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Vascular Resistance in Atelectatic Lungs: Effects of Inhalation Anesthetics
Author(s) -
Bjertnæs L.,
Mundal R.,
Hauge A.,
Nicolaysen A.
Publication year - 1980
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1980.tb01517.x
Subject(s) - medicine , enflurane , anesthesia , papaverine , hypoxic pulmonary vasoconstriction , atelectasis , vascular resistance , inhalation , lung , hypoxia (environmental) , vasoconstriction , halothane , hemodynamics , oxygen , chemistry , organic chemistry
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. enfluranr and ether on PVR in atelectatic lungs have been explored. Two pairs of isolated rat lung were perfused in series at constant flow. One of the preparations was made atelectatic by airway occlusion subsequent to ventilation with a high Po 2 gas (95% 02). Ventilation of the other preparation continued with hypoxic gas (2% 02). 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 PQ was increased (>66.5kPa). Histological examination revealed that two out of four preparations were completely atelectatic I 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.