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Biomedical subjects

R D Bevan

Publications and source records attributed to R D Bevan.

71 records · Page 4Linked to original sources
PubMed1976

Changes in the contractile response of arteires and veins from hypertensive rabbits to sympathetic nerve activity: assessment of some postsynaptic influences.

Contractile responses to field stimulation of intramural nerves of arteries and veins taken from rabbits made hypertensive by partial constriction of the abdominal aorta have been related to the carotid artery pressure. The increase in contraction of cephalic and short saphenous veins with rise in carotid artery pressure can be accounted for by an increase in sensitivity of the alpha-adrenergic receptor. The neurogenic contraction of the ear artery increased with carotid artery pressure rise. Changes in some of the extraneuronal factors that influence transmitter distribution and disposition in the tunica media were examined. In hypertensive animals, the percentage of released adrenergic transmitter entering the vessel wall might be expected to decrease due to an increase in medial thickness. However, this percentage was not significantly altered in the ear artery probably due, in part, to a concomitant increase in medial permeability to the transmitter. Extraneuronal transmitter disposition factors, i.e. extraneuronal uptake, monoamine oxidase, and catechol-O-methyltransferase activity are directly related to the wet weight of the vessel wall. Thus, their contribution to transmitter disposition would be expected to increase with increase in vessel wall thickness and tend to reduce the response to sympathetic activity. As the contractile response increased in the hypertensive vessels despite such changes, the increase in effector cell mass and density of neuronal terminal plexus, shown previously to increase with hypertension, are more important than these other considerations.

Animals↗
PubMed1976

Hyperplasia of vascular smooth muscle in experimental hypertension in the rabbit.

Evidence for smooth muscle cell hyperplasia was sought in elastic and muscular vessels of rabbits 2 weeks after hypertension had been induced by partial constriction of the abdominal aorta above both kidneys. In those arteries taken from the circulation proximal to the constriction, specifically the common carotid artery and the aorta, vessel length, wall thickness, weight, and deoxyribonucleic acid content were increased in proportion to the rise in arterial pressure. There was no change in the extracellular space of muscular arteries as measured by [14C]inulin. [3H]Thymidine uptake measured in a gastric artery increased in proportion to the rise in arterial pressure. As demonstrated by light microscope autoradiography, [3H]thymidine was incorporated into cells in all layers of the artery wall but predominantly into the smooth muscle cells. There was no change in the size of arteries below the ligature where the arterial pressure was within normal limits. The data demonstrated that the increase in vessel wall dimensions in this animal model of hypertension is due in part, during the acute phase, to an increase in the number of cells, particularly vascular smooth muscle cells.

Animals↗
PubMed1976

Facial vein in the rabbit. Neurogenic vasodilation mediated by beta-adrenergic receptors.

A segment of the facial vein of the rabbit, that opposite the buccal cavity, responds to norepinephrine (NE) and opposite the buccal cavity, responds to norepinephrine (NE) and transmural nerve stimulation (TNS) by a brisk biphasic dilation. The dilation in response to both procedures is reveresed by prior exposure to propranolol (10(-6)M). Pretreatment with phenoxybenzamine (10(-5)M) increases the size of the neurogenic response and displaces the NE dose-relaxation curve to the left. Histamine causes a constrictor response exclusively. Sympathetic stimulation of a segment of the facial vein proximal to this buccal segment, and also of the external jugular vein, results in constriction. Light microscopy showed no fequtres which can account for the dilation, and fluorescence histochemistry using a modified Flack technique showed a dense adrenergic nerve plexus extending throughout the thickness of the media. We found that frequency-response characteristics and neuronal uptake of 3H-NE were consistent with findings for a blood vessel with a heavy medial innervation. Also, monoamine oxidase and catechol O-methyltransferase activities were similar to those found in other rabbit veins. Furthermore, these results are consistent with an adrenergic neuroeffector organization in which there is a predominance of beta- over alpha-adrenergic receptors. In conclusion, the presence of a dilator response in this buccal segment of the facial vein may be related to its location in the wall of the cheek, where it may be subjected to considerable stretch.

Adrenergic beta-Agonists↗
PubMed1975

Effect of sympathetic denervation on smooth muscle cell proliferation in the growing rabbit ear artery.

The effect of sympathetic denervation on the uptake of 3H-thymidine (3H-Tdr) into the ear artery of a growing rabbit was studied in vitro and in vivo. Uptake into the right artery was compared with that into the left 2 and 3 weeks after left superior cervical ganglionectomy in 4-week-old rabbits. Denervation was confirmed by the absence of catecholamine fluorescence. The total uptake of 3H--Tdr was determined by scintillation spectrometry, and its distribution in the artery wall was studied by light microscope autoradiography. The denervated ear artery took up significantly less DNA precursor and exhibited fewer labeled vascular smooth muscle cell nuclie in the tunica media than did the control artery. These findings suggest that sympathetic innervation influences the proliferation of vascular smooth muscle in growing rabbits.

Animals↗
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.

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PubMedDate not supplied

Transient and persistent changes in rabbit blood vessels associated with maintained elevation in arterial pressure.

Arteries and veins of hypertensive rabbits were examined 8 weeks after partially constricting the abdominal aorta above both kidneys, and compared with those from sham-operated animals. Structural and functional changes in blood vessels after 2 weeks, when the arterial pressure first attained a new elevated level, have been described previously, and are now compared with changes 6 weeks later. The increase in blood vessel mass could be correlated with an increase in deoxyribonucleic acid (DNA) content. In contrast to the status at 2 weeks postoperatively, there was no increased uptake of 3H-thymidine, 3H-proline, or 3H-lysine at 2 months. Furthermore, at this time cell nuclei labeled with 3H-thymidine were infrequent. Some vessels showed evidence of change in the physical characteristics of their wall. Only minimal changes were observed in those parameters of adrenergic nerve function measured -- neuronal 3H-norepinephrine uptake and vessel wall catecholamine content -- that had been markedly changed at 2 weeks. The results of this work, together with those of other studies of this model, suggest two phases of response of the arterial wall to pressure rise: an initial dynamic proliferative cellular response mainly of vascular smooth muscle associated with changes in adrenergic neuronal parameters, and a subsequent equilibrium phase characterized by an increased number of smooth muscle cells, some changes in the extracellular components, and minimal changes in the adrenergic innervation.

Animals↗
PubMedDate not supplied

Trophic effects of peripheral adrenergic nerves on vascular structure.

In the rat and rabbit, evidence for a trophic action of sympathetic nerves on vascular pattern and structure has been reviewed. Effects have been identified by denervation and reinnervation techniques in blood vessels of different size from different regions. Following denervation, increased nonspecific sensitivity to constrictor agents occurs at all ages. In contrast, sympathetic trophic effects on muscle mass, extracellular artery components, and vessel number in the microvasculature were observed predominantly during growth. The mechanism of this action is not known, but the central ear artery in the rabbit was associated with nerve impulses.

Animals↗
PubMedDate not supplied

Cerebral artery mass in the rabbit is reduced by chronic sympathetic denervation.

Weights of matching right and left middle or posterior cerebral arteries and their main branches from the same animal were compared 8-10 weeks after unilateral denervation by superior cervical ganglionectomy. When compared in pairs, the denervated arterial systems weighed significantly less (mean 85%) than their innervated counterparts. This suggests that the sympathetic innervation exerts a trophic influence on extracerebral arteries.

Animals↗
PubMedDate not supplied

Functional arterial changes in chronic cerebrovasospasm in monkeys: an in vitro assessment of the contribution to arterial narrowing.

Cerebral arteries from monkeys with chronic cerebral vasospasm arising from experimental subarachnoid hemorrhage produced 5-6 days previously were examined for changes in their functional properties in an attempt to understand the basis of the narrowing. Hemorrhage was caused by puncture of the internal carotid artery just proximal to the circle of Willis. Segments taken close to the origins of the anterior and middle cerebral arteries consistently showed decreased distensibility. In addition, they exhibited large, prolonged, spontaneous increases in muscle tone. Other alterations observed include a marked reduction in the capacity of the vessel wall to contract, reduction in constrictor and dilator nerve influences on vascular tone, and some increased sensitivity to serotonin. Small pial arteries (150-200 micron o.d.) from the side of the injury showed large spontaneous irregular increases in tone. It is proposed that 5-6 days after experimental subarachnoid hemorrhage in monkeys the change most responsible for persistent narrowing in the larger arteries is an increased rigidity of the vessel wall. This is probably caused by an inflammatory response. In the smaller arteries, abnormal spontaneous contractile activity is a major factor in narrowing. This activity is not stretch-dependent. We suggest that the initial cause of the arterial narrowing after hemorrhage is the action of vasoactive substances released in the close vicinity of the arterial wall, which lead to tissue damage, abnormal tone, and an inflammatory response with fibrosis.

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PubMedDate not supplied

An in vitro study of prolonged vasospasm of a rabbit cerebral artery.

Longitudinal stretch of the rabbit basilar artery produces local injury followed by prolonged circular constriction. After stretching and rapid release in vitro localized constrictions promptly occurred. This could be prevented by prior treatment with cyanide or calcium-free solution. Once produced, constrictions persisted for more than 72 hours. Previously induced constriction was not reversed by treatment for two hours with cyanide or by removing calcium. Histological observation indicated that constricted areas were associated with a discrete circumferential rupture of the internal elastic lamina and disruption and thinning of the underlying media. Specific catecholamine fluorescence at the adventitio-medial junction was unchanged in constricted areas. The relationship between smooth muscle cell length and resting tension of artery segments with and without constrictions was compared. Segments with constrictions had a shorter muscle length for any given resting tension, which confirms that constriction was not due to passive collapse of the vessel wall. These findings suggest that injury of cerebrovascular smooth muscle may result in essentially irreversible vasoconstriction. Such a mechanism could contribute to the pathogenesis of prolonged cerebral vasospasm after SAH or traumatic injury to the cerebrum.

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