[Experimental study in partial liquid ventilation for acute respiratory failure after ischemia reperfusion pulmonary injury in a rabbit model].

Partial liquid ventilation (PLV) using perfluorooctylbromide (PFOB) was studied for use in treating experimental animal models in which acute respiratory failure was caused by hypoxia, oleic acid lung injury, or saline lung lavage. Clinical trials are currently being conducted in the United States. We studied the effectiveness of PLV with PFOB in treating acute respiratory failure after ischemia reperfusion pulmonary injury in a rabbit model; left lung ischemia was induced with a hilar clamp. Ninety minute later, the clamp was removed for reperfusion. Fifteen Japanese white rabbits weighing from 2.5 to 3.2 kg were divided into three groups-conventional mechanical ventilation (CMV) after reperfusion, PLV after reperfusion and controls (conventional mechanical ventilation without ischemia reperfusion injury). In the PLV group, a dose of 7 ml/kg PFOB was administered through an endotracheal tube. In the CMV group, PaO2 value decreased to 79 +/- 13 mmHg 120 min after reperfusion, significantly lower than in the PLV group 404 +/- 70- or controls -494 +/- 61-. PaCO2 was significantly higher in the CMV group-61.9 +/- 14.4 mmHg- than in the PLV group-45.7 +/- 6.1- or controls-32.1 +/- 2.2. Peak airway pressure was slightly higher in the CMV group-19.0 +/- 4.9-than in the PLV group-18.2 +/- 5.4- or controls-16.2 +/- 1.8. mPAP/mSAP did not differ significantly among groups. The heart rate decreased in the CMV and PLV groups, but was unchanged in controls. Microscopic studies revealed markedly reduced alveolar hemorrhage, lung fluid accumulation, and inflammatory infiltration in the PLV group, compared to the CMV group. PLV thus is effective in improving gas exchange and preventing pulmonary injury in acute respiratory failure after ischemia reperfusion injury in a rabbit model.

Impaired pulmonary oxygenation of diabetic origin in patients undergoing coronary artery bypass grafting.

The effect of a disposition to diabetes mellitus on pulmonary function was determined by dividing 70 consecutive patients who underwent coronary artery bypass grafting (CABG) into a group of 41 patients with such a disposition and a group of 29 without. Indices of pulmonary function studied were the ratio of the arterial partial pressure of oxygen to the inspired oxygen fraction (PaO2/FiO2), the alveolar-arterial oxygen gradient (A-aDO2) and the respiratory index (A-aDO2/PaO2). These were determined before CABG, at the maximum level of blood glucose and when FiO2 was in the range 0.4-0.7 within 6 h after CABG. Even before bypass, all indices were significantly worse in the group with a disposition to diabetes mellitus than in that without. After surgery, these dysfunctions were more severely exacerbated in the former group. FiO2 was the best predictor of the current state of pulmonary function in both groups. Variables that strongly affected pulmonary function were pulmonary arterial wedge pressure in the group with no diabetic disposition and central venous pressure in those with such a disposition. Thus, pulmonary dysfunction of diabetic origin exists not only before CABG, but also after the procedure. Attending physicians must be careful not to increase wedge pressure and central venous pressure.

[A case of open heart surgery associated with liver cirrhosis and pancytopenia].

A 58-year-old female was diagnosed as mitral regurgitation and tricuspid regurgitation, combined with liver cirrhosis (T. Bil 2.3 mg/dl, ICG-R 37%) and pancytopenia (Hb 9.4 g/dl, WBC 3,000, Plt 56,000). She underwent mitral and tricuspid annular plications. After extracorporeal circulation, the postoperative platelet count was maintained higher than preoperative one by transfusion of platelet-rich plasma. Administration of FOY was begun during operation. Levels of T. Bil. and BUN were highest at 15th postoperative day and decreased gradually. Postoperative pleural effusion was treated by administration of 25% albumin solution keeping the level of Alb. up 3.5 mg/dl.