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Biomedical subjects

M J Sole

Publications and source records attributed to M J Sole.

At least 91 records · Page 5Linked to original sources
PubMed1981

Decreased brain serotonin turnover after short term (two-hour) adrenalectomy in rats: a comparison of four turnover methods.

Within the first 2 h after adrenalectomy in rats there is a marked decrease in hypothalamic, brain stem, and hippocampal serotonin (5HT) turnover. This adrenalectomy-induced decrease in brain 5HT turnover was demonstrated in this study using four different methods. These include 1) accumulation of 5HT after monoamine oxidase inhibition with pargyline, 2) decline of 5-hydroxyindoleacetic acid after pargyline, 3) accumulation of 5-hydroxytryptophan after aromatic L-amino acid decarboxylase inhibition with m-hydroxybenzylhydrazine, and 4) accumulation of 5-hydroxyindoleacetic acid after probenecid. The adrenalectomy-induced decreases in 5HT turnover in these areas were prevented by glucocorticoid treatment with either corticosterone or dexamethasone. The similarity of the results obtained with four different methods of assessment of brain 5HT turnover provides strong evidence to suggest that the activity of 5HT neurons, in at least three brain areas, is decreased within the first 2 h after adrenalectomy. Also, it seems likely that glucocorticoid withdrawal is the important factor in this adrenalectomy-induced decrease in brain 5HT turnover. In addition, an increase in hypothalamic 5HT turnover in response to the surgical stress of sham adrenalectomy could be demonstrated. The adrenalectomy-induced decreases in brain 5HT turnover were also prevented by the administration of the serotonin receptor antagonist, pizotifen. In addition, serotonin receptor blockade with pizotifen inhibited the effect of corticosterone to normalize the adrenalectomy-induced changes in both the plasma ACTH concentration and brain 5HT turnover. These data provide further support for an interaction between glucocorticoids and brain 5HT neurons.

Adrenalectomy↗
PubMed1980

Plasma dopamine: source, regulation, and significance.

Plasma dopamine is present in free form in a concentration approximately equivalent to that of epinephrine and about 25% that of norepinephrine. It originates in a variety of tissues including sympathetic nerves and adrenal, and the percentage originating from the various sources remains unknown. Events that are associated with increases in sympathetic activity such as stress, exercise, standing, or hypovolemia are associated with increases in plasma dopamine concentration, although the responses may be of considerably smaller magnitude than those for plasma norepinephrine and epinephrine. The functional importance of dopamine in the periphery and of changes in circulating dopamine remain only poorly defined. These include possible roles in neurotransmission in sympathetic ganglia, altering renal vascular bed, modulation of aldosterone secretion and sodium excretion, mediation of certain stress responses, and others yet to be revealed.

Adrenal Glands↗
PubMed1980

Electrophoretic profiles of nonhistone nuclear proteins of human hearts with muscular subaortic stenosis.

Muscular subaortic stenosis (MSS) is a genetically determined cardiomyopathy, whereas right ventricular infundibular hypertrophy (IH) apparently is an acquired condition. Since genetic expression in eukaryotic cells may be regulated primarily by DNA-associated proteins, we isolated and characterized the proteins of heart nuclei from nine patients with MSS, eight with IH, and two with normal (N) hearts. More than 150 proteins could be identified by two-dimensional polyacrylamide gel electrophoresis. Proteins in the entire region from pH 7.0 to 9.0 with molecular weights (Mr) ranging from 35,000 to 41,000 and a protein focusing from pH 5.2 to 5.3 with Mr of 55,000 were strikingly reduced in MSS. Again the electrophoretic patterns of N and IH were similar. The electrophoretic patterns of nonhistone nuclear protein (NHNP) in MSS relative to N showed a striking resemblance to those demonstrated previously for the early stage (myolytic phase) of hamster cardiomyopathy relative to the matched control. Since NHNP interacting with DNA appears to play a major role in genetic expression, it is possible that some of the manifestations of MSS could be due to different components of NHNP in the affected hearts.

Animals↗
PubMed1979

Localization of pheochromocytoma by selective venous catheterization and assay of plasma catecholamines.

The diagnosis of pheochromocytoma rests primarily on determination of the 24-hour urinary excretion of catecholamines and their metabolites. In most cases nephrotomography and selective arteriography or venography, or both, are sufficient to localize the tumour. Selective venous catheterization and the assay of plasma catecholamines should be considered for pheochromocytoma localization in: (a) patients in whom standard techniques fail to localize the tumour; (b) patients who exhibit idiosyncratic reactions to the angiographic contrast materials; (c) young patients or patients with familial pheochromocytoma, including those with multiple neurofibromatosis or multiple endocrine adenomatosis, type 2; (d) patients with recurrent, malignant, or suspected multicentric or extra-adrenal tumours; and (e) patients excreting only norepinephrine in the urine. The validity of the results is particularly dependent on the skill with which venous catheterization is carried out.

Adrenal Gland Neoplasms↗
PubMed1979

Effects of bromocriptine on plasma catecholamines in normal men.

Administration of a single oral 2.5 mg dose of bromocriptine (Brc), a dopamine (DA) receptor agonist, to normal male volunteers results in comparable marked decreases in resting supine plasma concentrations of DA (decrement 2 h after drug administration was 67 +/- 5%; mean +/- SE), norepinephrine (NE; 63 +/- 3%) and epinephrine (E; 65 +/- 5%); decreases in all three plasma catecholamine (CA) concentrations were significant at p less than 0.001. This effect of Brc on plasma CAs was initiated more rapidly and was of briefer duration than the suppressive effect on serum prolactin (Prl). When Brc was administered daily for 1 week, its effect on plasma CAs had terminated within 4 h of its adninistration. A further oral dose after administration of Brc for 1 week produced identical suppressive effects on plasma CAs to those observed following the 1st dose. Brc did not prevent the incremental response of plasma DA, NE and E to standing. Also, orthostatic hypotension occurred on occasion, in spite of normal plasma CA responses to standing. Brc did not affect basal serum concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone or dihydrotestosterone. These data describing a suppressive effect of Brc on plasma DA, NE and E suggest that Brc inhibits release of these CAs from peripheral sympathetic nerve endings and adrenal medulla, and acts at least in part through presynaptic CA receptors in the brain. The suppressive effect of Brc on plasma CAs may prove useful as a test of normal presynaptic CA mechanisms.

Adult↗
PubMed1979

Catecholamines in coronary sinus and peripheral plasma during pacing-induced angina in man.

We measured aortic and coronary sinus dopamine (DA), epinephrine (E), and norepinephrine (NE) in eight patients with cardiac ischemia (I) and eight control subjects (C). Samples were taken at rest (73 +/- 3 beats/min in C and 68 +/- 3 beats/min in I) and during coronary sinus pacing to peak rates (144 +/- 4 beats/min in C and 136 +/- 6 beats/min in I). Arterial NE was higher in the ischemic patients at rest (254 +/- 25 pg/ml in C and 324 +/- 21 in I; p less than 0.05). There were no differences in arterial E and DA. Neither pacing nor angina affected peripheral catecholamine concentrations. Resting myocardial NE flux was similar for both groups. With pacing, coronary sinus flow and net myocardial NE release increased significantly in both groups. The maximum relative increase in net myocardial NE release was less in the ischemic patients than in the controls (575 +/- 145% in C and 255 +/- 40% in I; p less than 0.05). Thus, angina induced by pacing does not augment peripheral sympathetic activity. Furthermore, pacing-induced angina appears to be associated with a decrease in cardiac sympathetic tone compared with that found in paced controls.

Angina Pectoris↗
PubMed1979

The extraction of circulating catecholamines by the lungs in normal man and in patients with pulmonary hypertension.

We directly measured the net pulmonary extraction of circulating norepinephrine, epinephrine and dopamine in control patients and patients with primary or secondary pulmonary hypertension. Mixed pulmonary artery norepinephrine, epinephrine and dopamine were 314 +/- 13 pg/ml, 102 +/- 9 pg/ml, 51 +/- 5 pg/ml, respectively, for the control group; values were similar in patients with pulmonary hypertension. The pulmonary extraction of norepinephrine was 25.4 +/- 2.6% (clearance 266 +/- 62 ng/min) in control patients; epinephrine and dopamine were not extracted. There was no net extraction or production of any of the three catecholamines by the lungs in any of the patients with pulmonary hypertension. We conclude that the lungs play a significant role in the inactivation of circulating norepinephrine in man. This metabolic function of the lungs appear to be lost in pulmonary hypertension.

Adult↗
PubMed1978

Left ventricular receptors inhibit brain serotonin neurons during coronary artery occlusion.

Acute coronary artery ligation in pargyline-treated rats decreased serotonin and increased 5-hydroxyindoleacetic acid in the medulla and posterior hypothalamus. Lidocaine applied topically to the left ventricle completely prevented these alterations. No changes in serotonin were observed in the other brain regions examined. These data suggest a reflex inhibition of bulbar and hypothalamic serotonergic nerves by left ventricular receptors following acute coronary artery occlusion in the rat.

Animals↗
PubMed1978

Effects of clonidine on vulnerability to fibrillation in the normal and ischemic canine ventricle.

Clonidine infusion (10 microgram/kg, i.v.) elicited a 30% increase in repetitive extrasystole (RE) threshold in 6 chloralose-anesthetized dogs. A reduction in heart rate and arterial blood pressure accompanied the increased threshold. Intracisternal injection of clonidine (2 microgram/kg) in 6 dogs caused similar alterations in these parameters. Bilateral vagotomy, performed in 6 dogs prior to intravenous clonidine, prevented the increase in RE threshold but did not prevent the drug-induced bradycardia. Atropine (0.2 and 0.6 mg/kg), however, did not attenuate the effect of clonidine on RE threshold. Clonidine administration did not prevent the reduction in ventricular fibrillation threshold associated with a 10 min occlusion of the left anterior descending coronary artery or following reperfusion. We conclude that: (1) clonidine reduces ventricular vulnerability in the normal but not the ischemic heart, and (2) its protective effect is mediated by enhanced afferent vagal input to midbrain cardiovascular regulatory centers. This central nervous system action causes a reduction in sympathetic tone to the heart.

Animals↗
PubMed1978

Nuclear proteins in the heart of the cardiomyopathic Syrian hamster. Phosphorylation of phenol-soluble nonhistone proteins.

We examined incorporation of 32P into phenol-soluble nonhistone nuclear acidic proteins (NHNP) obtained from myolytic, hypertrophic, and failing phases of hamster cardiomyopathy. NHNP from these dystrophic hamster hearts were phosphorylated much less than their controls, despite a 9-fold increase in uptake of 32P into their nuclei. After fractionation of NHNP by isoelectrofocusing polyacrylamide gel electrophoresis, two major fractions focusing from pH 6.0 to 6.2 and 6.6 to 6.8 were highly phosphorylated in both the control and dystrophic hearts. The latter fraction was much more phosphorylated in the control. Two fractions of NHNP focusing at pH 4.9 and 5.1 were more highly phosphorylated in the dystrophic hearts than in the controls. Autoradiographs obtained from the two-dimensional polyacrylamide slab gel electrophoresis showed that two proteins (pH 4.9 and 5.1; mol wt 25,000 and 60,000, respectively) were highly phosphorylated in the dystrophic heart. There was no detectable phosphorylation of these proteins in the controls. These changes in the phosphorylation of cardiac NHNP may be important in determining the alteration of gene expression in hamster cardiomyopathy.

Animals↗
PubMed1978

Alterations in brain serotonin during congestive heart failure in the cardiomyopathic Syrian hamster.

Serotonin and its major metabolite 5-hydroxyindoleacetic acid were measured in the pons-medulla, midbrain, posterior hypothalamus, anterior hypothalamus, thalamus, and cerebellum of cardiomyopathic hamsters and their age-matched controls during the early and terminal stages of the cardiomyopathy. During the stage of cardiac decompensation, significant increases were observed in the concentration of serotonin in pons-medulla (2.30 +/- 0.07 vs 1.74 +/- 0.04; P less than 0.001) and posterior hypothalamus (3.49 +/- 0.04 vs. 3.04 +/- 0.11; P less than 0.005) and in 5-hydroxyindoleacetic acid in pons-medulla (1.42 +/- 0.05 vs 0.97 +/- 0.05; P less than 0.001) and posterior hypothalamus (1.65 +/- 0.02 vs 1.32 +/- 0.07; P less than 0.001). No changes were noted in any of the brain regions of control animals. We conclude that congestive heart failure may be associated with alterations in activity of bulbohypothalamic serotonergic nerves.

Animals↗
PubMed1977

Differential responsiveness of central noradrenergic and dopaminergic neuron tyrosine hydroxylase to hypophysectomy, ACTH and glucocorticoid administration.

Hypophysectomy leads to a small increase in tyrosine hydroxylase activity of all brain areas containing noradrenergic neurons or tuberoinfundibular dopamine neurons, but nigroneostriatal dopamine neurons are not so affected. ACTH or corticosterone treatment inhibited this effect of hypophysectomy in some noradrenergic neurons and in tuberoinfundibular dopamine neurons. These data showing differential responsiveness of tyrosine hydroxylase in different brain areas are compatible with differences in regulation or molecular form of tyrosine hydroxylase in central noradrenergic and dopaminergic neurons. The disparity between increased hypothalamic tyrosine hydroxylase activity and decreased norepinephrine turnover following hypophysectomy may result from a change in the rate-limiting step to the hydroxylation of dopamine.

Adrenocorticotropic Hormone↗