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Biomedical subjects

D E Donald

Publications and source records attributed to D E Donald.

At least 19 recordsLinked to original sources
PubMed1985

An outbreak of shingles?

7 of 101 staff within one department of a large office complex had shingles, as diagnosed by a general practitioner, within a three-month period. This incidence was significantly greater than that in the remaining workforce. Varicella-zoster-specific IgM antibody was detected in all 4 cases from whom early convalescent serum samples were obtained but in none of 22 controls. Within the index department there was evidence of clustering in time and by work area. A case/control study showed that a recent preceeding illness might have been a risk factor for shingles in the outbreak cases, but not for sporadic cases in other departments of the same office complex. This outbreak suggests that shingles can be provoked by reexposure to varicella-zoster virus.

Absenteeism↗
PubMed1983

Cardiopulmonary reflexes and arterial pressure during rest and exercise in dogs.

Mean arterial blood pressure, heart rate, and cardiac output were monitored at rest and during exercise of two grades of severity in conscious dogs under control conditions and after progressive interruption of the baroreflexes. Aortic arch denervation and vascular isolation and pressurization of the carotid sinuses were used to interrupt arterial baroreflexes. Subsequent interruption of cardiopulmonary afferents was produced by acute bilateral cervical vagotomy. The results indicate that 1) with the cardiopulmonary receptors alone operative, the arterial blood pressure response to exercise is abnormal, 2) cardiopulmonary receptors do not contribute to the moment-to-moment modulation of arterial pressure, and 3) the carotid sinuses, aortic arch, and cardiopulmonary receptors are all involved in determining the mean level of arterial blood pressure. It is concluded that vagally innervated cardiopulmonary receptors do not have a significant role in regulating arterial blood pressure during exercise but are involved in establishing the general level of arterial blood pressure.

Animals↗
PubMed1983

Inhibition by carotid baroreflex of exercise-induced increases in arterial pressure.

Mean arterial blood pressure, heart rate, and cardiac output were measured during continuous graded exercise (5.5 km/hr; 0, 7, 14, and 21% grades) in conscious dogs, under each of the following four conditions: (1) baroreceptors intact, (2) chronic aortic arch denervation, (3) chronic aortic arch denervation and surgical preparation of the carotid sinuses for later reversible vascular isolation, and (4) chronic aortic arch denervation and carotid sinuses vascularly isolated at a fixed pressure. Arterial blood pressure increased with increasing work load to a maximum of 12 +/- 3, 18 +/- 5, and 14 +/- 5 mm Hg above control in conditions 1, 2, and 3, respectively. In condition 4, the maximum increase in pressure during graded exercise was 51 +/- 7 mm Hg above control. Upon cessation of graded exercise, the increase in arterial pressure persisted through the 5-minute recovery period. Heart rate and cardiac output increased similarly in proportion to work load under all four conditions. In contrast to dogs in condition 4, three dogs with chronic sinoaortic denervation showed no work load-related increase in arterial pressure during exercise. Thus, during exercise, the carotid baroreflex acts to balance finely the opposing effects of sympathetic vasoconstriction and metabolic vasodilation.

Animals↗
PubMed1982

Response of large hindlimb veins of dog to aortic arch chemoreceptor stimulation.

Experiments were performed in chloralose-anesthetized dogs to examine the reflex effects on tone in the saphenous vein of stimulating the aortic arch chemoreceptors. The saphenous vein was perfused with cooled (30 degrees C) aortic blood at constant flow, and perfusion pressure was measured. In 13 animals the aortic arch chemoreceptors were stimulated by injection of cyanide (0.1 mg/kg) into the root of the aorta. Cyanide caused a decrease (20 +/- 2 mmHg) in saphenous vein perfusion pressure and an increase (44 +/- 4) in aortic pressure. These changes that occurred subsequent to aortic root cyanide injections were abolished by vagotomy or section of the aortic nerves (afferent pathway); section of the lumbar sympathetic chain at L4 and L5 abolished the dilator response of the vein (efferent pathway) but did not alter the increase in aortic pressure. Four dogs were prepared for cardiopulmonary bypass and separate perfusion of the systemic circulation and the isolated aortic arch. Delivery of hypoxic-hypercapnic blood to the isolated aortic arch caused a dilation of the saphenous vein and an increase in systemic arterial perfusion pressure. From these results we conclude that cutaneous venomotor tone can be reflexly reduced through the aortic chemoreflex.

Animals↗
PubMed1981

Inhibition of carotid pressor response by left aortic depressor nerve in dogs.

In 12 conscious dogs, the mean increase of 26 mmHg in arterial pressure during carotid occlusion was augmented by 52 mmHg after section of the left cervical vagus nerve and 6 mmHg after right vagal section. In 18 anesthetized dogs, in which the cervical vagal nerves were reversibly cold blocked, corresponding values were 33, 28, and 6 mmHg, respectively. In nine of these dogs, this left-sided dominance was present after bilateral section of the vagal cardiopulmonary afferents; it was absent after bilateral section of the aortic nerves in the other nine dogs. In five dogs on cardiopulmonary bypass with heart and lungs excluded, pressure within the isolated aorta and major intrathoracic arteries was raised from 120 to 220 mmHg. The resultant hypotension reflexly induced by activation of aortic baroreceptors was reduced by left but not by right vagal cold block. It was concluded that, in the dog, the left aortic nerve provided the major inhibition of the increase in arterial pressure after carotid occlusion.

Animals↗
PubMed1981

Maintained ability of carotid baroreflex to regulate arterial pressure during exercise.

In conscious dogs bilateral carotid occlusion increased arterial pressure by similar amounts at rest (+ 27 mmHg) and during graded exercise (+ 29 mmHg). During exercise stimulus-response curves for arterial pressure and heart rate derived from isolated carotid sinuses were displaced upward proportionately to the work load, but the curve characteristics were unchanged. After acute bilateral vagotomy similar responses to carotid occlusion were obtained at rest (+ 85 mmHg) and at 21% grade (+ 84 mmHg); the range and maximal slope of the arterial pressure stimulus-response curve during exercise was similar to that at rest, but the exercise curve was displaced downward and to the left. It was concluded that the carotid baroreflex was able to modulate arterial pressure as well during running as at rest. Dogs with neither carotid, aortic, or cardiopulmonary receptors able to respond to the exercise stress became and remained hypotensive during mild exercise; during severe exercise hypotension was present initially, but after 90 s arterial pressure recovered toward the preexercise level. The data indicated that arterial and cardiopulmonary baroreceptors have a major role in the support of arterial pressure in the first moments of exercise.

Animals↗
PubMed1980

Reversible vascular isolation of carotid sinuses in conscious dogs.

A surgical technique has been developed that permits reversible vascular isolation of both carotid sinuses in the conscious dog. Seven dogs so prepared were studied over periods of 4-12 wk. Repeatable stimulus-response curves relating arterial blood pressure to carotid sinus pressure were obtained for sinus pressures of 40-240 mmHg. Two studies gave evidence that the ability of the carotid baroreceptors to influence arterial pressure was not or was minimally affected by the surgical dissection. In 10 dogs one sinus was surgically prepared; 3 wk later the dogs were anesthetized and vagotomized. The steady-state stimulus-response curves for the chronically prepared sinuses showed no consistent differences from the curves for the opposite, acutely prepared sinuses. In 8 other dogs the hypertensive responses to bilateral carotid occlusion were compared before and after surgical preparation of both sinuses. The responses to carotid occlusion tended to be decreased after surgery but the differences were small and were significant only in 3 dogs.

Animals↗
PubMed1980

Reflexes from isolated carotid sinuses of intact and vagotomized conscious dogs.

Exposure of the vascularly isolated carotid sinuses of 8 conscious dogs to static pressures between 50 and 240 mmHg caused significantly smaller increases [23 +/- 5(SE) mmHg] than decreases (37 +/- 4 mmHg) in arterial pressure frossure and heart rate and shifted the stimulus-response curve upward. Bilateral cervical vagotomy in conscious dogs caused sustained (3 h) increases in arterial pressure (40 +/- 5 mmHg), significantly larger than after atropinization (7 +/- 2 mmHg). In anesthetized, but not in conscious dogs, high sinus pressure reversed the hypertension caused by vagotomy. After vagotomy, low sinus pressure resulted in arterial pressures greater than 200 -mHg. In conscious dogs the carotid baroreflex can widely vary arterial pressure and heart rate despite buffering by extracarotid baroreceptors with vagal afferents, but cannot fully compensate for the acute loss of the latter. Extracarotid baroreceptors actively participate with carotid baroreceptors in the regulation of arterial pressure and better buffer carotid baroreflex-induced increases than decreases in arterial pressure.

Anesthesia↗
PubMed1979

Cardiac receptors: normal and disturbed function.

Widely distributed throughout the heart is a network of fibers connected to the medullary cardiovascular centers by nonmedullated vagal afferent fibers. When the traffic in these fibers is interrupted by vagal cooling, and the input from the arterial baroreceptors is prevented, the arterial blood pressure increases. Thus, these receptors act to inhibit tonically the vasomotor center. The receptors in the atria alter their rate of discharge with changes in atrial transmural pressure and contractility and are most active during end-inspiration and early expiration when the transmural pressure is maximal. The receptors in the ventricles respond to changes in ventricular end-diastolic pressure (preload), to the pressure generated during systole (afterload) and to changes in ventricular contractility. The cardiac mechanoreceptors have an equal or greater effect on the renal bed than the arterial mechanoreceptors and this effect is enhanced by hypercapnia. In animals, the cardiac mechanoreceptors have less control of the muscle vessels than the arterial mechanoreceptors, but the reverse is true in man. Both the cardiac and arterial mechanoreceptors can modulate the output of renin from the kidney, but the cardiac mechanoreceptors are more sensitive to small changes in blood volume. During coronary occlusion, in association with the bulging of the ischemic myocardium, the rate of discharge of these cardiac receptors is greatly increased.

Animals↗
PubMed1979

Involvement of renal alpha- and beta-adrenoceptors in release of renin by carotid baroreflex.

In anesthetized vagotomized dogs with renal arterial pressure constant, carotid sinus hypotension (BCO) caused a reflex rise in systemic arterial pressure, a fall in renal blood flow, and a similar increase in renin release from both kidneys. Unilateral alpha-adrenoceptor blockade with phenoxybenzamine resulted in an increase in basal renal blood flow, a depression of basal renin release, and an abolition of the responses to BCO in the treated kidney. The untreated kidney responsed to BCO as before. Nonblocked and alpha-blocked kidneys released similar amounts of renin when renal blood flow was mechanically reduced by aortic constriction. Administration of propranolol to the nonblocked kidney prevented the release of renin but not the hemodynamic changes resulting from BCO. The experiments demonstrated that under certain conditions carotid sinus hypotension produced alpha-adrenoceptor-mediated changes in the kidney sufficient to cause increased renin release. A step in the renin release mechanism subsequent to the alpha-adrenoceptor-mediated changes in sensitive to propranolol.

Animals↗
PubMed1979

Role of vagal afferents in vasodepressor effects of PGE2 in spontaneously hypertensive rats.

In anesthetized, spontaneously hypertensive rats (Okamoto-Aoki), injections of 0.75, 1.5, and 3.0 microgram/kg PGE2 into the jugular vein caused transient decreases (mean +/- SE) in arterial pressure of 21 +/- 2, 37 +/- 3, and 78 +/- 6 mmHg, respectively, before cervical vagotomy and of 1 +/- 1, 15 +/- 4, and 15 +/- 6 mmHg after cervical vagotomy. The vasodepressor effect of jugular vein injections of 3.0 microgram/kg PGE2, but not of lower doses, was depressed by vagotomy in normotensive Wistar-Kyoto and Sprague-Dawley rats. Vagotomy did not reduce the hypotensive response to intra-aortic injections of PGE2 in these hypertensive and normotensive rats. The depressor effect of PGE2 thus appears to have a significant reflex component mediated through cardiopulmonary receptors subserved by vagal afferents, with hypertensive rats exhibiting a lower threshold than normotensive rats. A vagally mediated reflex component to the depressor effect of PGE2 could not be demonstrated in normotensive rabbits or in rabbits and rats with chronic renovascular hypertension. Thus, a naturally occurring vasoactive substance can stimulate cardiopulmonary receptors subserved by vagal afferents in the rat, and spontaneously hypertensive rats appear to be especially sensitive to this effect.

Afferent Pathways↗
PubMed1979

Contribution of prostaglandins to muscle blood flow in anesthetized dogs at rest, during exercise, and following inflow occlusion.

The role of locally formed cyclo-oxygenase products (endoperoxide intermediates, prostaglandins, or prostacyclins) in resistance to blood flow was studied in the hindlimbs of anesthetized dogs during rest, during exercise, and following release of inflow occlusion. Meclofenamic acid, indomethacin, or sodium meclofenamate reduced mean resting blood flows of 86, 113, and 118 ml/min to 54, 82, and 67 ml/min, respectively. Inhibitors of prostaglandin synthesis reduced the vasodilator response to arachidonic acid by 81%. In addition, prostaglandin synthesis inhibitors attenuated the hyperemic responses following inflow occlusions in the resting hindlimb. The attenuation was most marked following a 1-second occlusion (74%) and progressively less following a 10-second (44%) and a 300-second (24%) occlusion. However, the portion of the total postocclusive hyperemic response attributable to prostaglandins was constant and independent of occlusion duration. Inhibition of prostaglandin synthesis did not affect the hyperemia of exercise, but reduced significantly the postocclusion hyperemia that followed the release of a 1-second (63%) and a 2-second (43%) period of inflow occlusion in the exercising hindlimb; attenuation was minor following a 10-second occlusion (10%). In three of four exercising hindlimbs, the portion of the postocclusion hyperemia attributable to prostaglandins was inversely related to the duration of the occlusion. These data indicate that locally synthesized cyclo-oxygenase products, possibly prostaglandins, are important in the maintenance of blood flow in resting but not exercising muscle, contribute significantly to postocclusive hyperemia in resting and exercising hindlimbs, and mediate the hyperemia that follows occlusions of 5 seconds or less in resting and 2 seconds or less in exercising hindlimbs.

Animals↗