Biomedical subjects

S S Hull

Publications and source records attributed to S S Hull.

23 records · Page 2Linked to original sources

PubMed1986

Endothelium-dependent flow-induced dilation of canine femoral and saphenous arteries.

We have characterized the dilation response to increased blood flow in the canine femoral and saphenous arteries. An arterio-venous shunt was created and changes in arterial diameter measured by sonomicrometer crystals. Increasing shunt flow approximately 10-fold caused a 9% increase in femoral and 15% increase in saphenous artery diameter. The dilation response consisted of a transient decrease in diameter, followed by a rapid dilation and a slow return to control when flow was decreased. The increased diameter was not a result of decreased transmural pressure or alterations in pulse pressure. After removing the endothelial cells, the vessels did not dilate to increased flow or topical acetylcholine (10(-5) M), but responses to norepinephrine (10(-5) M) and sodium nitroprusside (10(-4) M) were unaltered. Indomethacin, theophylline or propranolol did not affect the flow-induced dilation. Quinacrine, an inhibitor of phospholipase A2, attenuated the dilation response in a dose-dependent manner. We conclude that increased blood flow affects endothelial cells, causing an active dilation of arterial smooth muscle.

Acetylcholine↗

PubMed1984

Mechanisms of central prostaglandin E2 hypertension in conscious dogs, sheep, and calves.

Intracarotid prostaglandin E2 (PGE2) infusions (10 ng X kg-1 X min-1) increased arterial pressure in conscious dogs, sheep, and calves. Total and regional peripheral resistances (renal, superior mesenteric, and iliac) increased in conscious calves. Arterial pH and CO2 tension did not change, implying no activation of the chemoreflex. The arterial baro-reflex was reset upward during intracarotid PGE2 infusion; arterial pressure increased with little heart rate change, but baroreflex sensitivity was unchanged. In contrast, equipotent intracarotid angiotensin II infusions (10 ng X kg-1 X min-1) both reset the baroreflex upward and decreased baroreflex sensitivity. Pretreatment with alpha-, but not beta-, adrenoceptor blocking agents attenuated the intracarotid PGE2 pressor effect. Increasing PGE2 infusions (10-200 ng X kg-1 X min-1) caused dose-related arterial pressure increases; plasma renin activity was increased only at the largest infusion rate. Pretreatment with captopril, an inhibitor of the angiotensin-converting enzyme, attenuated the PGE2 pressor effect. During barbiturate-halothane and chlorolose-urethan anesthesia, no pressor effect was observed during intracarotid PGE2. We conclude that intracarotid PGE2 acts centrally to augment sympathetic vasomotor outflow. The central action of PGE2 is not affected by activation of the arterial chemoreflex or alteration of baroreflex sensitivity and has a small renin-angiotensin component.

Anesthesia↗

PubMed1981

Role of prostaglandin E in the biphasic fever response to endotoxin.

Biphasic fevers were induced in sheep with intravascular infusions or injections of 4-10 mug (80-200 ng/kg) of endotoxin, whereas monophasic fevers were obtained with doses of 1-2/mug (20-40 ng/kg). A marked increase in arterial blood pressure invariably accompanied the onset of fever; the latency of responses to the higher and lower doses of endotoxins averaged 26 min and 42 min, respectively. Prostaglandin (PG) assays of plasma from the carotid artery and jugular vein during fever episodes revealed a surge of PGE and PGF coincident with the pressor response and the first phase of fever, but PG were not detected in plasma samples taken throughout the second phase of fever. PG measurements of arterial and venous plasma collected at a distal site (hind limb) showed a similar surge of PGE and PGF in association with the early fever response, indicating that intravascular PG synthesis and release represents a generalized systemic response to circulating endotoxin. Carotid arterial infusions of PGE(2) produced immediate monophasic fevers and pressor responses, whereas PGD(2) infusions produced an immediate pressor effect but no fever. Infusions of PGF(2alpha) or prostacyclin, however, evoked neither fever nor pressor effects. Intracarotid infusions of leukocyte pyrogen (LP) caused monophasic fevers with latent periods of 15-20 min but pressor responses were not seen and neither PGE nor PGF were detected in plasma samples from the carotid artery or jugular vein before or during fever. Indomethacin, a potent inhibitor of arachidonic acid metabolism, blocked fever responses to endotoxin and to LP. These findings implicate PGE as the mediator of the early phase of endotoxin fever and imply a role for another pyrogenic metabolite ofarachidonic acid in the mediation of the second phase of fever, i.e., the phase associated with circulating LP. It is possible that both pyrogenic metabolites are generated within the vascular compartment, reaching thermoregulatory centers of the brain by transfer across the blood-brain interface.

Animals↗

PubMed1980

Comparative luteolytic effects of prostaglandin F2 alpha and its 13-dehydro analogs in vivo.

Several 13-dehydro analogs were shown to be luteolytic in both the cyclic sheep and cyclic primate models studied. The fact that these luteolytic analogs have diminished uterine smooth muscle activity suggests that the receptors governing the smooth muscle effect on the one hand, and the luteolytic effect on the other, may possess different structural specificities. In both species studied, the analogs showed marked resistance to the PG-15-OH-dehydrogenase in vivo as shown by their activity when infused intravenously. In the early pregnant monkey, the reduced luteolytic activity of the 13-dehydro analogs suggests that mCG may have a protective effect on the corpus luteum to PGs in general. Thus, the early pregnant monkey, or possibly the hCG-treated cyclic monkey, would appear to be "essential" models in the study of luteolytic agents in the primate. Finally, previous reports of termination of early pregnancy in monkeys with luteolytic PG analogs may have depended, at least in part, on their intrinsic smooth muscle activity on the uterus.

Animals↗

PubMedDate not supplied

Heart rate--QT relationships during baroreceptor stimulation with diminished autonomic influence on the ventricles. Ventricular autonomic tone and QT interval.

The shortening of the QT interval of the electrocardiogram coincident with acceleration of heart rate and vice versa has been accepted for many years as evidence that the action potential duration and hence QT are necessarily dependent on heart rate. Exceptions to this rule have been attributed to the intervention of counteracting autonomic effects. In order to test this assumption, 26 conscious dogs divided into three groups were tested during baroreceptor stimulation by a bolus injection of phenylephrine. Seventeen dogs had been used in earlier studies in which they had undergone an experimental anterior myocardial infarction with apparent full recovery. A group of those dogs underwent beta-adrenergic blockade by intravenous atenolol 30 min prior to the baroreceptor activation. To test the intactness of the baroreceptor responses in the previously infarcted dogs, a third group of nine dogs that had had no prior myocardial infarction was included. All dogs were adapted to the laboratory environment and were not sedated during experiments. Simultaneous recordings of RR, QT interval, and phasic arterial pressure were made in all dogs before and during baroreceptor stimulation. In the normal group, and the previously infarcted group that received no atenolol, baroreceptor stimulation elicited a small (8/msec), but significant prolongation of the QT associated with a nearly 50% reduction in heart rate. The QT interval of the atenolol-treated dogs, although significantly more prolonged before stimulation, remained unchanged during the reflex. The data indicate that withdrawal of ventricular sympathetic tone may prolong the QT interval, thereby confirming the role of sympathetic innervation in the control of QT.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗