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Biomedical subjects

P Hamosh

Publications and source records attributed to P Hamosh.

At least 109 records · Page 6Linked to original sources
PubMed1977

The effect of prolactin on the lecithin content of fetal rabbit lung.

1 mg ovine prolactin was injected intramuscularly into rabbit fetuses (24th day of gestation) located in one of the two uterine horns exposed by laparotomy (n = 12). Fetuses in the other uterine horn were injected with an identical volume of vector and served as controls (n = 13). 2 days later the fetuses were removed by a second laparotomy and sacrificed. Analysis of lung tissue composition yielded the following results: (a) the prolactin-treated group of fetuses showed 40% higher total lung phospholipid content (17.0 +/- 0.8 micronmol/g) than the control group (12.2 +/- 0.5 micronmol/g); (b) the prolactin-treated group had a 67% higher lung lecithin content (8.7 +/- 0.8 micronmol/g) than the control group (5.2 +/- 0.4 micronmol/g); (c) dipalmitoyllecithin accounted for 67% of total lung lecithin in the prolactin-treated group and 44% in the control group. These differences were statistically highly significant (P less than 0.001). However, between the prolactin-treated and the control groups, there were no statistically significant differences in body weight and length, lung weight, the ratio of lung weight to body weight, DNA, protein and, water content. These results suggest that prolactin might be a trigger of lung surfactant synthesis in the rabbit fetus.

Animals↗
PubMed1977

Airway response to short-term inhalation of tobacco smoke. Lack of racial differences.

Airway response to short-term inhalation of cigarette smoke was studied in healthy black subjects. We have measured thoracic gas volume, airway resistance, maximum expiratory flow rates, and closing volume in 12 healthy black volunteers before and after smoking a cigarette. We found a significant reduction in airway conductance and midexpiratory flow rate after smoking the cigarette. The results are similar to those previously observed in white subjects. We conclude from our study that the response to short-term inhalation of cigarette smoke is identical in both white and black subjects.

Adult↗
PubMed1977

The effect on expiratory flow rates of smoking three cigarettes in rapid succession.

The effect of smoking three cigarettes in rapid succession on maximal and partial expiratory flow rates was studied in ten healthy smokers. The mean decrease in maximal midexpiratory flow and partial midexpiratory and end-expiratory flow was statistically significant. The response was maximal after the first cigarette. These results suggest that the instantaneous midexpiratory flow after 50% of the forced vital capacity has been exhaled is a useful indicator of irritation of the airways. Reduction of partial expiratory flow rates was three times greater than reduction of maximal expiratory flow rates. We suggest the use of partial expiratory flow curves as a screening test for irritants of the airways.

Adult↗
PubMed1976

Lipoprotein lipase in rat lung. Effect of dexamethasone.

The effect of hormone administration on the activity of lipoprotein lipase in the lung was studied in the rat. The following hormones were administered: dexamethasone, L-thyroxine, estradiol-17beta and progesterone. In addition, lung lipoprotein lipase activity was studied in diabetic and lactating rats. Lipoprotein lipase activity was measured in dried, defatted preparations of rat lung using double labeled ([14C]palmitate, [3H]glycerol) chylomicron triacylglycerol as substrate. Dexamethasone administration caused a rise of 70% in the level of activity of lipoprotein lipase in acetone powders of lung and a 100% increase in the amount of enzyme released during heparin infusion into isolated, perfused lungs. Enzyme activity was higher in lungs of females than of male rats; however; the level of activity was unaffected by estrogen or progesterone administration to either male or ovariectomized rats. Diabetes, hyperthyroidism or lactation did not change lipoprotein lipase activity in the lung. The constant presence of lipoprotein lipase activity in the lung suggests that this organ is able to maintain a steady supply of triacylglycerol-fatty acids under a variety of physiological and pathological conditions. Stimulation of enzyme activity by dexamethasone could lead to increased uptake of triacylglycerol-fatty acids by the lung and may thus be a contributing factor to corticosteroid-induced enhanced surfactant synthesis.

Animals↗
PubMed1976

Aspirin and exercise-induced asthma.

In four subjects with exercise-induced asthma, aspirin and placebo were administered prior to exercise in a double blind study. Pulmonary function tests did not reveal any difference between the response after aspirin or placebo. We conclude that in these four subjects aspirin did not prevent the bronchoconstrictor response. This might suggest that prostaglandins have no significant role in exercise-induced asthma.

Adult↗
PubMed1975

Lipoprotein lipase in rat lung. The effect of fasting.

We measured lipoprotein lipase activity in dried defatted preparations of rat lung using doubly labeled chylomicron triglyceride as substrate. The enzyme activity was linear for the first hour of incubation at 37 degrees C, had a pH optimum of 8.1 and was completely inhibited by 0.5 M NaC1. Lungs from fed rats hydrolyzed chylomicron triglyceride at a rate of 13.00 mumoles/g per h; the activity rate was unchanged by fasting 8-72 h. Heparin infusion into isolated lungs caused immediate release of lipoprotein lipase to the venous effluent. The activity released was equivalent to about 10% of total lung lipoprotein lipase activity in both fed and fasted rats. Since the ability to remove blood triglyceride is directly related to the level of lipoprotein lipase activity, these findings indicate that the lung is one of the few tissues able to remove efficiently blood triglyceride during fasting.

Animals↗
PubMed1975

The effect of prostaglandin F2beta on expiratory flow rates.

Prostaglandin F2beta (PGF2beta), a stereoisomer of F2alpha was administered by ultrasonic nebulization to eight patients with bronchial asthma and four normal subjects in increasing doses up to 200 mug maximum dose. Maximum expiratory flow (MEF) and forced vital capacity (FVC) were analyzed at 5, 15, 30, 60 and 120 minutes after administration of aerosol. All expiratory flow rates were reduced after 5 minutes. Some increase in terminal flow rates was observed after 60 minutes. We conclude that PGF2beta in not an effective bronchodilator at this dose level.

Asthma↗
PubMed1975

The effect of estrogen on the lipoprotein lipase activity of rat adipose tissue.

The effect of 17beta-estradiol or progesterone administration on adipose tissue lipoprotein lipase activity was studied in male and ovariectomized female rats. Lipoprotein lipase activity was measured in acetone-ether-extracted preparations of adipose tissue with doubly labeled (14C-fatty acid, 3H-glyceryl) chylomicron triglyceride as substrate. Administration of 17beta-estradiol to male rats lowered adipose tissue lipoprotein lipase activity from 8.22 plus or minus 1.8 U/g (1 U = 1 mumol triglyceride hydrolyzed per h) to 4.96 plus or minus 0.5 U/g in the treated group. Ovariectomy increased adipose tissue lipoprotein lipase activity from 10.4 plus or minus 1.8 U/g in controls to 22.7 plus or minus 4.3 U/g. 17beta-Estradiol administration to ovariectomized rats cuased a marked fall in adipose tissue lipoprotein lipase activity: 17beta-estradiol (2.5 mug/day) lowered the enzyme activity to 9.00 plus or minus 1.2 U/g, whereas 25 mug/day further decreased lipoprotein lipase activity to 3.2 plus or minus 0.6 U/g. Blood triglyceride levels increased from 0.8 plus or minus 0.05 mumol/ml in ovariectomized rats to 1.4 plus or minus 0.09 mumol/ml in 25 mug/day 17beta-estradiol-treated rats. Progesterone administration did not affect adipose tissue lipoprotein lipase activity in either male or ovariectomized rats. Heart and lung lipoprotein lipase activity was unaffected by hormone treatment. We suggest that the rise in blood triglyceride concentrations, which accompanies high palsma estrogen levels, could be due to the marked inhibition of adipose tissue lipoprotein lipase activity.

Adipose Tissue↗
PubMed1971

Left ventricular function in acute myocardial infarction.

Left ventricular catheterization was carried out in 40 patients with acute myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) was elevated in 85% of the patients studied. In 14 patients with apparently uncomplicated infarcts, LVEDP averaged 15 mm Hg, and cardiac index (2.98 liter/min/m(2)), stroke volume (38.3 ml/m(2)), and stroke work (49.2 g-m/m(2)) were within normal limits. In 12 patients with clinical signs of left ventricular failure, LVEDP averaged 29.9 mm Hg, cardiac index was at the lower limit of normal (2.79 liter/min/m(2)), but stroke volume (31.6 ml/m(2)) and stroke work (37.3 g-m/m(2)) were reduced. In 14 patients with clinical signs of shock, LVEDP averaged significantly lower than in the heart failure group (21.1 mm Hg), but cardiac index (1.59 liter/min/m(2)), stroke volume (16.5 ml/m(2)), and stroke work (11.1 g-m/m(2)) were markedly reduced. A large presystolic atrial "kick" (average amplitude 9.5 mm Hg) was an important factor in the high LVEDP in the patients with heart failure but not in those with shock. The first derivative of left ventricular pressure was significantly lower in shock than in the nonshock group. Although right atrial pressure (RAP) and LVEDP were significantly correlated (r = 0.49), wide discrepancies in individual patients rendered the RAP an unreliable indicator of the magnitude of left ventricular filling pressure. THESE DATA SHOW THE FOLLOWING: (a) LVEDP is usually elevated in acute myocardial infarction, even in absence of clinical heart failure; (b) cardiac output apparently is supported by increased LVEDP and compensatory tachycardia; (c) in patients with shock, left ventricular function usually is markedly impaired, but inadequate compensatory cardiac dilatation or tachycardia could contribute to the reduced cardiac output in some individuals; (d) lower LVEDP in shock than in heart failure may represent differences in left ventricular compliance.

Adult↗