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Biomedical subjects

A J Suggett

Publications and source records attributed to A J Suggett.

29 records · Page 2Linked to original sources
PubMed1982

The effects of localized hypoventilation on ventilation/perfusion (V/Q) ratios and gas exchange in the dog lung.

1. Hypoventilation of one lobe of lung was studied in open-chest anaesthetized dogs. Lobar blood flow, pulmonary-artery pressure and gas exchange were measured, the latter from breath-by-breath analysis with a mass spectrometer. 2. Hypoventilation of the lobe by reducing the respiratory pump stroke led, at each step, to a reduction in blood flow to that lobe. The flow (Q) reduction was variable, but always less than the ventilation (VE) reduction, so that the V/Q ratio to the lobe was reduced. O2 tension and pH fell and CO2 tension rose in effluent blood. Thus V/Q regulation achieved by flow reduction varied between individuals and was of low gain. 3. Anatomical or series dead space (VD series) was reduced in proportion to ventilation. When VD series was less than the apparatus dead space, some gas exchange still took place. 4. Oxygen uptake (VO2) and CO2 output (VCO2) were reduced during hypoventilation. VCO2 fell more than VO2, so that the respiratory exchange ratio (R) was reduced. 5. Whether the deterioration in gas tensions in effluent blood during hypoventilation of the lobe was due to shunt of blood past unventilated alveoli, or to V/Q mismatching, was not resolved. 6. The plateau phase of the CO2-output curves at low tidal volumes was usually regular; thus either hypoventilation was uniform, or some ventilation units were totally closed.

Animals↗
PubMed1981

Quantitative significance of hypoxic vasoconstriction in the ferret lung.

Stimulus-response curves for the pulmonary vascular bed to alveolar hypoxia have been measured in ferrets under conditions of perfusion either at constant pressure or a constant flow in vivo or in isolated lungs. In all circumstances the relationship between alveolar oxygen tension and the fall in blood flow or rise in pulmonary artery pressure was sigmoid although there were important differences between the in vivo and in vitro preparations. The significance of these observations in constant pressure and constant flow preparations in relation to pulmonary hypertension and ventilation/perfusion regulation is discussed.

Animals↗
PubMed1980

The effects of vincristine on platelet aggregation studied by a filter loop technique in the rat.

1 A method for measuring aggregation of platelets of adenosine diphosphate (ADP) is described using a filter inserted into the flowing aortic blood in the rat. 2 Repeated infusions of ADP resulted in a fall in the calculated aggregation index without significant changes in the platelet count. 3 Vincristine (0.05 mg/kg) intravenously caused significant inhibition of ADP-induced platelet aggregation. 4 Infusion of ADP caused some peripheral vasodilatation though it is unlikely that this contributed to the effects seen to any great extent.

Adenosine Diphosphate↗
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↗
PubMedDate not supplied

Angiotensin, hypoxia, verapamil and pulmonary vessels.

1. The action of angiotensin II on lung vessels was compared in dogs, cats, ferrets and rats using isolated perfused lungs and lobes of lungs perfused in vivo, both at constant flow, so that increases in inflow pressure at constant outflow pressure indicated increases in resistance. 2. Angiotensin II caused some increases in resistance in dogs, cats and rats but not ferrets. The increases were small compared with changes in the systemic circulation. Larger increases could be obtained in isolated lungs where there was no interference from rises in left atrial pressure. 3. All four species showed pulmonary vasoconstriction during hypoxia and ferret lungs were especially responsive. Thus angiotensin II cannot be the mediator of hypoxic vasoconstriction in all these species. 4. Angiotensin II significantly increased the response to hypoxia in isolated cat and rat lungs while also increasing baseline inflow pressure; the response to hypoxia was not altered in ferrets. Angiotensin II may therefore enhance reactivity of pulmonary vessels. 5. Verapamil, an inhibitor of calcium transport across cell membranes, reduced the response to hypoxia in rats and ferrets more than it reduced the response to angiotensin II in rats or prostaglandin F2 alpha in ferrets. Thus hypoxic pulmonary vasoconstriction probably involves transport of calcium.

Angiotensin II↗
PubMedDate not supplied

Effect of almitrine bismesylate on breathing pattern during hypoxia/hypercapnia in rats and ferrets.

1. Ventilatory measurements and functional residual capacity (FRC) were recorded from anaesthetized rats and ferrets using a whole body plethysmograph. Simulation of aspects of human chronic obstructive airways disease (COAD) was attempted by making animals acutely hypoxic or hypoxic and hypercapnic by causing them to breath appropriate gas mixtures or by increasing the tracheal resistance or dead-space. Some chronically hypoxic rats, which have muscularized pulmonary arterioles similar to COAD patients, were also studied. 2. In 18 chronically hypoxic (CH) rats and 17 littermate control rats (C), breathing air, doses of almitrine bismesylate caused greater increases in ventilation (VE) in C than in CH rats. FRC, which was initially greater in CH rats, increased significantly in both groups after almitrine. 3. In C rats, breathing hypoxic or hypoxic/hypercapnic gas mixtures caused large increases in VE. Slow infusions of almitrine caused a further increase in VE usually via an increase in tidal volume (VT) but not frequency (f). 4. In two series of rats (n = 9; n = 6) severe and moderate degrees of tracheal obstruction caused a fall in PaO2 and a rise in PaCO2, a fall in VE due to both VT and f and large changes in oesophageal pressure (Poes), which often became positive on expiration. Almitrine infusions usually caused a rise in PaO2, a rise in VT and no change in f; with moderate obstruction, Poes also rose. The results were thought to depend on the balance between improved ventilation and increased O2 demand of the respiratory muscles. 5. Eleven ferrets were made hypoxic and hypercapnic by adding a large dead-space to the trachea. A slow infusion of almitrine caused a significant rise in PaO2 before any significant change in VE was detected; PaCO2 fell at some time during the infusion, but not significantly. The initial significant rise in PaO2, at 2.5 min, was not associated with significant changes in T1 (time of inspiration) and VT/TI. At 5 min VT/TI and PaO2 were all significantly altered. 6. Infusions of almitrine into hypoxic and hypercapnic animals caused improvements in the arterial oxygen tension which were associated with subtle changes in the breathing pattern; inspiratory time and inspiratory flow rate changed in the absence of an increase in total VE. Possible conclusions with respect to the action of almitrine in patients with COAD are discussed.

Airway Obstruction↗
PubMedDate not supplied

Effect of alpha-methyldopa on lung microembolism in the rat.

The effect of chronic pretreatment with alpha-methyldopa on acute pulmonary hypertension induced by lung microembolization with Sephadex particles in the rat was studied. Alpha-methyldopa was administered twice a day for 10 days by oesophageal gavage (20 mg X kg-1 of body weight) prior to embolization. Rats were anaesthetized with urethane. A catheter was positioned in closed chest rats in the pulmonary artery and 50 microliter of Sephadex suspension in saline were injected. The control group was not pretreated with alpha-methyldopa. In a subgroup of control and pretreated rats, the cardiac output was measured by the dye dilution technique before and after lung microembolization. Rats pretreated with alpha-methyldopa had less pulmonary hypertension, higher cardiac output and more severe arterial hypoxaemia 15 min after lung microembolization than untreated animals. There was no difference in platelet counts prior and after embolization. We suggest that pulmonary hypertension after lung microembolization in the rat includes a vasoconstrictor component which can be suppressed by alpha-methyldopa, and that severe arterial hypoxaemia in pretreated rats is probably the result of a decrease of the ventilation/perfusion ratio in unobstructed areas, which in untreated rats may be prevented by active vasoconstriction.

Animals↗