Alexander S. Geha

Effect of pulsatile cardiopulmonary bypass on cerebral metabolism

Abstract The effects of pulsatile normothermic highflow cardiopulmonary bypass on cerebral metabolism in the dog were studied with and without the addition of carbon dioxide to the ventilating gas by measuring the pH, P O 2 , and P Co 2 , and the levels of lactate and pyruvate in the arterial blood and CSF. The findings were also compared with those in a similar group of dogs subjected to nonpulsatile cardiopulmonary bypass under identical conditions. The present results do not indicate the development of selective cerebral hypoxia or anaerobiosis at any time, even in the presence of moderately severe respiratory alkalosis. Lactate accumulation in the blood was less than with nonpulsatile perfusion, and P CSF O 2 was higher with pulsatile bypass, but alveolar-arterial oxygen gradients increased markedly after pulsatile perfusion with the Army artificial heart pump. Comparison with nonpulsatile bypass points out the lack of definitive evidence that pulsatile perfusion is more beneficial to cerebral metabolism.

Role of adrenergic mechanisms in the development of cardiac hypertrophy.

Summary This experiment was designed to study the role of cardiac beta-adrenergic mechanisms in the development of hypertrophy in rats. The suprarenal abdominal aorta was banded, resulting in an increase in cardiac wt-body wt ratio. A group of rats received a sham operation. Half of the banded rats were treated with practolol, 2.0 mg/kg intraperitoneally every 12 hr for the 6 days after banding. The effectiveness of cardiac beta-adrenergic blockade was confirmed by absence of an increase in heart rate following intravenous isoproterenol at various times between practolol injections. Practolol did not affect the gradient in the banded groups. Six animals in each banded group were sacrificed daily for 6 days. The right and left ventricles were dissected separately and weighed. RV-body weight ratios increased similarly in both banded groups. LV-body weight ratio (g/kg) was 2.17 ± 0.043 in sham rats, and it attained maximal levels of 3.03 ± 0.10 within 6 days in banded untreated rats and 2.96 ± 0.14 in banded rats receiving practolol. Therefore, beta-adrenergic mechanisms were not involved in the development of hypertrophy due to increased afterload. Also, these findings are not consistent with the Meerson hypothesis, since hypertrophy occurred despite the reduction in myocardial O2 consumption due to practolol.

Value of the cerebrospinal fluid as an indicator of cerebral metabolic changes

Abstract Ventilation with a gas mixture containing 8% O2 produces cerebral hypoxia in the dog and a shift to anaerobic metabolism and increases the release of lactate by the brain, which is evident immediately in the CSF. These changes were detected within 10 minutes and would indicate that the CSF is an adequate and sensitive indicator of cerebral metabolism. The CSF parameters, therefore, seem to be a true reflection of cerebral metabolic status and confirm the reliability of the use of CSF to study alterations in brain metabolism.

Bilateral carotid nerve stimulation in the treatment of angina pectoris.

Presented at the Nineteenth Annual Meeting of the American College of Angiology, San Juan, Puerto Rico, January 21-25, 1973. From the Departments of Surgery and Medicine, Washington University School of Medicine, and the Divisions of Thoracic and Cardiovascular Surgery, and Cardiology, The Jewish Hospital of St. Louis, St. Louis, Missouri 63110. Supported in part by Research Grant #5RO1-HL 13088 from the National Heart and Lung Institute, National Institutes of Health, U.S. Department of Health, Education and Welfare. Angina pectoris is believed to be the result of an imbalance between myocardial oxygen requirements and the availability of oxygen to the myocardium. A variety of surgical approaches to ischemic heart disease aiming at increasing the blood supply to the ischemic myocardium have been introduced in the past, often with considerable enthusiasm, only to meet with frustrating and frequently tragic results. Skeptics readily recall the disappointments following attempts to restore blood flow by implanting systemic vessels into the left ventricular myocardium, or to expand the lumen of damaged coronary vessels using patch grafts. However, there is little doubt that coronary bypass surgery, which utilizes a segment of saphenous vein or a systemic artery to link the aorta and the affected coronary vessel, can accomplish what the other approaches could not, namely immediate perfusion of the region of ischemic myocardium by establishing flow from a source above the obstruction to a relatively healthy portion of the artery beyond it.l5 This approach seems to be a sound one physiologically, and following introduction of saphenous vein bypass surgery for the management of chronic ischemia about five years ago, experience at a number

Surgical Treatment of Lesions of the Outflow Tract of the Left Ventricle

Presented at the Nineteenth Annual Meeting of the American College of Angiology, San Juan, Puerto Rico, January 21-25, 1973. From the Department of Surgery, Washington University School of Medicine, and the Division of Thoracic and Cardiovascular Surgery, The Jewish Hospital of St. Louis, Missouri. Supported in part by Research Grant No. HL-13088 from the National Heart and Lung Institute, United States Public Health Service, Department of Health, Education and Welfare. Left ventricular outflow lesions have become amenable to accurate corrective surgery with the advent of diagnostic methods which permit differentiation of the various pathologic states that may be present, and with open-heart surgery which permits appraisal of the pathologic anatomy and precise correction under direct vision. Until recently, many of these conditions had been of academic interest only. Lesions of the outflow tract of the left ventricle may be congenital or acquired, and are more completely defined in connection with the following classification: 1. Obstructive lesions A. Valvular stenosis 1. Congenital valvular stenosis

Effects of occlusion of the brachiocephalic vessels on cerebral metabolism in the dog

Abstract Cerebral and systemic metabolism were studied by measurement of gas tensions, pH, and lactate and pyruvate concentrations in CSF and arterial blood in dogs subjected to simultaneous occlusion of the carotid and vertebral arteries in the neck, or simultaneous intrathoracic occlusion of the brachiocephalic vessels and their branches. No appreciable change in cerebral metabolism was demonstrated with cervical occlusion of the vertebral and carotid vessels and all the dogs recovered with no detectable alterations in their gross clinical behavior. On the other hand, simultaneous interruption of the brachial and cephalic blood flow was associated with severe cerebral hypoxia and lactic acidosis, and with irreversible brain damage, leading eventually to death. Canine cerebral metabolism and function appear to remain intact after bilateral interruption of the carotid and vertebral arteries in the neck. Brain integrity, however, is then dependent upon the extensive collateral circulation between branches of the brachial vessels and of the cerebral vessels, particularly the vertebral arteries. Additional interference with flow of blood through the brachial vessels rapidly results in cerebral metabolic failure and irreversible brain damage.

Lactate production in blood circulating in a pump oxygenator: effect of carbon dioxide.

Abstract Blood gas tensions, pH, and glucose, lactate, and pyruvate concentrations were determined in whole blood circulated through a pump-oxygenator, ventilating the oxygenator with 100% O 2 and 93% O 2 -7% CO 2 in random order. Blood to which insulin or glucose had been added also was studied in a similar fashion. A high P O 2 was maintained throughout the study, thus eliminating any element of cellular hypoxia. Blood utilized glucose and produced lactate at a constant rate during conditions of cucapnia, and at an accelerated rate during conditions of severe hypocapnia and respiratory alkalosis. Eucapnia after hypocapnia slowed the rate of lactate production and glucose utilization but did not stop them, nor did it decrease the level of lactate in the blood. Pyruvate concentrations decreased then stabilized with hypocapnia and increased with eucapnia. Blood alone, however, seems to account for only a small fraction of the hyperlactatemia of hyperventilation in vivo . The mechanism of lactate production in blood alone with adequate oxygen levels is due to red blood cell metabolism being primarily anaerobic through the Embden-Meyerhof pathway. Whether this is accentuated by hyperoxia is not known. Also, why lactate is not decreased with hypercapnia in blood alone as occurs in vivo is not understood.

Distribution of High-Energy Phosphates in the Heart

Summary Dogs were anesthetized with sodium pentobarbital and ventilated with a respirator. Pressures were monitored in each chamber. Tissue samples from the beating heart were rapidly removed from uniform sites in the left ventricle (LV), right ventricle (RV), left atrium (LA), and right atrium (RA) and analyzed for ATP, ADP, and creatine phosphate (CP). The concentrations of ATP, ADP, and CP were distributed in the following order: LV > RV > LA > RA. This is the same order as the mean pressures developed in the various chambers, but the relationship between mean pressure and high-energy phosphate stores was not linear. The finding that ATP, ADP, and CP concentrations were highest in the LV, the chamber which performs the most work, suggests that differences in the distribution may be due to differences in the rates of production.

Organization of a cardiac surgical unit.

From the Departments of Surgery, Washington University School of Medicine, and The Jewish Hospital of St. Louis, St. Louis, Missouri 63110. Supported by Army contract DADA-17-69-9165 and U.S. Public Health Service Grant 2 RO 1 HL 12278-04. Presented at the nineteenth annual meeting of the American College of Angiology, San Juan, Puerto Rico, January 21-25, 1973. * Edison Professor of Surgery, Washington University School of Medicine and Surgeon-inChief, Jewish Hospital of St. Louis, St. Louis, Missouri. t Assistant Professor of Surgery, Washington University School of Medicine and Director, Division of Thoracic & Cardiovascular Surgery, Jewish Hospital of St. Louis. ‡ Instructor in Surgery, Washington University School of Medicine and Assistant in Thoracic & Cardiovascular Surgery, Jewish Hospital of St. Louis, St. Louis, Missouri. The title of this presentation suggests a technical treatise on how to do it; how