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Biomedical subjects

M Cain

Publications and source records attributed to M Cain.

At least 19 recordsLinked to original sources
PubMed2000

Assessment of the value of the vertebral heart scale in the radiographic diagnosis of cardiac disease in dogs.

In order to assess the influence of the vertebral heart scale (VHS) on the accuracy of the radiographic diagnosis of cardiac disease, thoracic radiographs of 50 dogs with proven cardiac disease, 26 with other thoracic diseases, and 50 with no clinical signs of cardiovascular or respiratory disease were mixed and examined by three independent, blinded observers chosen to represent a range of radiographic abilities. They first examined all the radiographs without making measurements of VHS and made a diagnosis. They then re-examined the radiographs, and measured VHS on both lateral and dorsoventral or ventrodorsal radiographs before again recording a diagnosis without reference to their original diagnoses. For all the observers, the dogs with cardiac disease had a higher mean VHS than the normal dogs. A VHS over 10.7 on the lateral radiograph was a moderately accurate sign of cardiac disease. The observers' accuracy of diagnosis did not change significantly as a result of using VHS as an adjunct to a subjective assessment of the radiographs.

Animals↗
PubMed1989

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.

Adrenal Glands↗
PubMed1988

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.

Adolescent↗
PubMed1987

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.

Animals↗
PubMed1987

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.

Adult↗
PubMed1986

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.

Adrenalectomy↗