocardiography in coronary disease.

Animals↗
PubMed1977

Distribution of coronary artery flow to the canine right atrium and sinoatrial node.

We assessed segmental distribution of blood flow to the right atrium and the region of the sinoatrial node using micropheres (7-10 mum) in 20 anesthetized dogs. Mean right atrial flow averaged 83+/-7 (SE) ml/min X 100 g, which was 56% of the left ventricular blood flow. The distribution of right atrial flow was not homogeneous. For example, flow to anterior right atriaater (105+/-8 ml/min X 100 g) than mean right atrial flow. Following ligation of the sinus node artery, perfusion of the segment containing the sinus node decreased by only 36%. Relative preservation of perfusion to the sinus node following sinus node artery ligation may explain why ligation of the sinus node artery does not alter heart rate. Furthermore, we also found that cannulation and pump perfusion of the sinus node artery at pressures 10 and 50 mm Hg greater than systolic pressure did not alter the distribution of right atrial flow. Thus, because cannulation and perfusion of the sinus node artery do not artifactually distort regional right atrial blood flow, we conclude that this should be a useful method for evaluating responsiveness of the sinus node to various interventions.

Acetylcholine↗
PubMed1977

Effects of intermittent pressure loading on the development of ventricular hypertrophy in the cat.

Although the effects of persistent pressure loading on the development of ventricular hypertrophy have been studied extensively, the effects of intermittent pressure loading have not been examined. To study the effects of intermittent pressure loading we subjected the right ventricle of cats to intermittent pulmonary artery constriction over a 2-week period. Two intermittent pressure loading schedules were employed. The first consisted of a right ventricular systolic pressure of 60 mm Hg for 3.5 days and normal right ventricular pressure for 3.5 days; and the second consisted of a right ventricular systolic pressure of 60 mm Hg for 2.3 days and normal right ventricular pressure for 4.7 days. The intermittent pressure-loaded cats were compared with normal unoperated controls, sham-operated controls, and cats with persistent right ventricular pressure load for either 1-week or 1- to 2-month duration. The data indicate that intermittent pressure loading caused significant right ventricular hypertrophy. Since significant residual ventricular hypertrophy was present in both intermittent pressure loading groups, regression of ventricular hypertrophy involves a slower process than the progression of hypertrophy.

Animals↗