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Biomedical subjects

J L Morris

Publications and source records attributed to J L Morris.

At least 109 records · Page 6Linked to original sources
PubMed1984

Development of the vascular bed in the rabbit ear: scanning electron microscopy of vascular corrosion casts.

The development of the vascular bed in the rabbit ear was investigated using vascular corrosion casts from animals of various ages. Examination of the casts revealed that the arrangement of the major auricular arteries and veins was determined before birth and was maintained during postnatal growth of the ear. Furthermore, the number of arteries branching off the central ear artery and the lateral arteries did not increase with increasing ear length. Scanning electron microscopic examination of lateral segments of adult ear casts revealed many anastomoses between marginal arteries and veins. These arteriovenous anastomoses (AVAs) occurred singly, in pairs, or in clusters of three to six. Their size and shape were variable, even in the same cast. The central segment of many AVA casts showed surface impressions of endothelial cell nuclei which were different from the impressions on adjacent arteries and veins. Arteriovenous anastomoses were also detected in ear casts from animals as young as 8 days. The density of AVAs in lateral ear segments ranged from 95-165 cm-2 in 8- to 11-day-old rabbits to 80-115 cm-2 in adults. However, estimates of the total number of AVAs in the lateral ear margin indicated that AVAs continued to be formed at a steady rate during growth of the ear. During the early neonatal period the cutaneous capillary plexuses developed prominent tufts projecting toward the skin surface, which were apparently associated with developing hair follicles. These capillary tufts were not seen in casts from fetal or adult rabbits.

Animals↗
PubMed1984

Catecholamines increase urine formation in isolated toad (Bufo marinus) kidneys perfused at constant rate.

Infusion of catecholamines into isolated kidneys of the toad (Bufo marinus) perfused at constant rate, produced increased arterial pressure accompanied by increased glomerular filtration rate, urine formation rate and sodium excretion. These parameters were all increased by arterial infusion of adrenaline or noradrenaline, or by infusion of adrenaline via the renal portal veins. Portal venous pressure increased slightly after arterial or portal infusion of adrenaline, but decreased after arterial infusion of noradrenaline. Estimation of segmental pressure gradients indicated that the efferent glomerular arterioles were selectively constricted by low concentrations of adrenaline or noradrenaline (3 X 10(-9), 3 X 10(-8) mol l(-1)). Higher concentrations of these amines constricted the preglomerular, as well as the postglomerular vasculature. These results demonstrate that the pericytes and/or endothelial cells which form the walls of the efferent arterioles in B. marinus are capable of active contraction.

Animals↗
PubMed1983

Innervation of the renal vasculature of the toad (Bufo marinus).

The innervation of the dorsal aorta and renal vasculature in the toad (Bufo marinus) has been studied with both fluorescence and ultrastructural histochemistry. The innervation consists primarily of a dense plexus of adrenergic nerves associated with all levels of the preglomerular vasculature. Non-adrenergic nerves are occasionally found in the renal artery, and even more rarely near the afferent arterioles. Many of the adrenergic nerve profiles in the dorsal aorta and renal vasculature are distinguished by high proportions of chromaffin-negative, large, filled vesicles. Close neuromuscular contacts are common in both the renal arteries and afferent arterioles. Possibly every smooth muscle cell in the afferent arterioles is multiply innervated. The glomerular capillaries and peritubular vessels are not innervated, and only 3-5% of efferent arterioles are accompanied by single adrenergic nerve fibres. Thus, nervous control of glomerular blood flow must be exerted primarily by adrenergic nerves acting on the preglomerular vasculature. The adrenergic innervation of the renal portal veins and efferent renal veins may play a role in regulating peritubular blood flow. In addition, glomerular and postglomerular control of renal blood flow could be achieved by circulating agents acting via contractile elements in the glomerular mesangial cells, and in the endothelial cells and pericytes of the efferent arterioles. Some adrenergic nerve profiles near afferent arterioles are as close as 70 nm to distal tubule cells, indicating that tubular function may be directly controlled by adrenergic nerves.

Adrenergic Fibers↗
PubMed1983

Effects of renal nerve stimulation on vascular resistance in the toad kidney.

Stimulation of the renal nerves to the perfused toad kidney produced an increase in intravascular pressure. This response was always abolished by bretylium, indicating that it was mediated by adrenergic nerves. The response was usually reduced by tubocurarine, indicating that some of the fibres in the renal nerve trunks were preganglionic. The vasoconstrictor response was abolished by treatment with yohimbine or phenoxybenzamine, but was only partially reduced by phentolamine. It is postulated that adrenaline released from nerve terminals acts primarily on "junctional" adrenoceptors which are not antagonised by phentolamine. However, part of the vasoconstrictor response appears to be due to occupation of nearby "extra-junctional" receptors by neurally-released adrenaline: only this part of the response can be antagonised by phentolamine. The vasoconstrictor response was enhanced by propranolol in both summer and winter. This indicates that neurally-released adrenaline can occupy beta-adrenoceptors, to antagonise the effects of alpha-receptor occupation, at both times of the year. In this respect, the beta-receptors mediating the effects of renal nerve stimulation are different from those acted upon by perfused adrenaline. A non-adrenergic vasodilatation was sometimes revealed after abolition of the vasoconstrictor response, but the nature of the nerve fibres mediating this response could not be determined.

Action Potentials↗
PubMed1983

6-Hydroxydopamine produces a weight increase in toads.

A large increase in body weight occurred after injection of 6-hydroxydopamine (6-OHDA, 100 mg kg-1) into the iliac lymph sac of toads. The body weight increase was apparently due to retention of fluid and only occurred when toads could not avoid contact of their ventral skin with water. Lower doses of 6-OHDA (25 or 50 mg kg-1) did not cause a weight increase although they were sufficient to eliminate fluorescence from peripheral adrenergic nerves. A peripheral injection of 6-OHDA did not affect the appearance of central aminergic nerves. Removal of the pituitary and median eminence did not affect the weight increase. Although the primary action of 6-OHDA in upsetting water balance in toads has not been revealed by this study, it is clearly not related to the chemical sympathectomy of adrenergic nerves.

Adrenergic Fibers↗
PubMed1982

Seasonal variation in responses of the toad renal vasculature to adrenaline.

Adrenaline and noradrenaline produced both constriction and dilatation of the toad renal vasculature: constrictor effects were mediated by alpha-adrenoceptors; dilator effects were mediated by beta-adrenoceptors. Vasoconstriction was the predominant response to these amines. Dilatation was only revealed after blockade of alpha-adrenoceptors and constriction of the vasculature. There was a marked seasonal variation in the constrictor responses to adrenaline, but not to noradrenaline. The maximal increase in renal vascular resistance produced by adrenaline in summer was greater, by a factor of three, than the maximum constrictor response in winter. The response to adrenaline in summer was also significantly greater than the responses to noradrenaline in both summer and winter. However, after treatment with propranolol there was no difference between the maximum vasoconstrictions to these two amines, in summer or in winter. Determination of dissociation constants for phentolamine indicated that adrenaline and noradrenaline acted on the same population of alpha-adrenoceptors in both summer and winter. The enhanced vasoconstriction to adrenaline in summer appears to be due to a reduced potency of adrenaline on renal vascular beta-adrenoceptors. The reduction in potency may be caused by a subtle configurational change in the beta-adrenoceptors, perhaps induced by hormonal changes associated with the onset of breeding.

Animals↗
PubMed1982

Somatostatin is contained in and released from cholinergic nerves in the heart of the toad Bufo marinus.

The heart of the toad Bufo marinus contained a substance with somatostatin-like immunoreactivity which eluted with somatostatin on reverse phase high pressure liquid chromatography. Immunoreactivity to somatostatin was localised histochemically to nerve fibers in muscle bundles of the sinus venosus, atria and ventricles and to nerve cell bodies in the sinus venosus and inter-atrial septum. Nerve cell bodies were localised both by interference contrast microscopy and immunohistochemistry; all detectable intracardiac neurons were immunoreactive. Synthetic somatostatin inhibited the rate and force of beat of atrial preparations, but did not affect the driven ventricle. Vagal stimulation caused inhibition of all cardiac chambers. After muscarinic blockade with hyoscine, vagal stimulation with 3 Hz or more still caused inhibition of the pacemaker and atrium, but not of the ventricle. The hyoscine-resistant vagal effects were diminished by about 60% after induction of tachyphylaxis to somatostatin. When when the vagus nerves were stimulated intermittently for 1 h at 10 Hz, in the presence or absence of hyoscine, the effect of somatostatin was reduced by about 60%. It is concluded that the cholinergic postganglionic neurons of the cardiac vagus contain somatostatin. When the vagus is stimulated at 3 Hz or more, the neurons release sufficient somatostatin to inhibit the pacemaker and atrial muscle.

Animals↗
PubMed1981

Structure and function of ciliated peritoneal funnels in the toad kidney (Bufo marinus).

Scanning electron microscopy revealed 600-800 ciliated peritoneal funnels opening onto the ventral surface of each kidney in Bufo marinus. The size and configuration of funnel apertures vary greatly, but individuals course beneath the kidney surface before opening into peritubular blood vessels. Injections of India ink into the peritoneal cavity demonstrate that cilia lining the peritoneal funnels create a current carrying peritoneal fluid into the renal vasculature. Clearance of fluid by the funnels was dependent on pressure in the peritubular vessels, and was increased by arginine vasotocin. Ciliated peritoneal funnels may provide an important route for return of lymphatic fluid from the peritoneal cavity to the vasculature.

Animals↗
PubMed1981

Resistance of adrenergic neurotransmission in the toad heart to adrenoceptor blockade.

Stimulation of sympathetic nerves to the toad heart produced increases in both the rate and force of cardiac beat. Although these responses were abolished by treatment with bretylium (10-6 mol.1-1) or 6-hydroxydopamine (100 mg.kg-1), and surgical sympathetic denervation, they were not abolished by treatment with propranolol (10-6 mol-1-1) and phentolamine (3 X 10-6 mol.1-1), either alone or in combination. The responses remaining after adrenoceptor blockade could not be ascribed to the effects of neurally released dopamine, ATP, adenosine, histamine or a variety of neuropeptides, although the participation of an as yet unidentified co-transmitter cannot be ruled out. Quantitative analysis of the interactions between propranolol and adrenaline on cardiac adrenoceptors, after blockade of alpha-receptors and amine uptake mechanisms, revealed that these interactions do not comply with the conditions for simple competitivity. Therefore, in addition to its action on beta-receptors, adrenaline seems to be producing excitation of the toad heart by acting on adrenoceptors which cannot be classified as either alpha- or beta-receptors. These results, together with the existence of close neuromuscular gaps (less than 50 nm) in the toad heart, are consistent with the hypothesis that sympathetic excitation of the toad heart is mediated by both "extra-junctional" beta-adrenoceptors, and "junctional" adrenoceptors which are neither alpha- nor beta-receptors.

Animals↗
PubMed1980

A head rest for cervical myelography.

A simple device for maintaining a patient's head position while performing cervical myelography is described. This holder permits patients to assume a comfortable position and is especially ideal when using lateral puncture at C1-2.

Contrast Media↗
PubMed1980

Rapid regression of pituitary prolactinomas during bromocriptine treatment.

Therapy for large prolactinomas remains controversial. Surgery is often unsuccessful in restoring endocrine function to normal. However, medical therapy with bromocriptine, a dopamine agonist, not only suppresses PRL levels, but may also lead to a reduction in tumor size. Previous reports have demonstrated radiographic evidence of tumor regression only after 3 or more months of bromocriptine therapy. We have now documented, for the first time, objective evidence of extremely rapid reduction in tumor size in two patients harboring large PRL-secreting pituitary tumors (mean pretreatment serum PRL levels, 2350 and 3900 ng/ml) who were prospectively treated with bromocriptine (7.5 mg/day) in preference to surgical intervention despite marked visual impairment in one of the patients. After 2 and 6 weeks of therapy, respectively, marked reduction in tumor size was demonstrated radiographically in both patients. Headache, visual acuity, and visual fields had improved after only 3 days. Although the mechanism of bromocriptine's antitumor activity is unclear, we believe that a large prospective trial to study the effects of bromocriptine therapy on the size of PRL-secreting macroadenomas is urgently needed to determine whether medical therapy should become the primary modality of treatment to reduce tumor size as well as restore endocrine function.

Adenoma↗