Because our measurements based on respiratory gas analysis include only metabolic requirements met through direct diffusion of alveolar gas into the lung tissue, total lung oxygen consumption may have been underestimated because of the unknown proportion of need met by the bronchial circulation. From lung transplantation it is known that the bronchial circulation can be abolished without causing any obvious dysfunction in gas exchange, although there is much better healing of the tracheal-bronchial anastomosis when the bronchial arteries are anastomized. However, it remains unclear from these studies how much the bronchial circulation actually contributes to gas exchange during total CPB. Baile et al., using the same approach, reported much higher values of about 140 ml/min (range, 8 to 1,043 ml/min). The same authors found a decrease in bronchial blood flow when alveolar pressure was increased. found values of about 22 ml/min for healthy patients, 89 ml/min in patients with heart failure, 76 ml/min in patients with mitral stenosis, and 40 ml/min in patients whose lungs are ventilated with dry air. Bronchial blood flow in humans during total CPB has been assessed by measuring the amount of blood returning the left heart. We believe that the alveolar walls derive oxygen chiefly from the alveolar air, whereas the bronchi, the smaller air passages, and major portions of the visceral pleura use oxygen carried by the bronchial flow. The major portion of this blood supplies the bronchial walls and the visceral pleura and is drained into the bronchial veins. In the normal lung, total bronchial blood flow is estimated to be about 1% of cardiac output, contributing a small amount to pulmonary capillary blood flow and gas exchange. Nasopharyngeal, rectal, and blood temperatures (during CBP) were monitored continuously. During this period, the lungs were ventilated with low tidal volumes (150 ml) at a rate of 6 breaths/min and with a positive end-expiratory pressure of 3 mmHg. Systemic hypothermia (28 degrees Celsius, alpha-stat pH management) was induced by blood cooling and maintained for at least 30 min. Blood was oxygenated by a membrane oxygenator (Cobe, Arvada, CO), and a nonpulsatile flow rate of 2–3 l min sup -1 m sup -2 was regulated by a roller pump (Stockert, Munich, Germany) to a mean arterial pressure of 50–80 mmHg. The left ventricle was vented in all cases. During total CPB, all blood from the caval veins was drained into the cardiotomy reservoir and the caval veins were occluded by banding so that pulmonary artery flow ceased completely. Cardiac arrest and hypothermia of the myocardium was achieved by intracoronary infusion of cardioplegic solution (modified Bretschneider) in association with systemic hypothermia (28 degrees Celsius).
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