The effects of acute and chronic atelectasis on pulmonary hemodynamics

Elebute, E. A.; Masood, Abdul-Mannan; Faulkner, Charles S.; Yu, Paul N.; Schwartz, Seymour I.

doi:10.1016/s0022-5223(19)43446-6

The Journal of Thoracic and Cardiovascular Surgery

1966

DOI: 10.1016/s0022-5223(19)43446-6

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The effects of acute and chronic atelectasis on pulmonary hemodynamics

E. A. Elebute¹,

Abdul-Mannan Masood²,

Charles S. Faulkner³

et al.

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1969

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Cited by 5 publications

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“…NLINN (1977) has presented evidence for a 50% rise in vascular resistance within atelectatic lung regions. Others, however, have observed either unchanged or even reduced vascular resistance (AVIADO 1960, NIDEN 1964, ELEBUTE et al 1966. The mechanism behind a rise in vascular resistance in atelectatic regions is also disputed.…”

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confidence: 99%

Vascular Resistance in Atelectatic Lungs: Effects of Inhalation Anesthetics

Bjertnæs¹,

Mundal²,

Hauge³

et al. 1980

Acta Anaesthesiol Scand

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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.

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mentioning

confidence: 99%

Vascular Resistance in Atelectatic Lungs: Effects of Inhalation Anesthetics

Bjertnæs¹,

Mundal²,

Hauge³

et al. 1980

Acta Anaesthesiol Scand

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Pulmonary function, cardiac status, and postoperative course in relation to cardiopulmonary bypass

Andersen

Ghia

1970

The Journal of Thoracic and Cardiovascular Surgery

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Traumatic Rupture of the Right Main Bronchus in an Eight-year-old Child Successfully Repaired Eight Years after Injury

et al. 1970

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The effects of acute and chronic atelectasis on pulmonary hemodynamics

Cited by 5 publications

References 24 publications

Vascular Resistance in Atelectatic Lungs: Effects of Inhalation Anesthetics

Vascular Resistance in Atelectatic Lungs: Effects of Inhalation Anesthetics

Pulmonary function, cardiac status, and postoperative course in relation to cardiopulmonary bypass

Traumatic Rupture of the Right Main Bronchus in an Eight-year-old Child Successfully Repaired Eight Years after Injury

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