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Biomedical subjects

F M Abboud

Publications and source records attributed to F M Abboud.

At least 163 records · Page 9Linked to original sources
PubMed1975

Regulation of blood flow in Paget's disease of bone.

Previous studies have demonstrated an increase in blood flow to extremities involved by Paget's disease of bone. It has been assumed that the increase in blood flow is through bone, but warmth of skin overlying Pagetic bone suggests that cutaneous blood flow might be increased. In three patients with Paget's disease involving one extremity, we compared blood flow in "Pagetic" extremities with flow in the contralateral normal extremities. Resting blood flow (measured with water plethysmographs) was 14.2plus or minus2.9 (meanplus or minusSE) ml/min times 100 ml extremity in the Pagetic limbs. The contribution of cutaneous flow to the increase in extremity blood flow was evaluated with epinephrine iontophoresis, which suppresses flow to skin but not to underlying tissue. Epinephrine iontophoresis of the Pagetic extremities decreased blood flow from 14.2plus or minus2.9 to 3.6plus or minus1.5 ml/min. Local heating (which increases cutaneous flow only) failed to increase blood flow in the Pagetic extremities as much as it did in the normal extremities. This suggests that cutaneous vessels in the Pagetic extremities were already dilated. During heating, blood flow in the normal extremities was similar to resting flow in the Pagetic extremities; this indicates that increases in cutaneous flow could account for most of the increase in total blood flow in the Pagetic extremities. Adrenergic control of blood flow to the Pagetic extremities was compared with that of the normal extremities. Vasoconstrictor responses to reflex stimuli in the Pagetic extremities were reduced; when vasoconstriction occurred it was gradual and sustained after termination of the stimuli, which suggests an exaggerated humoral response but reduced neural response to the stimuli. Intravenous epinephrine produced vasoconstriction in the Pagetic extremities and vasodilatation in the normal extremities. In summary, responses to epinephrine iontophoresis and heating suggest that the increase in blood flow in Pagetic extremities is primarily the result of cutaneous vasodilatation.

Blood Vessels↗
PubMed1975

Selective beta-1 receptor blockade with oral practolol in man. A dose-related phenomenon.

The purpose of this study was to test the hypothesis that oral administration of a low dose of practolol in man produces selective beta-1 receptor blockade, whereas oral administration of a high dose blocks both beta-1 and beta-2 receptors. Normal men were studied 2-4 h after a single oral dose of practolol (1.5 or 12 mg/kg) and after placebo. Effects on beta-1 receptors were studied by measuring heart rate responses to exercise. Effects on beta-2 receptors were tested by measuring forearm vascular responses to brachial arterial infusions of isoproterenol. Neither dose of practolol altered base-line heart rate, forearm vascular resistance, and arterial pressure, Both low and high doses significantly attenuated heart rate responses to exercise. Forearm vasodilator responses to isoproterenol were attenuated by the high dose, but not the low dose, of practolol. Serum concentrations of practolol 2 h after administration of the drug and at the time of the studies of forearm vascular responses averaged 0.5+/-0.1 (SE) and 5.9+/-1.0 mug/ml for low and high doses of practolol, respectively. The results indicate that the phenomenon of selective beta-1 receptor blockade in man is related to the dose and serum concentration of practolol selectively block beta-1 receptors; a high dose and serum concentrations block both beta-1 and beta-2 receptors.

Administration, Oral↗
PubMed1975

Response of muscular and cutaneous vessels to physiologic stimulation of chemoreceptors (38505).

Experiments were performed to determine whether physiologic stimulation of carotid chemoreceptors produces different responses in blood vessels of skin and muscle. Carotid chemoreceptors of anesthetized dogs were stimulated with hypoxic and hypercapnic blood and responses were observed in the isolated, perfused gracilis muscle and hindpaw. Chemoreceptor stimulation produced vasoconstriction in the muscle and vadodilatation in the paw (a predominantly cutaneous vascular bed). Responses to hypoxia without hypercapnic acidosis tended to be less pronounced. The study indicates that physiologic stimulation of carotid chemoreceptors produces contrasting responses in different vascular beds.

Acidosis↗
PubMed1975

Efferent pathways of the coronary chemoreflex.

This study was performed to identify the efferent pathways which mediate vasodilation during activation of the coronary chemoreflex and to compare the reflex responses in vessels in skeletal muscle and skin. Reflex vasodilator responses (decreases in perfusion pressure) were measured in innervated, perfused gracilis muscle and hindpaw of dogs during activation of the coronary chemoreflex with intracoronary injections of nicotine. Reflex vasodilator responses to intracoronary nicotine (1.25 and 2.50 mu-g per kilogram) averaged -14 plus or minus 5 (S.E.M.) and -34 plus or minus 6 mm. Hg, respectively, in muscle, but only -5 plus or minus 2 and -10 plus or minus 4 mm. Hg, respectively, in paw. Atropine, tripelennamine, and propranolol did not alter the vasodilation. Guanethidine blocked reflex vasodilation in muscle. The reflex vasodilator responses in paw were slight and were not significantly attenuated by guanethidine. The results indicate that sympathetic cholinergic pathways to skeletal muscle do not participate in the coronary chemoreflex. The reflex vasodilation in muscle results from withdrawal of adrenergic constrictor tone. The efferent pathway demonstrates that the coronary chemoreflex does not produce striking withdrawal of adrenergic tone in paw. The results indicate, therefore, that activation of the coronary chemoreflex results in greater withdrawal of adrenergic constrictor tone and greater vasodilation in muscle than in skin.

Animals↗
PubMed1975

A simplified neck suction device for activation of carotid baroreceptors.

Application of negative neck pressure is a valuable research technique for activation of carotid baroreceptors in man, but its use has been limited because a simple, effective, comfortable neck suction chamber has not been available. We have developed a new neck suction device which may have significant advantages over earlier models. Construction details are illustrated for this chamber which has the following attributes: (1) it is simple and inexpensive to construct, (2) one model fits most adults in relative comfort, and (3) the design of the chamber permits rapid initiation of neck suction to preselected levels leading to stimulus-related cardiac slowing and arterial hypotension.

Blood Pressure↗
PubMed1975

Effect of hypoxemia on responses to norepinephrine and angiotensin in coronary and muscular vessels.

The purpose of this study was to determine the relative effects of acute hypoxemia on constrictor responses to norepinephrine and angiotensin in two vascular beds, the coronary and skeletal muscle. The left circumflex coronary and gracilis muscle arteries of anesthetized dogs were perfused at constant flow. Practolol or propranolol was administered to block indirect myocardial effects of norepinephrine on coronary resistance. When Po2 of arterial blood perfusing the coronary and muscle beds was reduced from 101 to 44 mm while systemic Pco2 remained normal, constrictor responses to both norepinephrine and angiotensin were inhibited in coronary vessels but not in muscle vessels. When local Po2 was reduced to 27 mm Hg, inhibition of responses was again observed in the coronary circulation with both drugs; in the muscle, responses to angiotensin but not to norepinephrine were depressed significantly. Since intracoronary infusion of adenosine increased, rather than inhibited, vasoconstrictor responses to angiotensin, it is unlikely that release of adenosine during hypoxemia accounts for inhibition of vasoconstriction in the coronary circulation. Indomethacin did not alter the inhibition of coronary vasoconstrictor responses to angiotensin during hypoxemia, which suggests that releease of prostglandins during htpoxemia is not the primary mechanism for inhibition of coronary vascular responses. When contractions in the gracilis muscle were produced by electrical stimulation, vasconstrictor responses to norepinnephrine were inhibited during hypoxemia. We conclude that depression of constrictor responses by hypoxemia is more pronounced in the coronay circulation than in resting muscle, but when muscle is contracting, vasoconstrictor responses are impaired during hypoxemia.

Adenosine↗
PubMed1974

Interaction of baroreceptor and chemoreceptor reflexes. Modulation of the chemoreceptor reflex by changes in baroreceptor activity.

The purpose of this study was to determine whether the level of arterial pressure and degree of baroreceptor activation affect responses to stimulation of chemoreceptors. Chemoreceptors were stimulated by injecting nicotine into the common carotid artery of anesthetized and paralyzed dogs. Responses were observed in the innervated gracilis muscle, perfused at constant flow while perfusion pressure was measured. Arterial pressure was lowered by bleeding the animals and raised by transient occlusion of the descending aorta. Vasoconstrictor responses to stimulation of chemoreceptors were enhanced by hypotension and inhibited by elevation of arterial pressure. Potentiation of the chemoreceptor reflex by hemorrhagic hypotension was not the result of altered vascular resistance in the gracilis muscle, sensitization of chemoreceptors by catecholamines or acidosis, or changes in cerebral perfusion pressure. Additional studies were done in which we excluded the possibility that the changes resulted from direct effects of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were isolated and perfused. On one side, pressure was raised to stimulate the carotid sinus baroreceptors. On the other side, the carotid body chemoreceptors were stimulated by nicotine or by hypoxic and hypercapnic blood. Activation of baroreceptors on one side attenuated the vasoconstrictor response to chemoreceptor stimulation on the other side. This excludes a direct effect of changes in arterial pressure on the chemoreceptors and suggests a central interaction of these reflexes. We conclude that vasoconstrictor responses to stimulation of chemoreceptors are potentiated by hypotension and inhibited by transient hypertension. These effects appear to result at least in part from a central interaction of chemoreceptor and baroreceptor reflexes.

Animals↗
PubMed1974

Mechanisms mediating bradycardia during coronary arteriography.

Cardiac slowing occurring during diagnostic coronary arteriography was studied in 78 patients. Comparable degrees of slowing occurred with injections into the right and into the left coronary arteries into the contralateral artery, and with injections into the coronary artery giving rise to the sinus node artery and into the contralateral artery. Rapid intracoronary injections of isosmotic dextrose solution produced significantly less slowing than comparable injections of contrast medium. Slow injections of contrast medium produced cardiac slowing comparable to that caused by rapid injections of contrast medium. However, the cardiac slowing was significantly greater than that produced by rapid injections of dextrose solution. Inhalation of 100% oxygen did not alter the heart rate response to injections of contrast medium. Atropine produced dose-related attenuation of cardiac slowing. Bradycardia persisting after cholinergic blockade was significantly greater after injections into the coronary artery supplying the sinus node than it was after injections into the contralateral artery. Coronary arteriography produced transient, occasionally profound, arterial hypotension in 38 of 41 patients in whom arterial pressures were recorded. Arterial pressure did not change in three patients. This study suggests that the cardiac slowing which occurs during coronary arteriography in man is due primarily to a cholinergic reflex which may be a human counterpart of the Bezold-Jarisch reflex, observed heretofore only in experimental animals. This slowing appears to be mediated primarily by receptors sensitive to contrast medium, rather than by changes of coronary artery pressure, and secondarily, by direct depression of sinus node function by contrast medium.

Adult↗