Search PubMed⌕ Search

Biomedical subjects

A Hauge

Publications and source records attributed to A Hauge.

At least 37 records · Page 2Linked to original sources
PubMed1984

Cardiovascular responses to face immersion and apnea during steady state muscle exercise. A heart catheterization study on humans.

The cardiovascular adjustments to face immersion and apnea (FIA) in human beings during steady-state muscle exercise (163 and 98 watt) have been investigated. Using a triple lumen flow directed catheter inserted into the pulmonary artery we were able to measure cardiac output (CO) by thermodilution technique, pulmonary arterial pressure (PPA) right atrial pressure (PRA) and left ventricular filling pressure (PAD). Phasic arterial blood pressure (BP) was measured via a cannula in the radial artery. A 12 lead ECG was recorded continuously. FIA caused an immediate rise in BP (median 61%), the highest level being 25.33 kPa. CO during the last half of FIA was reduced by 49% (range 46-59, n = 7) systemic vascular resistance increased by median 200% (range 111-280). Myocardial oxygen demand determined by the heart rate pressure double product fell from median 33.6 to 16.8 (163 W) and 28.5 to 19.1 (98 W) given as beats/min X kPa X 10(2). Mean reduction was by 42%. PPA and PRA immediately increased and remained constant until a further pronounced increase was seen towards the end of FIA when pulmonary vascular resistance (PVR) went up. PACO2 and PAO2 at the end of 30 sec FIA (163 W) was 10.0 and 5.6 kPa, respectively, values which expectedly would cause pulmonary vasoconstriction. Our findings demonstrate that humans are able to make principally the same cardiovascular adjustments to diving as aquatic mammals, although the response patterns are slower and less efficient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Acute effects of acetazolamide on cerebral blood flow in man.

We have followed the time course of the effect of the carbonic anhydrase inhibitor acetazolamide injected i.v. in unanesthetized healthy human beings. The dose administered was 500 mg as a bolus. Cerebral blood flow (CBF) was measured continuously before, during and after the injection, using a pulsed ultrasound doppler system, which measured the instantaneous mean velocity across the lumen of the internal carotid artery, just below its entrance into the skull. Ventilation, heart-rate, end-expiratory PCO2, arterial PCO2, pH and systemic blood pressure was also measured. We found that acetazolamide caused a rise in CBF which could be detected as early as 2 min after the injection. A maximal average response of 75% increase in CBF was seen after 25 min. The half-time of the declining phase of the response was 95 min. There were no systematic differences in the CO2 reactivities, given as delta CBF/delta PACO2 in % of CBF at normocapnia, before and after acetazolamide injection, regardless of the absolute PACO2 level. The present dose of the drug caused no change in ventilation, alveolar and arterial PCO2 or in arterial blood pH indicating that the carbonic anhydrase was not fully inhibited. Our observations show that acetazolamide nevertheless caused a rapid vasodilation in the brain and over a wide range of PCO2's. We suggest that this agent has a local vasodilator effect on the cerebral arterioles, unrelated to its specific effects as a carbonic anhydrase inhibitor.

Acetazolamide↗
PubMed1982

Fluid Exchange in the isolated perfused lung.

The advantages of an isolated, perfused lung preparation in studies of transvascular fluid shifts are described. We find the permeability characteristics of the exchange vessels in the rabbit lung preparation to be similar to those obtained in lungs in situ. The filtration coefficient is similar during plasma and during Krebs-Ringer dextran T 70 perfusion. Therefore proteins in the perfusate do not modify the permeability of the exchange vessels in these lungs as had been reported for other vascular beds. Interstitial fluid pressure in both the alveolar walls and the alveolar corner regions increases with a rise in alveolar pressure. The result is a reduction in the fluid filtration rate under both zone-III and zone-I conditions. The resistance of the extravascular pathway and the fluid pressure in the periarterial/perivenous spaces both appear to be reduced when lung volume is increased by a reduction in pleural pressure. The net effect of positive airway pressure on the transvascular fluid exchange will depend on the relative contribution of the alveolar pressure effects and the lung volume effects. Fluid reabsorption can be observed to occur in the isolated, perfused rabbit lung. This reabsorption does not take place at the level of the loose perivascular tissue spaces since the interstitial fluid pressure at these sites is much lower than the microvascular pressure. We suggest that fluid reabsorption takes place at the thick part of the air-blood barrier, which, most likely, has a higher fluid pressure.

Albumins↗
PubMed1980

Hypoxia-induced pulmonary vasoconstriction: effects of fentanyl following different routes of administration.

Recent investigations have revealed that intravenous anesthetics, including fentanyl, do not reduce the pulmonary vasoconstrictor response to alveolar hypoxia. In contrast, the response is markedly reduced or abolished by inhalation anesthetics. Recent investigations have demonstrated that the route of administration is of importance. Halothane, which inhibits the response when administered via the airways, behaves more like an intravenous anesthetic following administration via the blood stream, provided the alveolar concentration has been kept low (Bjertnaes et al. 1977). It was therefore a distinct possibility that the lack of any damping effect of fentanyl on the response could be due to the route of administration rather than to a different pharmacological property. We have tested this hypothesis by introducing fentanyl in nebulized form via the airways in one group of isolated rat lungs, and via the blood stream in another group. We found, however, no effect of fentanyl on the pulmonary vasoconstrictor response to hypoxia, regardless of the route of administration. Plasma concentrations of fentanyl were determined by radioimmunoassay and compared with those encountered in anesthetic practice.

Anesthesia, Inhalation↗
PubMed1980

Vascular resistance in atelectatic lungs: effects of inhalation anesthetics.

We have investigated the relative contribution of mechanical obstruction and hypoxia-induced vasoconstriction to the increased pulmonary vascular resistance (PVR) in atelectatic lungs. For this purpose we have utilized the previous observation that inhalation anesthetics inhibit the vasoconstrictor response to pulmonary hypoxia. The effects of halothane, enflurane and ether on PVR in atelectatic lungs have been explored. Two pairs of isolated rat lungs were perfused in series at constant flow. One of the preparations was made atelectatic by airway occlusion subsequent to ventilation with a high PO2 gas (95% O2). Ventilation of the other preparation continued with hypoxic gas (2% O2), resulting in a gradual increase in PVR in both preparations. When maximum PVR was reached, one of the above inhalation anesthetics was administered to the atelectatic lungs via the ventilated lung preparation. This caused a dose-dependent, reversible reduction of PVR. The same effect was observed when pulmonary arterial PO2 was increased (greater than 66.5 kPa). Histological examination revealed that two out of four preparations were completely atelectatic 1 h after airway occlusion, whereas atelectasis was nearly complete in the other two. In two groups, airways were occluded for 1 h. In the first group PVR increased to 163% (median) above baseline level, as found during ventilation with high PO2. High arterial PO2 reduced PVR in the atelectatic lungs to 50% (median) above baseline, whereas papaverine induced a further PVR reduction, to 7% (median) above baseline. In the other group, papaverine was given before airway occlusion, and PVR increased to 10% (median) above baseline. Comparison of the two groups shows that mechanical obstruction accounts for about 6% (10/163) of the overall rise in PVR during atelectasis.

Animals↗
PubMed1980

Constant flow- vs. constant pressure-perfusion for studies of pulmonary vasoactive responses.

We have compared the pulmonary vascular responses to a standardized hypoxic vasoconstrictor stimulus (FIO2 = 0.02) obtained during 1) constant volume inflow, with pulmonary arterial pressure as the dependent variable, and 2) constant inflow pressure, with flow as the dependent variable. Isolated rat lungs were perfused at different baseline transvascular pressures. The experimental arrangement allowed changes between the two types of perfusion. Hypoxia at constant pressure perfusion gave a higher percentage rise in pulmonary vascular resistance (PVR) at all pressure levels. This advantage was however, more than offset by the finding that a) vascular closure (total or partial) often occurred, particularly below arterial pressure of 3 kPa, making detection of graded responses impossible, and b) the control situation was rarely regained. Responses obtained during constant flow were less reduced by elevations in baseline transvascular pressure, and the control situtaion was rapidly and completely regained. The observation that hypoxic vascular closure may occur in the pulmonary vascular bed supports the hypothesis that high altitude edema is caused by precapillary occlusion of a major part of the vascular bed, thereby subjecting still perfused regions to very high pressure and flow.

Animals↗
PubMed1980

Pulmonary O2 transfer during pulsatile and non-pulsatile perfusion.

The importance of the perfusion pattern for the oxygen transfer has been examined in isolated rabbit lungs perfused with plasma at constant volume inflow. The lungs were ventilated with constant tidal volume and constant end-expiratory pressure. Following a standardized rise in FIO2 the rate of rise in pulmonary venous PO2 (delta PO2/delta t) was measured during alternately pulsatile and non-pulsatile perfusion in normal lungs and in lungs made edematous by elevation of left atrial pressure. In normal lungs there was no difference in delta PO2/delta t when the two modes of perfusion were compared. In edematous lungs delta PO/delta t was statistically higher during pulsatile perfusion, indicating a beneficial effect of flow- and pressure pulsations, e.g. a better distribution of V/Q ratios throughout the lungs. In a separate series of expts. the advancement of a high O2 front through the airways was measured, and the two perfusion patterns compared. Since no difference was found, we suggest that the phenomenon of "cardiogenic gas mixing" in the airways in vivo is a result of a direct action of the heart on the lungs rather than arterial pulsations.

Animals↗
PubMed1980

The pulmonary vasoconstrictor response to hypoxia. The hypoxia-sensitive site studied with a volatile inhibitor.

Recent investigations have revealed that a number of inhalation anesthetics, including halothane, inhibit the pulmonary vasoconstrictor response to hypoxia without affecting other vasoconstrictor stimuli. Various injectable anesthetics do not show this effect. This discrepancy could be due either to different pharmacological properties or to the different routes of administration. There is no general agreement on whether the response to hypoxia is elicited mainly by airway hypoxia or by blood hypoxemia, i.e. where within the lungs hypoxia acts. This work is an attempt to localize the hypoxia-sensitive site employing halothane. We have studied the reduction of standardized vasoconstrictor responses to hypoxia during administration of halothane via: (1) the airways, (2) the pulmonary artery and (3) the pulmonary veins (backward perfusion). Our experimental model has been two pairs of series-perfused hyperventilated isolated rat lungs. An equimolar concentration of halothane most effectively inhibits the response when presented to the alveoli, less when presented to the arterial- and least when presented to the venous segments of the pulmonary vasculature. We suggest that the response to hypoxia is inhibited by halothane at some extravascular site on the arterial side of the pulmonary vasculature, functionally closer to the alveoli than to the responding vessels. A model which combines all the data into an unifying concept has been presented.

Animals↗
PubMed1980

Changes in cerebral blood flow during hyperventilation and CO2-breathing measured transcutaneously in humans by a bidirectional, pulsed, ultrasound Doppler blood velocitymeter.

We have used a bidirectional pulsed ultrasound doppler system which measures the instantaneous mean velocity across the lumen of a blood vessel in order to determine the relationship between alveolar PCO2 (PACO2) and blood flow in the four arteries supplying the brain in humans. Both high and low PACO2-values were explored. Six subjects, 3 males and 3 females (22-40 years) were studied by use of this non-invasive technique. To increase the PACO2 the subjects were breathing 4, 6 and 8% CO2 in air. PACO2 was reduced by voluntary hyperventilation down to a chosen end-expiratory PCO2 value of about 2.2 kPa. We found a linear relationship between arterial blood flow expressed as a percentage of control level and PACO2 in the range from 3.3 to 7.3 kPa. At the very lowest PACO2 values a levelling off of the response, with flow values of 40 to 45%, was observed. The CO2-reactivities in the 6 persons varied between 28.1 and 30.0%/kPa. The time course and the magnitude of the flow response were similar in all four arteries.

Adult↗
PubMed1980

Determinants of transvascular fluid shifts in zone I lungs.

We studied the fluid shifts in isolated, plasma-perfused rabbit lungs kept completely within zone I. The rate of fluid filtration or reabsorption was determined gravimetrically. A rise in alveolar pressure at constant pleural and vascular pressures reduced th rate of filtration or increased the rate of reabsorption in seven of eight lungs. In seven of seven lungs a reduction in pleural pressure at constant alveolar and vascular pressures increased the rate of filtration or decreased the rate of reabsorption. Thus, a given rise in lung volume had opposite effects depending on whether this rise was caused by an increased alveolar or reduced pleural pressure. Therefore, the exchange vessels studied cannot be true extra-alveolar vessels, which always expand (reflecting a rise in transmural pressure) with a rise in lung volume. When alveolar and pleural pressures were equally increased at constant vascular pressure, the rate of filtration was reduced in four of four lungs. The results can be explained through the existence of exchange vessels situated neither in the alveolar septae proper nor among the true extra-alveolar vessels. The vessels in the alveolar junctions are the most likely candidates.

Animals↗
PubMed1979

The importance of flow pulsatility for the rate of transvascular fluid filtration in lungs.

1. The rate of transvascular fluid filtration has been studied with a gravimetric technique in isolated perfused rabbit lungs during periods of elevated left atrial pressure (PLA). 2. Fluid filtration was expressed as the filtration coefficient, Kf (g/min x 100 g bloodless lung x mmHg PLA) and determined during alternately pulsatile and non-pulsatile perfusion in six zone III and three zone II/I lung preparations. Perfusion pattern was changed without interruption of flow. Mean in- and outflow pressures were kept constant. 3. In all the lungs it was found that Kf was higher during pulsatile than during non-pulsatile flow (P less than 0.01). Mean Kf (+/- S.E. of mean) for the zone III preparations was 0.42 (+/- 0.089) and 0.27 (+/- 0.057) for pulsatile and non-pulsatile perfusion, respectively. The corresponding figures for the zone II/I preparations were 0.11 (+/- 0.035) and 0.04 (+/- 0.030). 4. We suggest that the difference is due to a larger filtration area and/or a higher mean microvascular hydrostatic pressure during pulsatile than during non-pulsatile flow and not to a rise in hydraulic conductivity due to pressure pulsations ('stretched pores'). 5. When the water-exchange function of the lung is considered, flow pattern should be taken into account as an entity in its own right in addition to the steady state or the mean component of blood flow.

Animals↗
PubMed1978

Prostaglandin content in blood and lung tissue during alveolar hypoxia.

The aim of the present work was to investigate whether prostaglandins (PGs) are synthetized and released from isolated blood-perfused rat and cat lungs secondary to vasoconstriction induced by alveolar hypoxia. The lungs were perfused with autologous blood with constant volume inflow via the pulmonary artery in a recirculating system. They were ventilated with constant volume positive pressure, and acute alveolar hypoxia was induced by ventilation with a gas containing 2% O2. A superfusion bioassay technique was used to measure PG-like activity in the perfusate from the lungs, the blood being re-oxygenated before reaching the assay tissues. The oxygenator prevented the perfusate hypoxia induced by ventilation hypoxia to affect the bioassay tissues. The assay tissues were rat stomach strip, rat colon and chick rectum. They were sensitive to calibrating doses of 0.5--1 ng/ml PGE2 and 1--2 ng/ml PGF2alpha. In another series of experiments PGs of the F-series were measured in lung tissue from normoxic and hypoxic lungs with radioimmunoassay technique. No increase in PG-like activity could be detected in the venous effluent by means of bioassay during hypoxia, nor was the lung tissue content of immunoactive PGF increased by hypoxia. The present findings indicate that alveolar hypoxia does not stimulate PG-synthesis in lungs, refuting that PGs are important mediators of the pulmonary vasoconstrictor response to alveolar hypoxia. It is concluded that PGs play no significant role in producing the pressor response to alveolar hypoxia.

Animals↗