A hypoxic pulmonary vasoconstrictor response in dogs during and after infusion of sodium nitroprusside.
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Biomedical subjects
Publications and source records attributed to M K Sykes.
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Follow-up of the sites of 839 peripheral arterial punctures has confirmed the technique as safe and free from major sequelae. Minor complications, mainly bruising and tenderness, occurred at 39% of sites; this incidence is much less than that previously reported following short-term arterial cannulation. At only 2% of sites was there any significant pain or tenderness. There was a small incidence of pulse diminution particularly at the radial site but no case of arterial occlusion. The use of a smaller needle (23 s.w.g.) significantly reduced the overall incidence of complications.
The effect of orciprenaline on hypoxic pulmonary vasoconstriction and arterial oxygen tension (PaO2) was studied in 8 dogs by measuring the redistribution of blood flow in response to unilateral alveolar hypoxia. The distribution of blood flow was recorded continuously by measuring the radioactivity of the mixed expired gas from each lung during the continuous intravenous infusion of xenon-133. The hypoxic vasoconstrictor response was significantly depressed by an infusion of 1.0 micrograms/kg/min of orciprenaline but not by a dose of 0.1 micrograms/kg/min. PaO2 during unilateral hypoxia was significantly lower during the infusion of the high dose of orciprenaline than it was in the control periods before or after the infusion. A bolus dose of 0.5 mg significantly increased blood flow to a lung with established hypoxic vasoconstriction and also caused a significant reduction in PaO2. Since these effects were produced in the absence of airway pressure or pulmonary vascular pressure changes, it is concluded that orciprenaline may depress the hypoxic pulmonary vasoconstrictor response in dogs.
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The action of halothane on the pulmonary vasoconstrictor response to unilateral alveolar hypoxia was studied in two groups of dogs. In the first group the redistribution of blood flow between the two lungs was studied with a radioactive isotope method, which provided intermittent measurements, whilst in the second group the distribution of blood flow was observed continuously. In both groups there was no significant alteration of the hypoxic vasoconstrictor response with inspired halothane concentrations varying from 0.5 to 1.5%.
The cardiorespiratory effects of intermittent positive pressure ventilation with zero end-expiratory pressure (IPPV), continuous positive airway pressure breathing (CPAP) and spontaneous breathing (SR) were studied in 11 patients 3--20 h after open-heart surgery. The transition from IPPV to CPAP resulted in a significant reduction in tidal volume and significant increases in respiratory frequency, PaCO2, oxygen transport and mean arterial pressure, but there were no significant changes in cardiac output or PaO2. There were no significant differences in any of the measurements between CPAP and SR.
Cyclopropane was found to produce no significant changes in pulmonary vascular resistance or the pulmonary vasoconstrictor response to alveolar hypoxia in isolated cat lungs perfused at constant flow.
No significant changes were found in heart rate, blood pressure, cardiac output, arterial blood gases or physiological deadspace: tidal volume ratio before and after clamping and unclamping the abdominal aorta below the renal vessels. Nevertheless, drugs should be available to reduct the afterload on the heart if any evidence of myocardial ischaemia appears during the period of aortic clamping. The importance of maintaining an adequate circulating blood volume at all times is stressed.
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Hypoxic pulmonary vasoconstriction is a protective mechanism diverting pulmonary blood flow away from hypoxic areas toward more optimally oxygenated lung units. Venous admixture is reduced and arterial oxygenation improved. Hypoxic pulmonary vasoconstriction was demonstrated during acidosis, alkalosis and normal pH in the isolated perfused cat lung under conditions of constant flow and constant left atrial and airway pressures. Two per cent diethyl ether markedly reduced hypoxic vasoconstriction under all acid-base conditions, the hypoxic pressor response returning after wash-out of diethyl ether. Modification of hypoxic pulmonary vasoconstriction during acid-base disturbances and possible implications of concurrent anaesthetic administration are discussed.
Local pulmonary vasconstriction in response to alveolar hypoxia is a protective mechanism reducing blood flow to poorly oxygenated areas of lung. Pulmonary blood flow is thereby directed to better oxygenated lung units and venous admixture and the resulting arterial hypoxaemia is reduced. The effect of nitrous oxide on the pulmonary pressor response to alveolar hypoxia was assessed in the isolated perfused cat lung preparation under conditions of constant flow and constant left atrial and airway pressures. Nitrous oxide, in concentrations of 50 per cent and 75 per cent, was found to produce a reversible depression of the hypoxic pulmonary pressor response. The importance of hypoxia pulmonary vasconstriction and the possible implications of its reduction by anaesthetic agents are discussed.
The magnitude of the pulmonary vasoconstrictor response to alveolar hypoxia may be studied by measuring the reduction in blood flow when one lung is ventilated with nitrogen. A radioisotope technique has been developed which permits the distribution of blood flow between the two lungs to be measured continuously. This technique was evaluated in dogs and found to be satisfactory.
The activity of the pulmonary vasoconstrictor response to alveolar hypoxia was assessed by measuring the redistribution of pulmonary blood flow in response to the ventilation of one lung with nitrogen. The vasoconstrictor response was depressed during the administration of 5% diethyl ether but returned when the ether was withdrawn. It is suggested that depression of the hypoxic vasoconstrictor mechanism may be one cause of the increased alveolar-arterial Po2 difference noted during ether anaesthesia.
The pulmonary vasoconstrictor response to alveolar hypoxia was assessed by measuring the redistribution of blood flow in response to the unilateral administration of nitrogen or nitrous oxide. The response was diminished when nitrous oxide was administered and returned to previous levels when hypoxia was produced again by nitrogen. It is postulated that depression of the hypoxic vasoconstrictor response by nitrous oxide may contribute to the increased alveolar-arterial Po2 difference during anaesthesia.
The effects of halothane and diethyl ether on pulmonary vascular resistance and the pulmonary vasoconstrictor response to alveolar hypoxia were studied in the innervated perfused cat lung. A left and right heart bypass technique was used to allow perfusion of the lungs at constant flow. Neither anaesthetic agent caused a significant change in pulmonary vascular resistance but both agents caused a depression of the pulmonary vasoconstrictor response to hypoxia.
Data on arterial oxygen tension (PaO2) and alveolar-arterial PO2 difference (PAO2--PaO2) have been obtained from 337 patients awaiting elective surgery. Statistical analysis of these data has assessed both the individual and the combined influence of various factors on PaO2 and (PAO2-PaO2). The factors of importance in relation to PaO2 include age, smoking habits, body build and PAO2. In relation to (PAO2-PaO2) the significant factors include age, PaCO2, weight and smoking habits.
During pregnancy there is a fall in functional residual capacity and expiratory reserve volume. The point of airway closure in relation to vital capacity and the expiratory reserve volume was determined in 11 post-partum patients who had previously been studied during pregnancy. The lung volume at which airway closure occurred in pregnancy and the post-partum period did not change in relation to the vital capacity whereas the expiratory reserve volume did, so that airway closure became imminent in the pregnant women during tidal ventilation, especially whilst in the suping position. The significance of this alteration in pulmonary function to obstetric anaesthesia is discussed.
The effects of methoxyflurane on pulmonary vascular resistance and the pulmonary vasoconstrictor response to alveolar hypoxia were studied in isolated cat lungs perfused at a constant flow. Methoxyflurane decreased pulmonary vascular resistance and depressed the pulmonary vasoconstrictor response to hypoxia.