Biomedical subjects

C Su

Publications and source records attributed to C Su.

At least 181 records · Page 10Linked to original sources

PubMed1975

Nonsympathetic dilator innervation of cat cerebral arteries.

The results presented provide strong support for the presence of vasodilator innervation in the cat cerebral arteries. The dilator innervation is neither adrenergic nor cholinergic and does not originate in the superior cervical ganglia. The nature of the vasodilator transmitter is unidentified. Such innervation, however, may be involved in the regulation of cerebral blood flow, especially in view of the capability of some cat cerebral vessels to develop intrinsic muscle tone.

Acetylcholine↗

PubMed1975

Development of autonomic control of fetal circulation.

Development of parasympathetic and sympathetic reflexes controlling heart rate, vascular pressures, and blood flows was investigated in fetal lambs weighing 300-5,800 g (65-165 days' gestation). Cardiovascular responses to veratridine injections, atrial stretching, bilateral cervical vagotomy, and cholinergic blockade with atropine were used to test parasympathetic activities. Responses to propranolol and phenoxybenzamine were used to test beta- and alpha-adrenergic activities. Autonomic ganglionic blockade and stimulation provided additional information on both cholinergic and adrenergic systems. Fetal responses to various tests were compared to those of the mother. Results show: a) little parasympathetic tone on resting heart rate and other circulatory functions exists prior to fetal maturity; b) despite the feeble resting tone, the parasympathetic system is capable of exerting significant control when stimulated in both premature and mature fetuses, the capability increases as fetus approaches term; c) alpha- and beta-adrenergic tone in control of resting heart rate and peripheral circulation exists in early fetal life and increases as the fetus reaches maturity, and both adrenergic receptors respond strongly to stimuli in immature, premature, and mature fetuses; d) in immature fetuses, veratridine does not elicit a vagally mediated reflex; instead, it produces a centrally mediated alpha- and beta-adrenergic stimulation; e) the fetal cardiovascular response to any given test is dampened by the existence of the various vascular shunts, the umbilicoplacental circulation and, possibly, by incomplete maturation of vasomotor tone.

Anesthetics↗

PubMed1975

Effects of phenoxybenzamine and norepinephrine on transmitter release in the pulmonary artery of the rabbit.

The effects of phenoxybenzamine and norepinephrine (NE) on the release of tritiated NE were studied in spiral strips of the rabbit pulmonary artery. Phenoxybenzamine increased the tritiated NE efflux induced by transmural stimulation at 4 Hz by a factor of three. The magnitude of this effect was inversely related to the frequency of stimulation. NE (2.5 times 10- minus 6 M) decreased the enhancing effect of short exposure but not long exposure to phenoxybenzamine, probably by surmounting the phenoxybenzamine blockade of the alpha-adrenergic receptors on the adrenergic nerve terminal. The transmitter output per pulse increased with the frequency from 4 to 16 HZ and decreased at 32 HZ. This evidence suggests that a negative feedback mechanism does operate in this vascular preparation but, probably because of the wide neuromuscular cleft, is less effective than in tissues with a narrower synaptic interval.

Animals↗

PubMed1975

Systemic and pulmonary hemodynamic responses to adrenergic and cholinergic agonists during fetal development.

Systemic and pulmonary hemodynamic responses to adrenergic and cholinergic agonists were investigated in fetal lambs between 60 days and term gestation. The cardiovascular response to these agents increases with fetal age, and the increase is related to maturation of the effector system rather than the vascular receptors. The fetal pulmonary vascular bed and the ductus arteriosus are the primary components responding to acetylcholine; the systemic response is secondary to the occuring in the lung. Both fetal systemic and pulmonary vascular beds are under alpha-adrenergic control whereas the fetal heart is under beta-adrenergic control.

Acetylcholine↗

PubMed1975

Analysis of changes in reactivity of rabbit arteries and veins two weeks after induction of hypertension by coarctation of the abdominal aorta.

Vessel dimensions and characteristic responses to norepinephrine were measured in various arteries and veins of the rabbit made hypertensive by partial constriction of the upper abdominal aorta. The ear, radial, and basilar arteries taken from the circulation proximal to the ligature (the hypertensive arteries) were thickened in proportion to the rise is arterial blood pressure. The water, sodium, and potassium contents of these and all other vessels were not significantly changed in the hypertensive rabbits. The maximum response to norepinephrine in the ear artery, a representative vessel from the hypertensive part of the rabbit, was increased, whhereas the sensitivity of this vessel to norepinephrine expressed as the ED50 did not alter with changes in the arterial blood pressure. In contrast, the thickness and the maximum response to norepinephrine of the saphenous artery, representative of vessels distal to the ligature (normotensive vessels) and of the saphenous and cephalic veins were unaltered. The sensitivity as indicated by the norepinephrine ED50 of the veins, but not of the saphenous artery, increased with a rise in carotid artery blood pressure. These results suggest that the increased responsiveness to norepinephrine of arteries proximal to the ligature is due to changes in muscle mass and that the increased responsiveness of the veins is due to increased sensitivity to norepinephrine.

Animals↗

PubMed1975

Evidence for an increase in adrenergic nerve function in blood vessels from experimental hypertensive rabbits.

The possibility of changes in the adrenergic innervation of blood vessels in experimental hypertension was investigated by measuring arterial norepinephrine content, neuronal uptake of norepinephrine, and the neurogenic contractile response in rabbits made hypertensive by partial constriction of the abdominal aorta proximal to the kidneys. Two to 3 weeks after surgery, norepinephrine content was increased in the arteries above the ligature, where arterial blood pressure was increased, but not in the arteries below the ligature, where arterial blood pressure was normal, in the heart, or in the veins. Neuronal norepinephrine uptake per unit length of vessel and the neurogenic contractile response increased with the rise in arterial blood pressure. The neurogenic contractile response can be taken as an indication of an increase in transmitter release. The results taken together suggest an increase in the function and possibly the amount of the adrenergic neuroneal terminal in hypertension. Since the distributions of the changes in the adrenergic innervation and the increases in smooth muscle cell proliferation in hypertension are similar, these two processes may be interrelated.

Animals↗

PubMed1975

Neurogenic release of purine compounds in blood vessels.

The isolated thoracic aorta, ear artery and portal vein of the rabbit concentrated tritiated material on exposure to tritiated adenosine, adenine and its nucleotides. 3H-adenosine was transformed and retained predominantly as 3H-adenosine triphosphate in the portal vein and aortic adventitia, but to a lesser extent in the aortic medial or muscle layer. On transmural stimulation, portal vein and aortic adventitial strips pretreated with 3H-adenosine released tritiated material, which was recovered mainly as tritiated adenosine and nucleotides. Guanethidine abolished this release in the aortic adventitia and greatly diminished it in the portal vein. Both the release and vasodilation induced by transmural stimulation in the portal vein were abolished by tetrodotoxin. It is suggested that purine compounds are released locally within vascular walls from both the adrenergic and nonadrenergic nerves. The results are compatible with the view that adenosine triphosphate or a related compound may function as an inhibitory modulator in association with the adrenergic nerves and as a vasodilator transmitter of the non-adrenergic nerves in the portal vein.

Adenine Nucleotides↗

PubMed1974