Separate lung blood flow in anesthetized dogs: a comparative study between electromagnetometry and SF6 and CO2 elimination.

Anesthetized, prone dogs were intubated with a double-lumen endobronchial tube, and the lungs were ventilated independently. Three methods of recording differential blood flow were compared during unilateral lung hypoxia: electromagnetic flow measurement, flow probes being fitted onto each main pulmonary artery after thoracotomy (QPr); SF6 elimination from each lung, the inert gas being continuously infused into a central vein (QSF6); and CO2 elimination (QCO2). During control conditions (100% O2 to both lungs), the test lung QPr was 54% of cardiac output, and corresponding QSF6 and QCO2 were 56% and 52%, respectively. Hypoxic challenge with 8% O2 to the test lung reduced QPR, QSF6, and QCO2 by 25%, 27%, and 7%, respectively. Ventilation of the test lung with pure nitrogen reduced its blood flow further, QPr, QSF6, and QCO2 being reduced by 39%, 42%, and 23%, respectively, from initial control. A strong correlation between test lung QPr and QSF6 was seen with a slope of 0.90 (r:0.89, P less than 0.001). Only 60% of the reduction in test lung blood flow was detected by CO2 elimination, as compared to electromagnetic flow measurement or SF6 elimination. The poor results obtained with CO2 elimination can be explained by its dependence on the ventilation-perfusion ratio and the effect of oxygen tension on the CO2 binding capacity of blood (Haldane effect). The findings emphasize the necessity of using an inert, poorly soluble gas for the measurement of separate lung blood flow.

Hypoxia-induced pulmonary vasoconstriction in the human lung. The effect of isoflurane anesthesia.

The influence of isoflurane on hypoxic pulmonary vasoconstriction (HPV) was studied in eight subjects prior to elective surgery. The lungs were ventilated separately with a double-lumen endobronchial catheter. After oxygen ventilation of both lungs for 30 min during intravenous barbiturate anesthesia, the test lung was rendered hypoxic by ventilation with 8% O2 in nitrogen. The control lung was ventilated continuously with 100% O2. Isoflurane was added to the inspired gas, so that end-tidal concentrations of 1% and 1.5% were obtained. Cardiac output (QT) was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the excretion of a continuously infused, poorly soluble gas (SF6). The hypoxic challenge during intravenous anesthesia resulted in a reduction in the fractional perfusion of the test lung from 54% to 41% of QT. Mean pulmonary arterial pressure increased by 46%, and pulmonary vascular resistance (PVR) of the test lung more than doubled. Arterial oxygen tension fell from 375 mmHg (50 kPa) to 101 mmHg (13.5 kPa). Adding isoflurane to the inhalation gas, first at a concentration of 1%, then 1.5%, caused no further significant change in the distribution of pulmonary blood flow, although six of the eight subjects showed a small increase in test lung blood flow at isoflurane 1.5%. There was no change in PVR or in any other circulatory variable. Arterial blood gases remained essentially unaltered. When the hypoxic challenge was discontinued, all variables returned to control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypoxia-induced vasoconstriction in human lung exposed to enflurane anaesthesia.

The degree of hypoxic pulmonary vasoconstriction was studied in eight subjects during enflurane anaesthesia and was compared with that during intravenous pentobarbital anaesthesia in the same subjects. The lungs were ventilated separately with the aid of a double-lumen endobronchial catheter. After preoxygenation of both lungs for 30 min, during intravenous anaesthesia, the right lung (test lung) was rendered hypoxic by ventilation with 6% O2 in nitrogen. The left lung (control lung) was ventilated continuously with 100% oxygen. Cardiac output (QT) was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the elimination of a continuously infused, poorly soluble inert gas (SF6). The hypoxic challenge resulted in a reduction of the distribution of perfusion to the test lung from 57% to 36% of QT. Mean pulmonary arterial pressure increased by 37% and pulmonary vascular resistance of the test lung doubled. Arterial oxygen tension decreased from 45.9 to 9.5 kPa. Administration of enflurane to an end-tidal concentration of 2% to both lungs caused no significant change in the distribution of the pulmonary blood flow, PVR, or any other circulatory variable. The arterial blood gases remained unaltered. When the hypoxic challenge was discontinued, all variables returned towards control values. The findings suggest that the inhalational anaesthetic enflurane does not reduce the hypoxic vasoconstrictor response in the human lung.

Hypoxic pulmonary vasoconstriction in the human lung: the effect of prolonged unilateral hypoxic challenge during anaesthesia.

The influence of time on the pulmonary vasoconstrictor response to hypoxia was studied in six subjects during general anaesthesia and artificial ventilation prior to elective surgery. The lungs were intubated separately with a double-lumen bronchial catheter. After preoxygenation of both lungs for 30 min, the test lung was rendered hypoxic for 60 min by ventilation with 5% O2 in N2, with the control lung still being ventilated with 100% O2. Cardiac output was determined by thermodilution, and the distribution of blood flow between the lungs was assessed from the excretion of a continuously infused poorly soluble gas (SF6). The fractional perfusion of the test lung decreased from 53% to 25% of cardiac output within the first 15 min of unilateral hypoxia. The pulmonary artery mean pressure increased by 14% and the pulmonary vascular resistance (PVR) of the test lung increased by 54%. Venous admixture increased from 21% to 39% of cardiac output, while the "true" shunt was maintained at about 15%. Arterial oxygen tension (Pao2) fell from 45 kPa to 12 kPa. Prolonging the unilateral hypoxic challenge caused no further change in the redistribution of the pulmonary blood flow, but cardiac output and pulmonary artery mean pressure continued to increase to 40%-50% above control values after 1 h of hypoxia. The PVR of the test lung remained unchanged. The findings suggest that there is an immediate vasoconstrictor response to hypoxia in the human lung and that there is no further potentiation or diminution, of the response during a 60-min period of hypoxia.