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Biomedical subjects

R Mundal

Publications and source records attributed to R Mundal.

24 records · Page 2Linked to original sources
PubMed1982

Latent ischemic heart disease in sea captains.

For 110 apparently healthy Norwegian captains on ocean-going ships a near maximal bicycle exercise test revealed a pathological exercise electrocardiogram for 10.0%, while the corresponding results for a comparable group of Oslo men and a group of Norwegian sea pilots were 4.6 and 11.8%, respectively. The significant difference in prevalence between the captains and Oslo men could not be explained by differences in serum lipids, blood pressure, or a family history of coronary heart disease. The captains were taller and more physically fit than the Oslo men, but they were significantly heavier and had a more rapid age decline in physical performance capacity and a higher prevalence of heavy smokers. Ten of the 11 captains with a pathological exercise electrocardiogram were, or had been, heavy smokers (greater than or equal to 20 cigarettes/d). A high caloric intake in relation to caloric expenditure, heavy smoking, and poorly defined factors such as stress, irregular workhours, and varying climatic conditions are factors to be considered as explanations for these findings. The claim by captains that they have a higher risk than average for developing coronary heart disease was to some extent corroborated in the present study.

Adult↗
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

The pulmonary vasoconstrictor response to hypoxia during enflurane anesthesia.

Previous investigations have shown that diethyl ether, halothane and methoxyflurane inhibit the vasoconstrictor response to hypoxia in isolated rat lungs. A damping effect of diethyl ether and halothane has been observed in the human lung as well. In the intact dog lung, however, other workers have recently denied any effect of halothane and enflurane on this vasoconstrictor mechanism. These findings challenged us to investigate the effect of enflurane on the basoconstrictor response to hypoxia in isolated rat lungs. We found that enflurane administered via the airways reduced the response in proportion to the end-tidal concentration of enflurane, as determined by mass spectrometry.

Anesthesia, Inhalation↗