Search PubMed⌕ Search

Biomedical subjects

M Finlay

Publications and source records attributed to M Finlay.

At least 37 records · Page 2Linked to original sources

Quantitative changes in the rat pulmonary vasculature in chronic hypoxia--relation to haemodynamic changes.

The anatomical basis of resistance and compliance changes of the pulmonary arterial bed was studied in rats exposed to chronic hypoxia (10% O2, 3 weeks) and the findings were compared with those of normoxic rats. The lungs were perfused with a Ba-gelatine mixture at different pressures and studied by radiology and histology. The diameter of the pulmonary arteries (greater than 0.5 mm), measured from X-rays, was less in chronically hypoxic than normoxic rats when filled at the same perfusion pressure. Diameters increased in both groups with increasing perfusion pressure but at a given pressure those of chronically hypoxic rats were always smaller than those of normoxic rats. We found evidence that arterial length was increased in chronically hypoxic rats. Arterioles of 50 micron or less in diameter adjacent to gas exchange units were of similar external diameter in normoxic and chronically hypoxic rats, but most of the latter had developed a muscular coat and a second elastic lamina internal to the single elastic lamina of control arterioles. These changes reduced the lumen by an estimated 10-14% and would increase pulmonary arteriolar resistance in chronically hypoxic rats, resulting in a changed pressure profile. We found no evidence of arteriolar loss in chronically hypoxic rats although at a given pressure, the Ba-gelatine mixture penetrated less far for reasons which are discussed.

Angiography↗

A new variant of serum leucine aminopeptidase in the mouse: its development and possible regulation.

Serum leucine aminopeptidase (LAP) isozymes were compared in four strains of inbred mice during postnatal development, adult life, and pregnancy. In pregnancy, no changes in the maternal serum LAP pattern were observed, in contrast to human studies. One strain, DD/S, differs from the other three in serum LAP. Polymorphism in serum LAP has not been previously described in the mouse. Neonatal DD/S mice exhibit a single band of serum LAP upon starch gel electrophoresis; however, between 14 and 18 days of age, two distinct bands appear, which persist throughout adult life. In the strains C57BL/6J, BALB/cJ, and DBA/2J there is a single band of activity at all stages. Crosses and backcrosses between DD/S and C57BL/6J show that the double-band variant is inherited as an autosomal recessive. The variant is independent of both the supernatant malic enzyme (Mod-1) and the intestinal LAP (Lap-1) loci, which are known to be linked on chromosome 9. The serum LAP variant is linked to an intestinal alkaline phosphatase variant. The presence of a separate structural gene is suggested by the genetic independence of the serum LAP variant from Lap-1. Also, the two serum LAP bands of DD/S are not interconverted by treatment with neuraminidase, beta-mercaptoethanol, or heat or by mixing the sera of DD/S and C57BL/6J prior to electrophoresis. The level of serum LAP activity in DD/S is approximately twice that in C57BL/6J. While these observations imply two structurally distinct proteins, the absence of any trace of the second LAP band in the heterozygote strongly suggests that the LAP variant protein is not the result of a separate structural gene. Intestinal LAP in DD/S migrates with the same electrophoretic mobility as the serum LAP variant, implying that the variant might originate in the intestine and its appearance in the serum be modulated by some factor at an unlinked locus.

Age Factors↗

Results of simple aspiration of pneumothoraces.

The results of simple aspiration in 30 cases of pneumothorax are presented. The procedure was successful in 33% of cases with known pre-existing lung disease, and in 83% of those without. Aspiration was also more successful in those patients under 50 years of age and if the estimated degree of lung collapse was less than 50%.

Adult↗

Cardiac output, pulmonary hypertension, hypoxaemia and survival in patients with chronic obstructive airways disease.

A prospective study of cor pulmonale in 74 patients relates pulmonary haemodynamics to survival. Mean arterial oxygen tension (PaO2) was 7.2 +/- 0.14 kPa and mean arterial carbon dioxide tension (PaCO2) 6.6 +/- 0.12 kPa at entry. Pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), and cardiac output (CO) sitting and supine and where possible on exercise, were measured every one or two years by a floating catheter technique. Survivors showed very little change in pulmonary artery pressure, pulmonary vascular resistance or cardiac output. Those who did not survive, showed a steady increase of PAP and PVR, whether or not they had received continuous oxygen therapy at home. Cardiac output remained normal or slightly elevated despite increasing pulmonary artery pressure. The relationship between VO2 (minute oxygen consumption) and cardiac output remained within the normal or greater than normal range, even on exercise. Although a deteriorating clinical situation may be paralleled by changes in pulmonary haemodynamics, it is questioned whether such changes are causally implicated in mortality.

Cardiac Output↗