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Biomedical subjects

H Purcell

Publications and source records attributed to H Purcell.

53 records · Page 3Linked to original sources
PubMed1991

Identification and localization of pertussis toxin-sensitive GTP-binding proteins in bovine kidney glomeruli.

The vascular tree and the mesangium in the glomerulus respond to various hormones, growth factors, and autonomic signals, leading to generation of second messengers and regulation of ion channels. Guanine nucleotide regulatory proteins (G proteins) mediate these effects in other systems. Glomerular G proteins were studied by immunoblotting and immunohistochemical techniques. Glomeruli were isolated from bovine kidney cortex by differential sieving. Glomerular proteins were resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and nitrocellulose transfers were immunoblotted with antibodies to G proteins. G alpha,common antiserum (P-960) recognized proteins with a molecular mass of 41 to 45 kDa. Antibodies against peptide sequences specific to Gi alpha and Go alpha demonstrated Gi alpha, 1/3 (molecular mass, 39 to 41 kDa), Gi alpha 2 (molecular mass, 40 kDa), and Go alpha (molecular mass, 39 kDa). Presence of these proteins was further confirmed by pertussis toxin-catalyzed ADP ribosylation of protein(s) with a molecular mass of 39 to 41 kDa in the glomeruli. Immunohistochemical staining of frozen sections from bovine kidney cortex revealed the presence of Gi alpha 2 in capillary loop distribution in glomeruli and interstitium, but Gi,1/3 or Go could not be demonstrated. The pattern of immunofluorescence with Gi alpha 2 antiserum suggested localization of Gi alpha 2 to the endothelium in glomerular and interstitial vasculature. The novel finding of Go in glomeruli requires localization of Go to specific cells and determination of its role in glomerular physiology. In conclusion, these studies demonstrate that bovine kidney glomeruli express alpha subunits of pertussis toxin-sensitive GTP-binding proteins Gi,1/3, Gi,2 and Go.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate Ribose↗
PubMed1991

Circadian patterns of myocardial ischaemia and the effects of antianginal drugs.

Chronopathology of cardiovascular disease is now well documented. Silent myocardial ischaemia involves the same pathophysiological changes as conventional ischaemia. Early morning peaks in angina and myocardial ischaemia call for adequate timing of medication. beta-blockers abolish the morning peak, and aspirin reduces morning infarctions. The effects of other antianginals on these phenomena are presently unknown.

Angina Pectoris↗
PubMed1978

The clinical value of digoxin in patients with heart failure and sinus rhythm.

Six patients in sinus rhythm with congestive heart failure due to either myocardial infarction or cardiomyopathy, were given oral frusemide to eliminate oedema. Symptomatic relief occurred as body weight was reduced, and after a 'dry' basal weight had been achieved, progressive-load exercise testing was done to examine any benefit that derived from adding oral digoxin to the diuretic. Three pairs of sub-maximal exercise tests were done at intervals over three months, and the responses of each patient when using digoxin and diuretics were compared with those when using diuretics alone. One patient did not complete this study, because more frequent premature beats and increased angina followed the withdrawal of digoxin. For the five patients who completed three pairs of tests, there was no significant change in symptoms, in workload achieved, or in heart rate, respiratory rate, ventilation and respiratory quotient, whether digoxin was added or removed. It is concluded that in these patients where salt and water retention was controlled with diuretics, digoxin did not improve the capacity for exercise, and it is suggested that for such patients with myocardial disease in sinus rhythm, treatment should begin with diuretics.

Adult↗
PubMedDate not supplied

Adrenal activation of carbon tetrachloride: role of microsomal P450 isozymes.

Previous investigations demonstrated that carbon tetrachloride (CCl4) was activated by adrenal microsomes, resulting in various functional changes and ultimately in necrosis of the zona reticularis of the gland. Experiments were done to identify the adrenal P450 isozyme(s) involved in the bioactivation of CCl4. Incubation of microsomes from the zona reticularis (ZR) of the guinea pig adrenal cortex with CCl4 plus NADPH caused initiation of lipid peroxidation, covalent binding of CCl4-derived radioactivity to protein, and degradation of cytochrome(s) P450. Preincubation of the microsomal preparations with inhibitory antibodies to P450(17 alpha) or P450C21 decreased the corresponding enzyme activities (17 alpha-hydroxylation and 21-hydroxylation), but did not affect the activation of CCl4. 1-Aminobenzotriazole (ABT), a suicide inhibitor of some P450 isozymes, decreased the enzyme activities catalysed by an adrenal 52,000 Da (52 kDa) isozyme, but had no effect on the function of P450(17 alpha) or P450C21. However, ABT completely inhibited the CCl4-induced LP and covalent binding in adrenal microsomes. The results indicate that adrenal CCl4 activation is catalysed by the 52 kDa P450 isozyme and not by the steroid hydroxylases. Localization of the 52 kDa isozyme to the ZR probably accounts for the selective necrosis of this region of the gland by CCl4.

Adrenal Cortex↗
PubMedDate not supplied

Improving outcome after acute myocardial infarction: what is the role of ACE inhibitors?

Acute myocardial infarction continues to be the number 1 killer in industrialised countries. While the more widespread use of thrombolytic therapy has made a dramatic impact on patient survival, changes in long-term prognosis after discharge from hospital have not improved radically and 5-year mortality remains at over 30%. The single most important determinant of survival in the long term is left ventricular function. The process of ventricular dilatation and remodelling begins early after infarction. While such changes may initially go unrecognised clinically, without intervention progressive functional impairment will ensue and the majority of patients will develop signs and symptoms of heart failure, which carries a worse prognosis than many forms of cancer. ACE inhibitors act on both the haemodynamic and neurohormonal mechanisms in heart failure. Several large-scale clinical trials have clearly demonstrated that early use of these agents in stable patients who are not hypotensive or in cardiogenic shock can reduce significantly the development of heart failure and death. A strategy for the early initiation of ACE inhibitor therapy is proposed to improve survival in AMI patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Structural changes in hypertension, the potential for their prevention, arrest and reversal: a focus on felodipine.

Hypertension is accompanied by a series of structural adaptations and pathological alterations in the heart and vessels. These include hypertrophy of the left ventricle and walls of resistance vessels, degeneration of elastic components in the walls of large arteries, atherosclerosis and glomerulosclerosis. In order to improve prognosis it is important that the antihypertensive drugs used can prevent or regress these processes, and this review focuses on the experience with the vascular selective calcium antagonist felodipine. Clinical studies show that antihypertensive treatment with felodipine promotes regression of left ventricular hypertrophy, increases compliance of large arteries, and has favourable effects on renal function. In addition, experimental data have shown that felodipine inhibits atherosclerotic plaque development. As structural cardiovascular changes appear early in hypertension, intervention with antihypertensive therapy is better initiated sooner than later. Vascular selective calcium antagonists, such as felodipine, appear effective in reducing blood pressure and in ameliorating hypertension-induced structural changes.

Felodipine↗