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Biomedical subjects

G D Buckberg

Publications and source records attributed to G D Buckberg.

At least 163 records · Page 9Linked to original sources
PubMed1983

Warm induction of cardioplegia with glutamate-enriched blood in coronary patients with cardiogenic shock who are dependent on inotropic drugs and intra-aortic balloon support.

This report reviews the initial clinical application of our experimental studies inducing cardioplegia with a warm (37 degrees C) glutamate-enriched blood solution in ischemically damaged hearts. Over 15 months, 23 consecutive coronary patients requiring preoperative intra-aortic balloon and inotropic drug support for cardiogenic shock underwent operation for left ventricular power failure. Twelve patients were given a warm glutamate-enriched blood cardioplegic solution during the first 5 minutes of aortic clamping before multidose cold (4 degrees C) glutamate blood cardioplegia was begun; 11 patients received standard multidose cold blood cardioplegia without glutamate. All patients had comparably depressed left ventricular performance preoperatively despite maximal inotropic and balloon support and showed evidence of extending myocardial infarction. They did not differ in the number of grafts placed (3.7 +/- 0.2), associated valve and aneurysm procedures (seven patients) or cross-clamp time (89 +/- 6 minutes). All patients received warm blood cardioplegic reperfusion before aortic unclamping. The perioperative mortality was 9% (2/23); both patients who died received cold blood cardioplegia without glutamate. In addition to lower mortality, patients receiving warm glutamate blood cardioplegia exhibited better hemodynamics, allowing earlier discontinuation of inotropic drug infusion (1.3 +/- 0.5 versus 2.7 +/- 0.8 days, p less than 0.05) and intraaortic balloon support (1.2 +/- 0.2 versus 3.6 +/- 0.5 days, p less than 0.05). Late mortality was 30%, resulting in a 65% overall survival rate (2 to 15 months) for the entire series of patients. The operative principles evolving from this early experience include (1) warm blood cardioplegic induction, (2) glutamate enrichment, (3) meticulous attention to cardioplegic distribution and grafting sequence, (4) warm cardioplegic reperfusion before unclamping, and (5) graft perfusion during construction of proximal anastomoses. Hopefully, further application of these techniques will improve results in these extremely high risk coronary patients requiring operation.

Aged↗
PubMed1983

Comparison of distribution beyond coronary stenoses of blood and asanguineous cardioplegic solutions.

In seven dogs on cardiopulmonary bypass, a critical stenosis (75% to 90%) of the left anterior descending coronary artery (LAD) was produced. Alternate 250 ml/min infusions of asanguineous and blood cardioplegic (4 degrees C) solutions were made for 3 to 5 minutes. Poststenotic flow (flowmeter), intramyocardial temperature, and aortic pressure were measured. During cardioplegic infusions of 250 ml/min, aortic pressure was 34 +/- 4 mm Hg higher with blood cardioplegia than with asanguineous cardioplegia (82 +/- 7 versus 48 +/- 8 mm Hg). Poststenotic cardioplegic flow was 39% +/- 9% higher (29 +/- 5 versus 18 +/- 5 ml/min) with blood cardioplegia. Consequently, blood cardioplegia resulted in more rapid arrest (20 +/- 2 versus 45 +/- 5 seconds) and lower myocardial temperature (6 degrees +/- 1 degree C) in the region of LAD blood supply; posterior ventricular myocardial cooling was similar (unobstructed vessels) with both solutions. These data show that the reduced viscosity of asanguineous cardioplegia compared to blood cardioplegia results in lower aortic pressure. Consequently, the higher aortic pressure with blood cardioplegia results in superior cardioplegic delivery beyond obstructed coronaries and better myocardial cooling. We conclude that the decreased viscosity of 4 degrees C asanguineous cardioplegia causes diversion of cardioplegic solution from the obstructed to the normal coronary bed.

Animals↗
PubMed1982

Left ventricular O2 requirements of pressure and volume loading in the normal canine heart and inaccuracy of pressure-derived indices of O2 demand.

The purpose of this study was to: 1) re-evaluate the left ventricular O2 requirements (MVO2) of pressure and volume-loading; and b) assess the accuracy of pressure-derived indices of left ventricular (LV) O2 demand under pressure-loading and volume-loading conditions. Using a right heart bypass preparation (heart rate 150 beats . min-1), mean arterial pressure (7.3 to 22.9 kPa) and cardiac output (0.8 to 6.0 litre . min-1) were varied independently. Adequate left ventricular O2 supply was demonstrated by normal transmural distribution of blood flow, normal myocardial lactate metabolism, and intact reactive hyperaemic responses. For equivalent increases in cardiac external work (from 2 to 4 joules . min-1) pressure-loading and volume-loading resulted in similar increases in O2 uptake (59% and 49%, respectively, P = 0.21). MVO2 was consistently greater for volume-loading than for pressure-loading at any SPTI, pressure-rate product, and triple product. The prediction of O2 demands by these indices under these loading conditions collectively was unreliable (r = 30 to 0.42). O2 requirements of the left ventricle with both pressure-loading and volume-loading were highly correlated (r = 0.82 to 0.99) with meridional wall stress. We conclude that: 1) volume-loading conditions have a greater O2 requirement than appreciated previously; 2) pressure loads and volume loads require similar O2 uptake in the normal canine heart for similar external work; 3) currently used pressure-derived indices are unreliable predictors of LV O2 demand when loading conditions are varied; and 4) O2 requirements are more uniformly related to meridional wall stress.

Animals↗
PubMed1982

Correlation of pancreatic blood flow and high-energy phosphates during experimental pancreatitis.

A dog model was used to measure the hemodynamic changes occurring during acute pancreatitis induced by intraductal injection of fresh trypsin-bile-blood mixture. Pancreatic blood flow was measured with 15-micrometer radioactive microspheres. Measurements of pancreatic adenosine triphosphate (ATP) and creatine phosphate (CP) were made under normal conditions and during acute hemorrhagic pancreatitis. Basal ATP and CP concentrations were 5.82 +/- 0.25 and 5.30 +/- 0.31 mmol/g wet tissue, respectively. Hemorrhagic pancreatitis was characterized by a severe reduction in pancreatic blood flow, followed by a 45% fall of ATP and a 70% lowering of CP. These results suggest that inadequate pancreatic tissue perfusion during acute pancreatitis results in a marked depletion of high-energy phosphate stores. We suspect this energy depletion reflects the progression of the disease from edematous to hemorrhagic pancreatitis and causes irreversible damage of pancreatic tissue.

Acute Disease↗
PubMed1982

Benefits of normothermic induction of blood cardioplegia in energy-depleted hearts, with maintenance of arrest by multidose cold blood cardioplegic infusions.

This study tests the hypothesis that warm induction of cardioplegia prior to prolonged maintenance by multidose infusions of cold blood cardioplegic solution would increase the tolerance of energy-depleted hearts to subsequent aortic clamping. Eighty percent depletion of subendocardial adenosine triphosphate (ATP) was produced in 30 dogs by 45 minutes of normothermic ischemia. This was followed either by unmodified blood reperfusion or 2 additional hours of aortic clamping with multidose cold blood cardioplegia. We compared a brief (5 minute) period of 37 degrees C cardioplegic induction to standard 4 degrees C blood cardioplegic induction to determine if warm induction would enhance metabolic and functional recovery. Warm cardioplegic induction resulted in more oxygen consumption than cold induction (16.9 versus 8.1 cc/100 gm), and lower levels of glucose-6-phosphate (G6P), suggesting better aerobic metabolism (0.97 versus 1.87 microM/gm wet weight). Prompt repletion of creatine phosphate (CP) occurred with warm and cold cardioplegic induction, although ATP levels levels remained low. Hearts undergoing ischemia and unmodified reperfusion consumed insufficient oxygen to meet basal metabolic needs during reperfusion (7 cc/100 gm below requirement) and recovered only 33% +/- 5% of control left ventricular performance. Better function occurred with cold cardioplegic induction (63% +/- 5%), and almost complete recovery (85% +/- 5%) occurred when warm induction of cardioplegia was used. We conclude that warm induction followed by prolonged cold multidose blood cardioplegic arrest enhances aerobic metabolism, results in normal left ventricular performance, and improves tolerance of aortic clamping in energy-depleted hearts.

Adenosine Triphosphate↗
PubMed1981

Critical importance of ensuring cardioplegic delivery with coronary stenoses.

This study examines the relative importance of the duration of ischemia versus the adequacy of cardioplegic distribution and protection in hearts with coronary stenoses. Of 18 dogs on cardiopulmonary bypass, 12 underwent critical narrowing (greater than 90%) of the left circumflex artery (LCA) and total occlusion of the anterior descending coronary artery (LAD). In six dogs (control) the coronary arteries were patent. A 16 degrees C blood cardioplegic solution was given at 20 minute intervals of aortic clamping. In control dogs and in six dogs with stenoses, the aorta was clamped for 60 minutes. In the latter group, the stenoses were removed after 20 and 40 minutes to simulate sequential completion of grafts and better cardioplegic distribution. In the remaining dogs with stenoses, the aorta was clamped for only 30 minutes, with stenoses removed after the heart had been returned to the beating empty state for 30 minutes to simulate doing distal grafts with cardioplegic protection and proximal grafts during reperfusion (traditional technique). With sequential grafting, myocardial temperature was lower (16 degrees C versus 22 degrees C) and incidence of reperfusion fibrillation less than with the traditional technique. Despite a greater ischemic interval, sequential grafting with adequate cardioplegic distribution resulted in less lactate washout (5 +/- 15 versus 35 +/- 6 cc/100 gm/min), greater recovery of compliance, and higher stroke work indices (1.32 +/- 0.12 versus 0.75 +/- 0.15 kg-m/min). We conclude that the success of myocardial protection with potassium cardioplegia in hearts with coronary stenoses is related more to ensuring its distribution than to limiting the duration of ischemic arrest with the false assumption that the heart is reperfused adequately while proximal grafts are completed in the beating empty state.

Animals↗
PubMed1981

Detrimental effects of premature use of inotropic drugs to discontinue cardiopulmonary bypass.

Ten dogs underwent 45 minutes of normothermic ischemic arrest. After 15 minutes of reoxygenation, none could support the systemic circulation independently. In five dogs, we could discontinue bypass (cardic output 70 to 100 cc/kg/min) by giving dopamine (10 to 30 mcg/kg/min). In five other dogs, total cardiopulmonary bypass was prolonged for an additional 30 minutes and no dopamine was given. During control and at 15 and 45 minutes after aortic unclamping, we measured myocardial blood flow (microspheres), metabolism (oxygen uptake and lactate), water content (wet/dry weight), left ventricular compliance (intraventricular balloon), and performance (isovolumetric and Starling function curves). Dogs treated with prolonged bypass showed progressive improvement in ventricular compliance, function, and water content and did not require inotropic drugs when bypass was discontinued 45 minutes after ischemia. In contrast, dogs receiving dopamine exhibited more myocardial edema (3.3% versus 1.7% water gain), worse ventricular compliance (18% versus 55% recovered at 25 ml left ventricular volume), poorer contractility (58% versus 70% recovery of +dP/dt), generated 50% less stroke work at a left atrial pressure of 25 mm Hg (0.25 versus 0.52 gm/kg), failed to augment oxygen uptake to meet the metabolic demands of the working heart (11% versus 45% increase in oxygen uptake), and required continued inotropic support to discontinue extracorporeal circulation. We conclude that (1) limited prolongation of total bypass enhances recovery from ischemic damage and (2) use of inotropic drugs to prematurely discontinue extracorporeal circulation will impede recovery by accentuating myocardial edema and further decreasing ventricular compliance, performance, and oxygen utilization.

Animals↗
PubMed1981

Reducing postischemic damage by temporary modification of reperfusate calcium, potassium, pH, and osmolarity.

This study was designed to determine if ischemic damage could be reduced by modifying blood composition upon reperfusion. After control data had been obtained in seven dogs on prolonged cardiopulmonary bypass, 71 dogs underwent 1 hour of ischemic arrest with topical hypothermia (left ventricular temperature 16 degrees C). We measured left ventricular performance (isovolumetric function curves), compliance (intraventricular balloon), blood flow (microspheres), metabolism (oxygen consumption), and water content (wet/dry weights) before and 30 minutes after ischemia. The initial reperfusate was 500 cc of oxygenated blood given over a period of 5 minutes. Without temporary reperfusate modification, postischemic left ventricular performance was depressed 40% +/- 3%, compliance fell 50% +/- 12%, water content rose 2.5% +/- 0.1%, and left ventricular blood flow and oxygen uptake increased only minimally when cardiac work was increased (function curve). These deleterious changes were reduced significantly, but not prevented, by the following isolated reperfusate modifications: (1) lowering amount of ionic calcium available for cell entry, (2) raising pH to 7.8 to counteract acidosis, (3) raising potassium level to maintain arrest and reduce metabolic demands, and (4) increasing osmolarity (mannitol, 360 mOsm) to counteract edema. In contrast, by combining these modifications to achieve a hypocalcemic, hyperkalemic, alkalotic, and hyperosmolar blood perfusate, it was possible to attain 104% +/- 1% recovery of myocardial performance, 80% +/- 1% restoration of compliance, 60% less postischemic edema, and near-normal augmentation of left ventricular flow and oxygen uptake to meet increasing needs.

Animals↗
PubMed1980

Superiority of blood cardioplegia over asanguinous cardioplegia--an experimental and clinical study.

This study compares experimental and clinical results using both an asanguinous and sanguinous vehicle for delivering the cardioplegic solution. Animals receiving blood cardioplegia had better left ventricular function after unclamping, significantly less post-ischemic myocardial edema, and a better ability to augment flow and oxygen consumption. Patients receiving blood cardioplegia had also better myocardial performance with high cardiac outputs and lower left atrial pressure, and showed less evidence of myocardial damage. We conclude that oxygenation of the cardioplegic solution provides superior myocardial protection to that seen when the same solution is used in an asanguinous vehicle.

Animals↗
PubMed1980

Effects of intensive exercise training on myocardial performance and coronary blood flow.

Five instrumented and eight noninstrumented dogs were progressively trained for 12-18 wk on a motor-driven treadmill. Data were compared with 14 instrumented and 8 noninstrumented control dogs. Gastrocnemius malate dehydrogenase activity was significantly increased in the trained dogs (887 +/- 75 vs. 667 +/- 68 mumol . g-1 . min-1). The trained dogs also showed significant increases in maximum work capacity, cardiac output (7.1 +/- 0.5 vs. 9.1 +/- 0.7 1/min), stroke volume (25.9 +/- 2.0 vs. 32.0 +/- 2.0 ml/beat), and left ventricular (LV) positive dP/dtmax (9,242 +/- 405 vs. 11,125 +/- 550 Torr/s). Negative dP/dtmax was not significantly different. Peak LV systolic pressure increased with exercise, but there was no significant difference between the trained and control dogs. LV end-diastolic pressure did not change with exercise and was the same in both groups. Tension-time index was lower in the trained dogs at rest and submaximum exercise (9.7 km/h, 10%) but was not different at maximum exercise. Diastolic pressure-time index was significantly higher in the trained dogs at rest and during submaximum exercise but was not different at maximum exercise. LV coronary blood flow was significantly reduced at rest (84 +/- 4 vs. 67 +/- 6 mo . min-1 . 100 g-1) and during submaximum exercise (288 +/- 24 vs. 252 +/- 8 ml . min-1 . 100 g-1). During maximum exercise flow was not significantly different (401 +/- 22 vs. 432 +/- 11 ml . min-1 . 100 g-1) between the control and trained groups. The maximum potential for subendocardial flow was unchanged with training despite the development of mild hypertrophy.

Animals↗
PubMed1980

[Effect of pH adjustment in deep hypothermia and circulatory arrest (author's transl)].

In 14 puppies, body temperature was lowered to 22 degrees C with surface hypothermia, then to 16 degrees C with textracorporeal circulation. During 60 min of circulatory arrest all hearts were protected with the same multidose blood cardioplegic solution. In seven dogs pH was kept at 7.4 and in seven others pH was varied as in poikilotherms (i.e. 7.95 at 16 degrees C) principally by adjusting pCO2 during cooling and rewarming. Appropriate pH adjustment allowed higher cardiac output with normal systemic lactate metabolism. Raising pH by lowering pCO2 to 10 mm Hg allowed twice as much cerebral blood flow. Postischemic myocardial performance was depressed by 50% by retaining pH 7.4 and was normal when pH was varied appropriately. These findings have major implications for the routine management of hypothermia during cardiac operations.

Animals↗
PubMed1980

Reversal of ischemic damage with amino acid substrate enhancement during reperfusion.

Twenty dogs underwent 15 minutes of normothermic ischemic arrest and 30 minutes of reperfusion while on cardiopulmonary bypass. In 10 control dogs, the reperfusate blood was not modified. In 10 other dogs, the aorta was reclamped and the heart reperfused for 5 minutes with blood containing L-glutamate (0.026M). We measured coronary blood flow (microspheres), left ventricular (LV) metabolism [O2 content, adenosine triphosphate (ATP)], LV compliance (intraventricular balloon), and LV performance (balloon and Starling curves) before and 30 minutes after ischemia. Fifteen minutes of ischemic arrest produced significant depression in contractility and oxidative metabolism. L-Glutamate infusion resulted in higher oxygen uptakes (9.7 versus 6.9 cc/100 gm/min) and allowed more complete recovery of ATP content (80% versus 67%). Glutamate-treated hearts had more complete recovery in the rate of contraction, +dP/dt, (96% versus 68%), and relaxation, --dP/dt (99% versus 72%), the best recovery of compliance (74% versus 88%), and complete (100%) recovery of stroke work index (1.55% versus 0.87% gm - m/kg). We conclude that the addition of L-glutamate to reperfusate blood reverses ischemic damage. We suspect that l-glutamate acts by replenishing Krebs' cycle intermediates lost during ischemia, thereby stimulating oxidative metabolism and enhancing ATP production.

Adenosine Triphosphate↗