Biomedical subjects
M Cain
Publications and source records attributed to M Cain.
Funding essential health services.
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Integrating technology into resident and student curricula.
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Working with communities for health.
Nurses must continue to build links with communities to enable communities to control their own health outcomes.
Reducing professional liability.
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Anaphylactic reaction to intravenous cyclophosphamide.
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Taking to the water with Manchester's midwives.
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Neuropeptide Y in the sympathetic control of blood pressure in hypertensive subjects.
Neuropeptide Y (NPY) coexists with noradrenaline in postganglionic sympathetic neurons and with noradrenaline and adrenaline in the central nervous system. The possibility that NPY is released into the circulation during activation of the sympathoadrenal system was investigated in ten moderately hypertensive volunteers using three different stimuli. In healthy moderately hypertensive volunteers cold pressor test, head up tilt and graded bicycle exercise resulted in increased blood pressure, heart rate and plasma catecholamine concentrations. While there was a trend for plasma NPY-like immunoreactivity (NPY-LI) to increase during cold pressor test and head up tilt, NPY-LI concentration only increased significantly during bicycle exercise, the stimulus of greatest duration. These results suggest that plasma NPY-LI can be released into the circulation on sympathoadrenal activation in moderately hypertensive subjects and demonstrate that the pattern of release is similar to that previously observed in normotensive subjects.
Plasma atrial natriuretic polypeptide concentrations during and after reversion of paroxysmal supraventricular tachycardias.
Plasma concentrations of immunoreactive atrial natriuretic polypeptide were raised in 22 of 23 patients with paroxysmal supraventricular tachycardia and in all seven patients with atrial flutter. Plasma concentrations of atrial natriuretic polypeptide rose soon after the onset of supraventricular tachycardia. A sample taken 30 minutes after reversion to sinus rhythm (pharmacological or non-pharmacological) showed a significant fall in 19 of the 23 patients with paroxysmal supraventricular tachycardia and all seven patients with atrial flutter. Because atrial natriuretic polypeptide has powerful natriuretic and diuretic properties, an increase may contribute considerably to the polyuria that is often associated with episodes of supraventricular tachycardia.
Complementary changes in plasma atrial natriuretic peptide and antidiuretic hormone concentrations in response to volume expansion and haemorrhage: studies in conscious normotensive and spontaneously hypertensive rats.
1. Plasma concentrations of atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) were measured in conscious stroke-prone spontaneously hypertensive (SPR), spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats before and after acute volume expansion or haemorrhage. 2. Plasma ANP concentration was reduced to one-third of resting values 30 min after a 1.5% haemorrhage (1.5 ml of blood per 100 g bodyweight). Plasma ADH concentration rose immediately 50-fold on haemorrhage and remained elevated at 30 min. 3. Plasma ANP concentration increased 2.5-fold relative to resting values 1 min after infusion of 2.0 ml per 100 g 5% dextrose; after 10 min plasma ANP remained elevated. Plasma ADH concentration tended to fall on volume expansion although no significant decrease was observed. 4. There was no difference in the basal levels of ANP and ADH, or in the changes produced by alterations in blood volume, in hypertensive SPR and SHR compared with normotensive WKY. 5. Thus, plasma ANP concentrations moved in opposite directions in response to two physiological stimuli: volume expansion and haemorrhage. Reciprocal changes were observed in plasma ADH.
Direct radioimmunoassay of human plasma atrial natriuretic peptide in various normal and pathophysiological states: increase in renal and cardiac failure during exercise.
We have used a sensitive direct radioimmunoassay to study the effects of exercise on plasma atrial natriuretic peptide (ANP) concentrations in man. Plasma ANP concentration increased three-fold in sixteen patients undergoing bicycle ergometer electrocardiographic tests for the investigation of chest pain. Resting ANP concentrations were higher in those patients in whom there was more evidence of heart disease, such as a positive exercise test, treatment with a beta blocker or history of myocardial infarction, although exercise resulted in increased ANP in both groups. We also confirm the increased plasma ANP concentration observed in patients with congestive cardiac failure and renal failure. In nine patients with renal failure routine haemodialysis was accompanied by a 30 per cent reduction in plasma ANP concentration. Plasma ANP concentrations were similar in treated hypertensive patients, untreated borderline hypertensive patients and normotensive subjects.
Relative importance of sympathetic nerves and of circulating adrenaline and vasopressin in mediating hypertension after lesions of the caudal ventrolateral medulla in the rat.
Electrolytic lesions of the A1 noradrenaline cells in the caudal ventrolateral medulla cause transient hypertension and bradycardia in the conscious rat, as previously described in the rabbit. The lesions produced 100-fold increases in plasma arginine vasopressin, 40-fold increases in plasma adrenaline and fourfold increases in plasma noradrenaline levels. Absence of circulating vasopressin [homozygous diabetes insipidus rats (DI)] or circulating adrenaline (adrenalectomized rats) did not affect A1 hypertension, but sympathectomy with systemic 6-hydroxydopamine (6-OHDA) significantly attenuated A1 hypertension. A factorial experiment was performed to assess the relative contributions of these three peripheral effector mechanisms in a quantitative manner, with combined deficiencies of any two or of all three of these effector systems. Results suggest A1 hypertension in the rat to be primarily mediated through increased sympatho-adrenal activity. The largest component of hypertension (66%) results from increased sympathetic vasoconstrictor nerve activity, and a smaller part (34%) reflects the action of circulating adrenaline. Increases in vasopressin levels do not contribute to A1 hypertension, although vasopressin makes a major contribution to A1 lesion bradycardia.
Post-partum pituitary necrosis presenting as anaemia.
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The mechanism of hypertension and bradycardia following lesions of the caudal ventrolateral medulla in the rabbit: the role of sympathetic nerves, circulating adrenaline, vasopressin and renin.
Lesions of the ventrolateral medulla of the rabbit, coinciding with the A1 noradrenaline cell bodies (A1 lesions) produced fortyfold increases in the plasma levels of vasopressin and adrenaline, a twofold increase in plasma noradrenaline and a substantial increase in plasma renin activity. These increases accompanied the hypertension and bradycardia that follow A1 lesions. The vasoconstriction and hypertension were completely abolished by phentolamine, an alpha-adrenoceptor antagonist, when it was administered before lesions and were markedly reduced when it was given after lesions. On the other hand, administration of an antagonist to the vasoconstrictor action of vasopressin (d(CH2)5Tyr(Me)AVP) or an angiotensin converting enzyme inhibitor had little effect. Prior removal of the adrenal glands prevented any rise in plasma adrenaline levels but had no effect on the pressure response to subsequent A1 lesions. These results indicate that the vasoconstriction and hypertension were predominantly mediated by alpha-adrenoceptor stimulation, acting mainly through sympathetic vasoconstrictor nerves. The fall in heart rate following A1 lesions was approximately halved by pretreatment either with d(CH2)5Tyr(Me)AVP alone, or by blockade of the vagus and sympathetic with scopolamine and propranolol; it was completely abolished by combined pretreatment with all three agents. The experiments show that vasopressin release makes a major contribution to the bradycardia acting at least in part through mechanisms that are independent of cardiac vagal or sympathetic nerves.
Biomimetic approach to potential benzodiazepine receptor agonists and antagonists.
Several beta-carbolines, isoquinolines, imidazopyridines , and canthin -6-ones prepared in biomimetic fashion were tested for their ability to bind to the benzodiazepine receptor. Methyl isoquinoline-3-carboxylate, methyl 6,7- dimethoxyisoquinoline -3-carboxylate (3b) 1-phenyl-3- carbomethoxyimidazopyridine , (6B,) and canthin -6- one ( 13a ) bound with moderate affinities, while 2- carbomethoxycanthin -6- one ( 13b ) bound to benzodiazepine receptors with an affinity comparable to several pharmacologically active benzodiazepines. The potency of 13b suggests that the benzodiazepine receptor(s) can tolerate substitution at positions 1 and 9 of a beta-carboline without loss of activity if the substituents are trigonal and maintain a planar topography. Moreover, displacement of the carbonyl group by two atoms from the aromatic ring (C) of the beta-carboline skeleton caused a marked decrease in binding to the benzodiazepine receptor. This observation supports the hypothesis that maximum binding affinity of beta-carbolines is achieved when the carbonyl group at position 3 is attached directly to the aromatic pyridine ring.
Hypertension after brainstem (A1) lesions in normal rats and in rats with adrenalectomy, sympathectomy or diabetes insipidus.
Lesions of the ventrolateral medulla coinciding with the A1 noradrenaline cell group, in either the rabbit or the rat, cause hypertension and bradycardia accompanied by 50-fold increases in plasma vasopressin and adrenaline and a two-to-four-fold increase in plasma noradrenaline. Following adrenalectomy in normal rats, the A1 hypertension and bradycardia were unchanged. In Brattleboro rats with diabetes insipidus, A1 hypertension was not altered but the bradycardia was reduced by 40%. In Brattleboro rats subjected to adrenalectomy, the hypertension was reduced by 50%. In normal rats, chemical sympathectomy with intravenous 6-hydroxydopamine (6OHDA) reduced the hypertension by about 50%, and when combined with adrenalectomy it abolished the hypertension altogether. In Brattleboro rats, 6OHDA reduced the hypertension after A1 lesions by about 40%. We suggest that A1 hypertension is predominantly mediated through increased activity of sympathetic vasoconstrictor nerves, and that circulating adrenaline and vasopressin only make a minor contribution to the increase in pressure.
Hyperkalemia in the elderly.
Hyperkalemia is a common and potentially dangerous condition in elderly patients. These subjects are more likely to have a disease or be taking medications that may induce this disorder. We describe three such cases where the increased concentration of potassium in plasma resulted from decreased renal excretion of this ion, and suggest a simple approach to the etiological diagnosis of hyperkalemia.