Salvatore M. Sancetta

Renal failure in patients with cirrhosis of the liver: III. Evaluation of intrarenal blood flow by para-aminohippurate extraction and response to angiotensin

Abstract Renal functional abnormalities associated with advanced liver disease were evaluated in twenty-two patients by determining the effects of angiotensin infusions and of increasing tubular loads of para-aminohippurate (PAH) upon the extraction of PAH. Angiotensin infused intravenously produced variable changes in renal blood flow, glomerular filtration rate and urinary excretion of sodium and water, but did not alter extraction of PAH. This agent did not change the distribution of blood flow within the kidney as estimated from PAH extraction. To the extent that in some patients renal ischemia and hypoxia may have been induced, these changes also had no effect upon the extraction ratio of PAH (E PAH ). The E PAH was below normal during control periods in eight of the twenty-two patients. Reduced E PAH was associated with, but was not a consequence of, decreased renal plasma flow and glomerular filtration rate and a poor urine flow response to water administration. Chronic renal disease, tubular necrosis, renal hypoxia, excessive tubular load of PAH or low urine flow rate could not be incriminated as causes of the decreased E PAH . The decreased E PAH and associated renal functional changes noted in some patients with cirrhosis are explained best by a hemodynamic alteration involving renal cortical vasoconstriction with relative increase in medullary blood flow. Ten patients were given a PAH load. Five responded normally. In the other five changes in E PAH were consistent with the presence of a defect in ability to transport PAH.

RELATION OF ACUTE POTASSIUM DEPLETION TO RENAL AMMONIUM METABOLISM IN PATIENTS WITH CIRRHOSIS

Neurologic findings characteristic of the impending hepatic coma syndrome occur in some cirrhotic patients treated with diuretic agents that may induce potassium losses (1-5). Even when diuretic agents are not employed, hypokalemia may be associated with this syndrome (6-8). Patients demonstrating these signs often improve after treatment with potassium salts. This result of therapy might indicate that potassium deficiency per se is a pathogenetic factor in the impending hepatic coma syndrome (9). Because of the extensive evidence relating abnormalities in nitrogen metabolism to hepatic coma (10), however, it seemed possible that some derangement of nitrogen metabolism might be associated with potassium deficiency. This hypothesis, relating potassium deficiency indirectly to the hepatic coma syndrome by an influence this cation has on ammonium metabolism, provided the rationale for undertaking this investigation. The relation of potassium to ammonium metabolism was studied in patients with cirrhosis of the liver and ascites rendered acutely potassium deficient by a diuretic regimen. The results of these studies demonstrate that metabolism of ammonium by the kidney is altered in potassium-deficient patients and that significant quantities of ammonium may be delivered to the cir-

Effect of Hypotension due to Spinal Anesthesia on Coronary Blood Flow and Myocardial Metabolism in Man

The induction of spinal anesthesia resulted in hypotension and decreased coronary blood flow and myocardial oxygen consumption. At the same time the myocardial extraction coefficient of oxygen was not increased, indicating myocardial oxygenation to be adequate for the lower work load. This does not imply that local ischemia might not occur in the presence of coronary artery sclerosis. The coronary arteriovenous differences of glucose, lactate and pyruvate were not changed during the period of hypotension.

The acute and chronic effects of phlebotomy on general hemodynamics and pulmonary functions of patients with secondary polycythemia associated with pulmonary emphysema

Abstract 1.1. Hemodynamic and pulmonary function studies were evaluated in 15 patients with secondary polycythemia associated with chronic pulmonary emphysema. 2.2. The studies were made before and after acute venesection and again after sufficient venesection to maintain hematocrits at nearly normal levels for periods of 5 to 6 weeks. 3.3. Significant decreases in hematocrit, right atrial and right ventricular systolic, end-diastolic, and mean pressures, and significant increases in arterial oxygen saturation and tension, oxygen consumption, and arteriovenous oxygen difference were noted in measurements carried out 1 hour after the initial phlebotomy. 4.4. In the total group, no changes occurred in pulmonary function studies after acute phlebotomy or repeat phlebotomies, or in hemodynamic studies after repeat phlebotomies. 5.5. In patients with high end-diastolic right ventricular pressures at the initial catheterizations, acute phlebotomy was followed by decreases in the residual lung volume and functional residual capacity, although these had increased to the control values after 6 weeks. 6.6. It is possible that the observed changes in O 2 gas studies and residual lung volumes may be related to changes in intrapulmonary blood volume or flow. 7.7. All of the changes observed after repeated phlebotomies can be explained by the mechanical removal of red blood cells. 8.8. There is no indication that polycythemia, of itself, is detrimental to the hemodynamic or pulmonary function status of these patients when heart failure has not supervened. 9.9. Venesection has a therapeutic role in the management of patients with secondary polycythemia associated with chronic pulmonary emphysema. Immediate phlebotomy should be helpful in controlling heart failure, and repeat phlebotomies, although not altering the hemodynamic or pulmonary function status of these patients, may be indicated because of the reduction in the viscosity, and, therefore, presumably for the effect on the incidence of thromboembolic complications. It would appear that the utilization of repeated phlebotomies should be determined by the degree of polycythemia rather than by the pulmonary function status of the patient.

EFFECTS OF HIGH SPINAL ANESTHESIA ON CEREBRAL CIRCULATION AND METABOLISM IN MAN

The effects of high spinal anesthesia on the general (1, 2), hepatic (3), and coronary (4) hemodynamics have been previously reported by our group. Because hypotension produced by high spinal anesthesia may be a potential hazard to the circulatory sufficiency of the brain, it was considered important to study the effects of high spinal anesthesia on the cerebral circulation and metabolism. Studies by others have been concerned with the effects of differential spinal block on the cerebral circulation of hypertensive individuals (5) and the effect of hypotensive drugs on the cerebral circulation of aged persons (6) and hypertensives (7). The majority of patients in this study are normotensive, but the effects of high spinal anesthesia on a small group of hypertensives is included. The anesthetic level is higher and the amount of spinal anesthetic agent employed is larger than in studies reported by others, simulating the dosage used in producing surgical high spinal anesthesia, although surgical procedures were not undertaken in these subjects.

Dissecting aneurysm of aorta with hemorrhagic infarction of the spinal cord and complete paraplegia

Abstract A case of dissecting aneurysm of the aorta is presented in which all the intercostal arteries were severed, causing hemorrhagic infarction of the spinal cord and complete motor and sensory paraplegia. To our knowledge it is the first such case reported in which spinal subarachnoid hemorrhage occurred.

Stokes-Adams Attacks Induced by Rectal Stimulation in a Patient with Complete Heart Block

This paper reports a case of complete heart block whose Stokes-Adams attacks were induced by straining at stool and invariably by digital stimulation of the rectum. Electrocardiograms during attacks exhibited high ventricular tachycardia or fibrillation and chaotic heart action.

Dynamic and Neurogenic Factors Determining the Hepatic Arterial Flow after Portal Occlusion

Acute ligation of the portal vein in the barbital-anesthetized dog produces a significant increase in the hepatic arterial flow when the perfusion pressure remains elevated in the artery. Evidence is presented which supports the concept that the immediate readjustment is solely dependent on dynamic changes. The late readjustments are probably conditioned by the interplay of neurogenic and humoral factors.

Congenital Heart Disease with Septal Defects in which Paradoxical Brain Abscess Causes Death

The presence of septal defects in congenital heart disease makes for a direct shunting of particulate matter from the venous to the arterial side of the circulation. In reviewing the literature we have been surprised to find that this phenomenon, with resultant brain abscess, has been second only to bacterial endocarditis as a septic cause of death. The subject deserves attention from the view-point of early diagnosis and cure, since the reported mortality has been almost 100 per cent.

Acute Hemodynamic Effects of Hexamethonium in Normotensive Man

The effect of intravenous hexamethonium bromide was studied in 10 normotensive human subjects in the steady state. In the absence of over-all change in cardiac output, the variable decrease in arterial pressure is accounted for by decrease in calculated total peripheral resistance.