In an attempt to clarify the effect of nitroglycerin (NTG) on the human pulmonary "venous" (P"V") system, short segments of volume-pressure (V-P) curves in the P"V" system were estimated in 50 patients before and after the sublingual administration of NTG. The pulmonary "venous" volume (P"V"V) was estimated with our own method, using radionuclide (RN) angiocardiography. The mean pulmonary artery wedge pressure ((PAW)^^^-) was measured using a Swan-Ganz catheter. The increments of P"V"V and (PAW)^^^- that occurred during passive elevation of the legs were clues to the estimation of V-P "curves" in this system before and after NTG. In order to calculate a short segment of a V-P curve, the P"V"V was plotted on the ordinate and the (PAW)^^^- on the abscissa. In addition, we presented the effective unstressed volume graphically by extrapolating each short segment of V-P curves towards the volume axis (ordinate). We obtained the following results from the present study; (1) The sublingual administration of NTG caused the P"V"V-(PAW)^^^--plots to shift to the left (-5.2 ± 3.6 mmHg, mean ± SD) and downwards (-19 ± 11 ml, mean ± SD). (2) The V-P curves appeared to shift steeper after NTG (19.2 ± 11.3 ml/mmHg, mean ± SD) than before NTG (12.4 ± 7.9 ml/mmHg). (3) The graphically-obtained effective unstressed volume was unchanged with NTG, at least within the operating range of (PAW)^^^-. (4) It is highly probable that NTG causes the tone of the P"V" system to be decreased by way of a relaxation of the vascular beds of the P"V" system.

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Some interesting features in the morphological study of rat cardiac cells were obtained by use of the light and phase-contrast microscopy. The histological approach and comparison of the ultrastructures of the cultured cardiac cells with uncultured cells were included in the studies as a control. Four main points are discussed: (1) the process of single beating cells that eventually constitutes the cell cluster and network, (2) the function and histological content of the network, (3) the mechanisms of synchronized beating cells, (4) the substance of the cell surface coat and intercellular connection.

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During the period from August, 1977 to December, 1984, a total of 3003 patients who received open heart surgery were treated postoperatively at the ICU of National Cardiovascular Center. Low cardiac output syndrome (LOS) developed in 669 (22.3%) patients. Organ failures due to LOS were studied in these patients. Although the overall mortality of postoperative patients was 5.6% and improved to around 4% in the later years, death rate of patients with LOS was persistently high (22.8%) and showed no tendency to improve even in the latest yeart. Moreover, the clinical results of those LOS patients who developed organ failure were extremely poor; the mortality of patients with respiratory failure (RF) accounted for 36.8% and that of patients with other organ failure exceeded 50%. The incidence of impaired organs in LOS patients was 49.9% in RF, 29.9% in acute renal failure (ARF), 18.4% in hepatic failure (HF), 16.4% in disseminated intravascular coagulation (DIC), 15.5% in central nervous system failure (CNSF), and 11.1% in gastrointestinal bleeding (GIB). Pathophysiological mechanisms as well as the management of these major complications caused by LOS are also discussed. Some patients developed multiple organ failure (MOF). Plasma exchange (PE) was performed on 16 patients who developed MOF. Improvement of various organ functions was obtained and consequently three patients were successfully treated by means of PE. Removal of various substances toxic cycle produced by the interaction of impaired organs in patients with MOF are major roles of PE in the treatment of MOF.

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In order to explore pulmonary dysfunction originating in cardiac decompensation, acquired heart diseases were classified into three selected categories; chronic compensated heart, chronic decompensated heart and acute decompensated heart with severe alveolar edema. Pathophysiology in each category was investigated. Hemodynamic variables were measured by cardiac catheterizations and a variety of pulmonary functions based on respiratory physiology were studied. Severe alveolar edema due to acute pump failure of the heart revealed a significant inverse correlation between PaO₂ and PaCO₂ indicating the appearance of decreased PaO₂. A-_aDO₂ remained still high despite a complete resolution of alveolar edema. There are some possibilities that pulmonary dysfunction might be accelerated by repetition of acute cardiac decompensation in chronic heart diseases. Chronic pulmonary involvements caused by chronically decompensated heart must be stressed most important for comprehensive treatments of cardiac pump failure. Lung volumes considerably decreased but ordinarily there was no obvious airflow obstruction in the large central airways. Chronic compromised lung with giant left atrium, however, showed appreciable decrease in FEV₁% (FEV₁/FVC), MMF, V₅₀ and V₂₅, indicating an apparent evidence of both central and peripheral airway obstructions. Patients with CTR over 70% were more seriously involved with a significant reduction in lung volumes in addition to total airway obstructions. Under these situations an inverse correlation between PaO₂ and PaCO₂ in chronic decompensated heart was observed showing a contrast difference in chronic compensated heart.

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The pathophysiology and treatment of pump failure with right ventricular overload due to chronic pulmonary diseases were discussed. When right ventricular overload occurs hypertrophy and dilatation of right ventricle follows and the heart as a whole, including left ventricle, is altered in morphology and function .Therapeutic measures for right ventricular overload are the key to management and treatment of pump failure. Pulmonary hypertension, as an etiological factor, is discussed and is divided into two categories, that is, mild to moderate pulmonary hypertension with hypoxia due to chronic obstructive lung disease, and severe pulmonary hypertension due to pulmonary vascular disease. In each category, effects of oxygen inhalation and vaso-dilating agents were evaluated. Oxygen did not decrease pulmonary vascular resistance in the state of chronic hypoxia, though a vasodilating agent was effective. In pulmonary vascular disease, vaso-dilating agents were effective to decrease pulmonary vascular resistance and pulmonary artery pressure, though the effect was less than 30% down in resistance.

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We studied the effects of positive end-expiratory pressure (PEEP) ventilation in ten patients with acute myocardial infarction (nine in Killip class III, one in Killip class IV; pulmonary capillary wedge pressure > 24 mmHg) and of extracorporeal ultrafiltration method (ECUM) in seven patients with refractory heart failure due to acute myocardial infarction and others. (1) Application of PEEP resulted in significant increases in PaO₂ and SaO₂ and decrease in PaCO₂. Significant reduction in mean pulmonary arterial and pulmonary capillary wedge pressures and heart rate was observed, while stroke work index increased significantly. There was a significant correlation between changes in stroke work index and PaO₂ after the application of PEEP. (2) The use of ECUM removed fluid of 1416 ± 662 ml (680-2800 ml) with the ultrafiltration flux rate being 478 ± 223 ml/hour. Significant decreases in mean pulmonary arterial, pulmonary capillary wedge and central venous pressures were observed, while PaO₂ increased significantly. BUN and serum creatinine levels increased significantly, and total protein and serum albumin tended to increase. There was a significant correlation between fluid removed and change in PaO₂ after the use of ECUM. Thus, PEEP and ECUM are beneficial for patients with refractory heart failure. The mechanism(s) are: (1) reduction in preload due to an increased intrathoracic pressure and a decreased systemic venous return with PEEP, or due to removal of excess fluid with ECUM, and (2) improvement of the oxygenation of the blood.

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To evaluate the influence of volume overload by pregnancy on heart diseases, the relations between cardiac status before pregnancy and clinical courses during pregnancy were studied, especially from the viewpoint of pulmonary circulation. In 206 pregnant cardiac patients whose prepregnancy laboratory data were known, the deterioration (appearance or advance of heart failure) during pregnancy was prospectively related to: pulmonary congestion (p < 0.05), enlarged left atrium (p < 0.05), atrial fibrillation (p <0.01) and right ventricular hypertrophy (p < 0.005) in mitral stenosis; cardiomegaly (p <0.05) and atrial fibrillation (p < 0.005) in mitral regurgitation; cardiomegaly (p < 0.005) in congenital heart diseases; and to previous congestive heart failure (p < 0.005) in total cases. All of the cases with systolic pulmonary artery pressure higher than 50 mmHg deteriorated during pregnancy. Some cases with no deteriorating laboratory findings showed dyspnea suddenly at the end of pregnancy. In 1033 cardiac patients who had experienced pregnancy, deterioration during pregnancy was seen more frequently in cases with mitral valvular diseases that in those with aortic valvular diseases. No deterioration was seen in pulmonary stenosis patients. Abnormal status of pulmonary circulation may be one of the important determining factors of deterioration by pregnancy in cardiac patients. The criteria for permitting pregnancy in cardiac patients are proposed.

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