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Biomedical subjects

J Herget

Publications and source records attributed to J Herget.

At least 55 records · Page 3Linked to original sources
PubMed1987

Dexamethasone potentiates hypoxic vasoconstriction in salt solution-perfused rat lungs.

Isolated rat lungs perfused with blood or plasma develop good hypoxic pressor reactivity, but those flushed of blood and perfused solely with physiological salt solution (PSS) show decreased or no hypoxic vasoconstriction. Because the handling of rats during collection of blood increases the plasma corticosterone levels, we wondered whether the difference between blood and PSS perfusion was due partly to higher glucocorticoid activity with blood than with PSS. Treatment of lung donors with the synthetic glucocorticoid dexamethasone (2 mg/kg im 3 h before isolation) or addition of dexamethasone (4.2 X 10(-6) M) to the perfusate increased markedly the hypoxic pressor reactivity of rat lungs perfused with PSS plus albumin (4 g/100 ml). In comparison, dexamethasone did not cause a significant increase in the already vigorous hypoxic pressor reactivity of blood-perfused lungs, but it reversed the blunted pressor reactivity of lungs perfused with blood collected from adrenalectomized rats. The potentiation of hypoxic vasoconstriction by dexamethasone required greater than 40 min to develop and was inhibited by a 100-fold higher concentration of progesterone, a glucocorticoid receptor antagonist. Although dexamethasone and the cyclooxygenase blocker meclofenamate (3.1 X 10(-5) M) caused similar decreases in perfusate levels of cyclooxygenase metabolites, the glucocorticoid was much more effective in inducing hypoxic vasoconstriction in PSS-perfused lungs. Thus a reduction of cyclooxygenase metabolism might have contributed to, but did not fully account for, the glucocorticoid effect. Dexamethasone also caused small increases in base-line perfusion pressure and in pressor reactivity to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1985

Effects of ouabain, low K+, and aldosterone on hypoxic pressor reactivity of rat lungs.

It can be postulated that inhibition of lung tissue Na+-K+-ATPase might potentiate hypoxic pulmonary vasoconstriction by depolarizing some excitable cell or, in contrast, that it might blunt the hypoxic response by reducing cellular metabolic rate and sensitivity to hypoxia. Thus the purpose of this study was to test in isolated rat lungs whether hypoxic pressor reactivity was related inversely or positively to Na+-K+-ATPase activity. Dose-pressor response curves to hypoxia, angiotensin II, or KCl were measured under control conditions and after exposure either to one of two inhibitors of Na+-K+-ATPase, ouabain, and low-K+ solution or to a stimulator of Na+-K+ pumping, aldosterone. Ouabain and low K+ depressed the response to hypoxia but had little effect on that to angiotensin II. The response to KCl was increased by ouabain. Aldosterone potentiated the hypoxic response. These results do not support the idea that membrane depolarization due to inhibition Na+-K+ pumping is a component of hypoxic vasoconstriction. They do suggest a positive relationship between Na+-K+-ATPase activity and hypoxic pressor reactivity and are consistent with the idea that Na+-K+-ATPase activity might influence hypoxic reactivity indirectly by altering cellular energy metabolism. It is also possible that the results were somehow due to changes in intracellular [Na+] or transmembrane Na+ gradient, rather than to changes in energy metabolism.

Aldosterone↗
PubMed1981

Pulmonary hypertension induced by repeated pulmonary inflammation in the rat.

The effect of repeated lung inflammation on the pulmonary vascular bed was studied in rats. Nonbacterial lung inflammation was induced by repeated carrageenan instillations into the lungs. Three days after the single carrageenan injection, the mean pulmonary arterial blood pressure was only slightly raised [16.3 +/- 0.6 (mean +/- SE) Torr in controls and 19.5 +/- 0.5 Torr in rats with lung inflammation, P less than 0.001]. A substantial pulmonary hypertension was found in rats 3 days after the sixth lung inflammation (24.6 +/- 1 Torr). In this group, arterial hypoxemia, hypercapnia, and right-heart hypertrophy were found. In the 14th day of recovery after the last injection of carrageenan, the mean pulmonary artery blood pressure decreased (18.5 +/- 0.9 Torr) but remained higher than in the control group. There was no difference in cardiac output measured by dye-dilution technique between the experimental and control groups. After repeated inflammation, the media of distal pulmonary vessels thickened and the number of pulmonary arterioles with distinct media increased.

Animals↗
PubMed1979

Pulmonary hypertension in rats with papain emphysema.

Lung emphysema was produced in 80 rats by tracheal chronic constriction and repeated instillations of 0.1% papain solution intratracheally. 17 animals survived 90 days of the experiment; a complete examination was performed on 14 experimental and 11 control animals. 9 rats of the experimental group had pulmonary hypertension, in 5 other rats the pulmonary arterial blood pressure was not different from that in the controls. The experimental animals with hypertension had arterial hypoxemia and increased weight of the right ventricle. All experimental rats (with and without pulmonary hypertension) had increased air spaces in the lung and thickened media of distal pulmonary vessels. After breathing 100% oxygen for 20 min, the pulmonary arterial blood pressure in animals with pulmonary hypertension decreased but did not reach the control level. The decrease of the mean pulmonary arterial blood pressure after oxygen breathing correlated well with the initial level of pulmonary hypertension and with the degree of hypoxemia during air breathing.

Animals↗
PubMed1978

The effect of acute and chronic hypoxia on thoracic gas volume in anaesthetized rats.

1. Thoracic gas volume at end expiration (functional residual capacity, FRC) was measured in chronically and acutely hypoxic anaesthetized rats by a plethysmograph method. 2. FRC, measured during air breathing, was 34-62% larger in rats which had been kept in an environmental chamber in 8, 10 or 12% O2 for 3 weeks than in littermate controls. FRC returned to normal after the rats had returned to air for 9 days. There was no constant difference in the pattern of breathing between control and chronically hypoxic rats. 3. Pressure-volume curves measured post mortem showed no difference in the volume of the lung at 25 cm H2O pressure or in the compliance of the lung between chronically hypoxic and control rats. Thus there was no gross mechanical change in the lung to account for the increase in FRC. 4. Acute hypoxia caused by breathing 12% O2 increased FRC in control but not in chronically hypoxic rats. The increase in FRC in control rats was abolished by combined blockade of the vagus nerves and carotid bodies (with procaine) but not by vagal blockade alone. 5. The combined vagal and carotid body blockade reduced FRC significantly in rats which had been in 10% O2 for 3 days but not in those which had been in 10% O2 for 21 days. 6. Lung area measured from radiographs was not reduced by a muscle relaxant in chronically hypoxic rats. Electromyograms from anterior intercostal muscles and the diaphragm showed no electrical activity in expiration in chronically hypoxic rats which might indicate an active muscular basis for their increased FRC. However when FRC was raised by acute hypoxia in control animals there was also no increase in electrical activity in expiration which could have explained their increase in lung volume. 7. We concluded that the increase in FRC during acute hypoxia in control rats was probably due to a reflex from the carotid body. The increase in FRC in chronically hypoxic rats, which was present while they breathed air, may have had an active muscular component in the early stages but later on there was possibly a structural factor in the chest wall.

Acute Disease↗
PubMed1978

Resolution of pulmonary hypertension and other features induced by chronic hypoxia in rats during complete and intermittent normoxia.

Rats subjected to 10% O2 (hypoxic rats) for various periods and recovery regimens were compared with control animals with respect to pulmonary artery pressure (Ppa), right ventricular hypertrophy (RVH), and muscularisation of small pulmonary vessels. Mean Ppa was measured in anaesthetised animals spontaneously breathing air and rose from 16 mmHg in controls to 36 mmHg in rats exposed to hypoxia for three weeks. Ppa had returned to normal after 20 weeks' recovery in air. RVH regressed a little more quickly, but muscularisation of small pulmonary vessels. Mean Ppa was measured in anaesthetised animals spontaneously breathing air and rose from 16 mmHg in controls to 36 mmHg in rats exposed to hypoxia for three weeks. Ppa had returned to normal after 20 weeks' recovery in air. RVH regressed a little more quickly, but muscularisation of small pulmonary vessels was still apparent after 20 weeks. Some hypoxic rats were subjected to an intermittent normoxic recovery regimen for either 40 or 80 hours a week in air, the remainder in 10% O2. Some reduction in RVH probably occurred after six weeks on the 80-hour regimen, but there was no reduction in Ppa or muscularisation of small pulmonary vessels. These results suggest that the pulmonary hypertension of chronic alveolar hypoxia resolves very slowly and is probably related to structural changes in the pulmonary vessels. Their relevance to human cor pulmonale and intermittent long-term oxygen treatment for these patients is discussed.

Altitude↗
PubMed1977

Effect of alpha-methyldopa on the pulmonary vascular changes induced by chronic hypoxia in rats.

1. Groups of young rats were kept in a hypoxic chamber or in air as control animals for 28 days. 2. Hypoxic and control animals were treated with either alpha-methyl-3,4-dihydroxyphenylalanine (alpha-methyldopa) or distilled water. 3. alpha-Methyldopa significantly reduced the increase in pulmonary artery pressure and right ventricular hypertrophy induced by chronic hypoxia and partially prevented the histological changes in the small pulmonary vessels.

Animals↗
PubMed1976

Causes of experimental pulmonary hypertension in rats.

Experimental pulmonary hypertension was induced in young male rats by means of tracheoconstriction and repeated injections of aqueous bean (Phaseolus vulg.) extract into the trachea. After 120 days, the blood pressure of the experimental and control animals was measured in the pulmonary artery with a shaped polyethylene catheter, without opening the chest. In all the experimental animals the blood pressure in the pulmonary artery was higher than in the controls. The mean pressure in the pulmonary artery of the experimental rats was 25 +/- 1 torr and in the controls 16 +/- 0.4 torr. The right ventricle of the experimental animals was larger than in the controls. No difference was found between the systemic blood pressure values, measured in the femoral artery, in the experimental animals and the controls. The experimental animals had a faster heart rate. Cardiac output, measured by the dye dilution method, was the same in the control and experimental animals and there was likewise no difference in the PO2 PCO2 and pH values in the arterial blood. The inhalation of oxygen instead of air did not affect the blood pressure in the pulmonary artery. The pulmonary blood vessels were evaluated quantitatively in histological sections of the experimental and control animal's lungs. There was no different between the thickness of the media of the distal pulmonary vessels, expressed as a percentage of the outer diameter of the vessel, in the experimental animals and the controls. A media thicker than 7% was found in 15% of the evaluated vessels from experimental animals and in 8% of those from the controls. No correlation between the mean thickness of the media and the mean blood pressure in the pulmonary artery was found in any of the animals.

Animals↗