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Biomedical subjects

M E Allison

Publications and source records attributed to M E Allison.

At least 55 records · Page 3Linked to original sources
PubMed1978

The early use of fine-needle percutaneous transhepatic cholangiography in an approach to the diagnosis of jaundice in a surgical unit.

Fine-needle percutaneous transhepatic cholangiography (PTC) was performed in a series of 46 patients with jaundice or suspected biliary tract disease. The ductal system was successfully outlined in each of 20 patients with dilated intrahepatic ducts and in 19 of 26 patients with intrahepatic ducts of normal calibre. There were two episodes of septicaemia after PTC, one of them fatal. Valuable accurate diagnostic information was obtained in all cases with biliary tract obstruction. A programmed approach to diagnosis of suspected obstructive jaundice is outlined. Fine-needle PTC is an acceptably safe procedure and need not be followed by immediate laparotomy.

Adult↗
PubMed1978

Structural changes of experimental glomerulonephritis in rats as revealed by microdissection.

Microdissection revealed striking alterations in the nephrons of animal models AICN and anti-GBMN. The most severely damaged AICN kidney in the series presented marked heterogeneity in the size and deformity of the proximal tubules, corresponding to the diverse and variegated nephrons described by Oliver in chronic Bright's disease. The severely damaged anti-GBMN kidneys revealed widespread alterations in the proximal tubules, which, however, tended to be fairly uniform among the affected nephrons. This uniformity, perhaps, reflected the shorter duration of disease in the anti-GBMN animals. The most characteristic proximal tubular alteration in either the AICN or anti-GBMN animals was that combining atrophy of the pars convoluta and hypertrophy of the pars recta in same tubule. The largest and smallest nephrons encountered in the entire study were found in the most severly damaged kidney in the AICN. This finding reflected the simultaneous existence of regressive and progressive changes in this kidney, as certain nephrons underwent hypertrophy to compensate for the atrophy and disappearance of others. The remarkable functional glomerulotubular balance of single nephrons known to exist in both AICN and anti-GBMN was matched by the evidence presented here of structural glomerulotubular balance among the severely altered nephrons of a representative kidney from each group. Microdissection studies directed toward the characterization of the nephronic alterations in both membranous glomerulonephritis and proliferative glomerulonephritis of man should be of interest in relation to the findings in these experimental rat models of human disease.

Animals↗
PubMed1975

Effect of intravenous frusemide on plasma renin concentration: suppression of response in hypertension.

1. Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium. 2. The renin response to frusemide was suppressed in patients with primary hyperaldosteronism. 3. In patients with low-renin hypertension and normal renin essential hypertension, the renin response to frusemide was similarly suppressed. 4. Suppression of the renin response to frusemide is therefore a feature of hypertension not confined to patients with primary hyperaldosteronism and low-renin hypertension. 5. Thus low-renin hypertension does not appear to constitute a distinct diagnostic entity. 6. It is suggested that suppression of the renin response is part of a long-term renal adaptation to high blood pressure.

Adult↗
PubMed1975

Response of plasma aldosterone to fludrocortisone in primary hyperaldosteronism and other forms of hypertension.

The response of plasma aldosterone to fludrocortisone administration (400 mug 12-hourly for 3 days) was studied in twenty-two patients with primary hyperaldosteronism. No difference was observed in the response between those patients with an adrenal adenoma and those with bilateral adrenocortical hyperplasia, there being no significant change in plasma aldosterone levels across the test period. No separation between the groups was seen when basal plasma renin concentration was related to the aldosterone level following fludrocortisone. It is concluded that the test is of little value in the pre-operative differentiation of these conditions. Twenty-three patients with no demonstrable cause for their hypertension and four with elevated levels of plasma deoxycorticosterone were similarly studied for comparison. These groups demonstrated a normal fall in plasma aldosterone levels following fludrocortisone.

Adenocarcinoma↗
PubMed1975

Hyperoncotic albumin infusion in experimental glomerulonephritis in rats: A micropuncture study.

The effect of infusion of hyperonciotic (25 g% salt-poor bovine plasma albumin) (0.06 g% of body weight) has been studied using clearance and micropuncture techniques in animals with two forms of immunologically induced experimental glomerulonephritis and in age-matched control rats. In control rats the significant natriuresis and diuresis after hyperoncotic albumin were associated with decreased fractional and absolute proximal reabsorption, decreased calculated efferent oncotic pressure, and a transitory rise in efferent arteriolar hydrostatic pressure. These findings, however, do not necessarily indicate a predominant role for peritubular "physical factors" in the control of proximal reabsorption. In glomerulonephritic rats a smaller diuresis and an insignificant natriuresis were found after hyperoncotic albumin, especially in anti-GBM nephritis, when no change in SNGFR or proximal absolute reabsorption occurred. In AICN there was a rise in SNGFR and a fall in absolute reabsorptive rate, especially in those nephrons with high filtration rates. There was no evidence that any alteration in efferent arteriolar hydrostatic pressure of calculated efferent oncotic pressure had occurred.

Animals↗
PubMed1974

Tuberculosis as a continuing cause of renal amyloidosis.

In 40 patients with renal amyloidosis seen in a ten-year period tuberculosis was the major preceding disease in 20, though it was active in only two at diagnosis. Most patients presented with renal failure, and only two survived for five years. This experience (at least, in the west of Scotland) conflicts with the generally accepted view that rheumatoid arthritis is the commonest cause of renal amyloidosis.

Acute Kidney Injury↗
PubMed1974

Pathophysiology of experimental glomerulonephritis in rats.

Micropuncture, clearance, immunofluorescence and light microscopy techniques were used to study kidney structure and single nephron function in rats with autologous immune complex nephritis (AICN), a membranous glomerulonephritis developing over 5 to 20 mo, in the more acute and proliferative glomerular basement membrane (GBM) nephritis and in controls. Both models are known to have clinical counterparts in human disease. Kidney functional abnormalities correlated with the degree of architectural derangement. In both AICN and anti-GBM nephritis filtration fraction fell in direct proportion to the fall in glomerular filtration rate (GFR), renal plasma flow being unchanged. Fractional electrolyte excretion increased as the GFR fell. Despite marked heterogeneity of single nephron filtration rate (SNGFR) (AICN, 5-93 nl/min; anti-GBM, 0-50 nl/min) and of proximal tubular hydrostatic pressure (4-48 mm Hg), each nephron showed almost complete glomerulotubular balance, absolute reabsorption to the late proximal convolution varying directly with filtration rate. In addition SNGFR could be related both to proximal intratubular hydrostatic pressure and to calculated glomerular capillary pressure (Pg), being lowest in those nephrons with the highest intratubular pressure. Nephrons with very high filtration rates did not apparently reach filtration equilibrium. Mean SNGFR was significantly lower in the anti-GBM group, while calculated Pg was the same in both. This probably reflects the acute and diffuse involvement of the anti-GBM lesion with different filtration characteristics from the more chronic AICN disease. Tubular damage was more marked in AICN, and extraction of p-aminohippurate was reduced in this group.

Blood Proteins↗
PubMed1972

High dosage metolazone in chronic renal failure.

Metolazone is a modified quinazolinesulphonamide and in a dose of between 4 and 7.5 mg is an effective diuretic in man with normal renal function. Fourteen patients with non-oedematous stable chronic renal failure (creatinine clearance ranging from 1.2 to 12 ml/min) were given metolazone in doses ranging from 20-150 mg. A noticeable increase in urine flow and sodium excretion occurred, free water clearance increased, and there was a small but significant increase in potassium excretion. No side effects were noted.

Adolescent↗