Although ethyl alcohol has a long medicinal history (1), its precise effects on the cardiovascular system have not been defined. Acute alcohol ingestion is known to result in triglyceride accumulation in the liver, which appears dependent upon an intact sympathetic nervous system (2). Evidence for stimulation of this system after ethanol ingestion has been advanced (3). Since sustained catecholamine infusion has been associated with lipid accumulation in the myocardium (4, 5), a study of the acute effects of ethanol on myocardial metabolism and function has been undertaken in animals considered nutritionally normal. The quantity given produced blood level concentrations usually associated with moderate intoxication. MethodsMongrel male dogs weighing 19 to 22 kg were anesthetized 18 hours postprandially with morphine sulfate, 3 mg per kg, and pentobarbital (Nembutal), 12 mg per kg, and studied without opening the chest. After insertion of an endotracheal tube, respiration was regulated with a Harvard respiratory pump, facilitating the maintenance of arterial oxygen saturation and pH in the normal range. Catheters were placed in the coronary sinus, pulmonary artery, aorta, and left ventricle for blood sampling and pressure determinations. Although initially the catheters were filled with dilute heparin, slow saline infusions or intermittent flushes were used during the experiment to maintain their patency. Since the level of arterial free fatty acids did not rise during the experiment, the earlier limited use of heparin did not appear to affect substrate concentrations.During the evaluation of cardiac performance in the intact animal in experiments of many hours duration, a direct measurement of contractility utilizing the forcevelocity relationship is not feasible, but less direct methods may be employed to characterize myocardial function. Thus, contractility change has been deduced from the relation of stroke output to left ventricular end-diastolic pressure (LVEDP) (6, 7).Sympathetic stimulation of isolated papillary muscle analyzed in terms of the force-velocity relationship has revealed an enhanced velocity of muscle shortening, representing a primary contractility increase (8). Sympathetic stimulation of the intact heart under conditions of controlled heart rate, before and after loading, has evoked an increase of stroke output as well as dp/dt maximum of left ventricular pressure as manifestations of primary contractility increments (9).A rise in LVEDP is normally associated with a corresponding stroke output increment (9), presumably a reflection of the rise in maximal isometric force without a velocity change that attends increased length of papillary muscle (8). The failure of stroke output to rise in this situation would appear to represent impaired muscle function (6,9,10) particularly when the duration of systole is prolonged or unchanged (6). In this present study the ventricular ejection rate was analyzed in terms of ventricular systolic duration and the maximal rate of rise of left ventricular pres...

SUMMARY A patient with glomerulonephritis and endocarditis is described who had evidence of feline Chlamydia psittaci infection. Treatment with antichlamydial drugs resulted in resolution ofthe glomerulonephritis and the endocarditis. It is recommended that screening for chlamydia is included in the investigation of patients with suspected or obscure endocarditis.Infective endocarditis is often caused by an unusual organism. The management of such cases is much more effective if the identity of the organism has been established (Friedberg, 1964;Hampton and Harrison, 1967).We describe a patient with infective endocarditis and secondary glomerulonephritis in whom there was strong evidence of infection with the feline keratoconjunctivitis agent (Chlamydia psittaci

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Plasma biochemistry, bone radiology and morphometry were studied in a group of 20 patients receiving maintenance hemodialysis. The aim was to determine if increasing the dialysate calcium concentration would decrease plasma parathyroid hormone and improve the radiologic appearances of bone in patients without producing serious side effects. Dialysate calcium concentration was increased stepwise from 4.5 to 6.0 and then to 7.0 mg/100 ml. Mean predialysis plasma calcium concentration increased from 9.4 to 9.7 and then to 10.0 mg/100 ml and mean predialysis phosphate concentration increased from 5.3 to 5.6 mg/100 ml. Parathyroid hormone concentration was elevated in all patients but the mean concentration did not change significantly although in seven patients a decrease occurred. Six patients had radiologic signs of renal bone disease, two patients showed improvement and three patients developed bone disease during the study. The patients with radiologic bone disease had the highest parathyroid hormone concentrations and the majority were female. Morphometric bone measurements showed that bone loss during the study occurred mainly in the male patients. Soft tissue calcification continued to appear during the study. Although the response to some patients to an increased dialysate calcium concentration was favorable, it was impossible to predict which types of patient would benefit from the use of a dialysate calcium concentration of 7.0 mg/100 ml.