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R F Hickey

Publications and source records attributed to R F Hickey.

At least 37 records · Page 2Linked to original sources
PubMed1994

Regional vasodilating properties of isoflurane in stunned swine myocardium.

Studies about the coronary vasodilating properties of isoflurane indicate that this drug induces coronary vasodilation. No work has examined isoflurane-induced vasodilation in known stunned myocardium. This study was conducted to determine isoflurane's coronary vasodilation potency in stunned myocardium and to compare the results obtained with normal myocardium. We determined the vasodilating properties of isoflurane in regionally perfused swine myocardium. Six domestic swine were anesthetized with pentobarbital and fentanyl. The left anterior descending artery (LAD) was cannulated and perfused with blood drawn from the carotid artery and passed thorough a membrane oxygenator. LAD arterial flow was controlled by a calibrated roller pump with continuous digital readout, and LAD arterial pressure was measured directly. The anterior interventricular vein was cannulated and dimension crystals placed in the LAD-perfused myocardium. Myocardial stunning was induced by reduction of coronary blood flow (CBF) to 30% of control flow for 20 minutes. One hour after reperfusion, the vasodilatory response to 0%, 1%, and 2% isoflurane administered via the membrane oxygenator was determined and compared to maximum vasodilatation produced by regional intracoronary administration of adenosine. Systemic blood pressure and heart rate remained constant throughout the experiment. At 2% isoflurane, systolic shortening and regional myocardial oxygen consumption decreased 53% and 17%, respectively. The same concentration increased CBF by 33% and reduced coronary vascular resistance (CVR) by 25%. One percent isoflurane affected neither CBF nor CVR. Regional coronary administration of adenosine produced much greater changes in CBF (+509) and CVR (-89.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Therapeutic hyperoxia diminishes myocardial stunning.

UNLABELLED: We used a model of isolated coronary perfusion to answer the question: Does high PO2 during low flow myocardial ischemia diminish postischemic myocardial contractile dysfunction? In 12 anesthetized, open chest swine, the left anterior descending (LAD) coronary artery was cannulated and perfused via an extracorporeal circuit. Normoxic arterial blood was pumped through a pediatric membrane oxygenator, which was used to control arterial PO2 in the perfusion bed. Myocardial stunning was created by reducing LAD coronary artery flow to 40% of control values for 30 minutes. After 5 minutes of ischemia, swine were randomized to either continued coronary normoxia or to coronary hyperoxia. In the hyperoxic group, oxygen was substituted for nitrogen in the oxygenator, thus increasing coronary PO2 to 382 +/- 32 mmHg. After 30 minutes of ischemia, all swine were reperfused with normoxic blood. RESULTS: There were no significant baseline differences between the two groups with regard to baseline hemodynamics, myocardial blood flow, or oxygen delivery parameters. Preischemic systolic shortening was comparable in the normoxic and hyperoxic groups: 23.6 +/- 6.8% and 24.9 +/- 3.9%, respectively. Increasing coronary arterial PO2 to 382 mmHg during ischemia led to a significant decrease in myocardial stunning in the hyperoxic group. Postischemic systolic shortening in the hyperoxic treatment group, measured at 15, 30, 45, and 60 minutes of reperfusion, was 14.8% +/- 6.3% (p < 0.05), 13.4% +/- 6.4% (p < 0.05), 13.8% +/- 6.7% (p < 0.05), and 14.3% +/- 5.8% (p < 0.05) compared to comparable measurements in the normoxic control group of 9.0% +/- 5.4%, 7.8% +/- 5.0%, 7.8% +/- 5.2%, and 7.2% +/- 5.1%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Coronary blood flow autoregulation and flow heterogeneity in the stunned heart.

We used an anesthetized swine model of regionally "stunned" myocardium to determine the effect of stunning on coronary autoregulation and blood flow heterogeneity. In 18 domestic swine, stunning was accomplished by reducing blood flow to the left anterior descending coronary artery (LAD) by approximately 75% of baseline for 15 min and restoring it to normal for 1 hour. We quantified coronary autoregulation using both the slope of coronary pressure-flow curves and an autoregulation index. We quantified blood flow heterogeneity using radioactive microspheres to determine the variability in flow (dispersion index) among forty 200 mg segments of myocardium from the center of the stunned, LAD-perfused left ventricle. Before and after stunning, we measured autoregulation, myocardial blood flow and flow heterogeneity, as well as hemodynamic indices of myocardial oxygen demand. Fifteen min of ischemia and 1 hour of reperfusion produced both a 46% reduction in mechanical function, and a 7% drop in systemic arterial pressure, but not change in heart rate or rate pressure product. Myocardial oxygen consumption was 15% reduced and myocardial blood flow 16% reduced in the stunned myocardium when measured at one hour of reperfusion. Fifteen min after reperfusion, the slope of the coronary pressure flow plots and the coronary venous oxygenation were increased whereas the autoregulation index decreased. These findings all indicate reduced autoregulation during early reperfusion. However, after one hour of reperfusion, the slope of the coronary pressure-flow relation (0.41 +/- 0.19 vs. 0.48 +/- 0.26 ml.100 g-1.min-1.mmHg-1) and the autoregulation index (0.43 +/- 0.16 vs. 0.30 +/- 0.32) were unchanged from control measurements (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Coronary pressure-flow regulation in the stunned myocardium.

In this study, we used a swine model to study coronary autoregulation in the stunned myocardium. In 18 domestic swine, the left anterior descending coronary artery was cannulated and flow to this artery controlled via an extracorporeal perfusion circuit. Stunning was induced by reducing pump flow to approximately 25% of the baseline value for 15 minutes followed by 1 hour of reperfusion. This ischemia/reperfusion protocol reduced systolic shortening to approximately 50% of control, at 1 hour of reperfusion. Neither the slope of the coronary pressure-flow relation (0.41 +/- 0.19 vs 0.48 +/- 0.26 mL/100 g per min per mmHg) nor an autoregulation index (0.43 +/- 0.16 vs 0.30 +/- 0.32) was significantly changed at 1 hour reperfusion (p > 0.05) compared to baseline. These findings argue against the hypothesis that the mechanical dysfunction of the stunned myocardium is due to suboptimal perfusion caused by poor coronary autoregulation.

Animals↗
PubMed1992

Effects of high arterial oxygen tension on function, blood flow distribution, and metabolism in ischemic myocardium.

BACKGROUND: Although oxygen inhalation therapy has long been used in the treatment of acute myocardial ischemia, experimental evidence that increased arterial PO2 has any beneficial effect in the absence of hypoxemia is equivocal. In this study, we used a swine model of subendocardial myocardial ischemia to determine the effects of arterial hyperoxia on regional myocardial contractile function (sonomicrometry), myocardial blood flow distribution (microspheres), and regional myocardial glycolytic metabolism (carbon isotope-labeled substrates). METHODS AND RESULTS: In 10 domestic swine, the left anterior descending coronary artery was cannulated and flow to this artery was strictly controlled via a roller pump in the perfusion circuit. Arterial PO2 was controlled by manipulating inspired oxygen concentration (FIO2). Low-flow myocardial ischemia was induced by reducing pump flow to 50% of the control value, which diminished regional endocardial systolic shortening to 30-50% of normal. After a 15-minute period of flow stability, each animal was exposed in randomized order to two additional 15-minute experimental periods: coronary normoxia (PO2 = 90-110 mm Hg) and coronary hyperoxia (PO2 greater than 400 mm Hg). At each level of oxygenation, we measured regional myocardial function, regional myocardial blood flow and metabolism, and hemodynamic indexes of myocardial oxygen demand. Myocardial ischemia during normoxia reduced systolic shortening to 10.9 +/- 5.3% in the ischemic zone. Hyperoxia increased ischemic zone systolic shortening substantially to 15.2 +/- 4.6%. During myocardial ischemia, endocardial blood flow was decreased to 0.26 +/- 0.06 ml.g-1.min-1 in the ischemic zone. During hyperoxia, endocardial blood flow rose to 0.34 +/- 0.10 ml.g-1.m-1. The endocardial: epicardial flow ratio was 0.45 +/- 0.18 in the initial ischemia period and rose to 0.61 +/- 0.23 in the hyperoxic period. Myocardial ischemia increased regional uptake of glucose, conversion of glucose to released lactate, and net myocardial lactate release. In the ischemic myocardium, coronary hyperoxia decreased both chemically measured lactate production and isotopically measured lactate release and decreased glucose extraction and the conversion of glucose to lactate. CONCLUSIONS: These data demonstrate for the first time that increasing arterial PO2 to high levels during acute low-flow myocardial ischemia improves both function and flow distribution in the ischemic myocardium and decreases glycolytic metabolism in the ischemic zone. The degree of improvement in contractile function (5% absolute increase in systolic shortening or 25% change normalized to preischemic values) is consistent with the observed increase in subendocardial blood flow.

Animals↗
PubMed1991

Characterization of metabolic performance of methanogenic granules treating brewery wastewater: role of sulfate-reducing bacteria.

Granules from an upflow anaerobic sludge blanket system treating a brewery wastewater that contained mainly ethanol, propionate, and acetate as carbon sources and sulfate (0.6 to 1.0 mM) were characterized for their physical and chemical properties, metabolic performance on various substrates, and microbial composition. Transmission electron microscopic examination showed that at least three types of microcolonies existed inside the granules. One type consisted of Methanothrix-like rods with low levels of Methanobacterium-like rods; two other types appeared to be associations between syntrophic-like acetogens and Methanobacterium-like organisms. The granules were observed to be have numerous vents or channels on the surface that extended into the interior portions of the granules that may be involved in release of gas formed within the granules. The maximum substrate conversion rates (millimoles per gram of volatile suspended solids per day) at 35 degrees C in the absence of sulfate were 45.1, 8.04, 4.14, and 5.75 for ethanol, acetate, propionate, and glucose, respectively. The maximum methane production rates (millimoles per gram of volatile suspended solids per day) from H2-CO2 and formate were essentially equal for intact granules (13.7 and 13.5) and for physically disrupted granules (42 and 37). During syntrophic ethanol conversion, both hydrogen and formate were formed by the granules. The concentrations of these two intermediates were maintained at a thermodynamic equilibrium, indicating that both are intermediate metabolites in degradation. Formate accumulated and was then consumed during methanogenesis from H2-CO2. Higher concentrations of formate accumulated in the absence of sulfate than in the presence of sulfate. The addition of sulfate (8 to 9 mM) increased the maximum substrate degradation rates for propionate and ethanol by 27 and 12%, respectively. In the presence of this level of sulfate, sulfate-reducing bacteria did not play a significant role in the metabolism of H2, formate, and acetate, but ethanol and propionate were converted via sulfate reduction by approximately 28 and 60%, respectively. In the presence of 2.0 mM molybdate, syntrophic propionate and ethanol conversion by the granules was inhibited by 97 and 29%, respectively. The data show that in this granular microbial consortium, methanogens and sulfate-reducing bacteria did not compete for common substrates. Syntrophic propionate and ethanol conversion was likely performed primarily by sulfate-reducing bacteria, while H2, formate, and acetate were consumed primarily by methanogens.

Biodegradation, Environmental↗
PubMed1991

Hyperoxemic reperfusion does not increase myocardial infarct size.

We tested the hypothesis that arterial hyperoxia during myocardial reperfusion increases reperfusion injury and infarct size. The anterolateral marginal coronary artery of 35 anesthetized rabbits was occluded for 45 min, then reperfused for 3 h with either normoxic [arterial PO2 (PaO2) = 96.7 +/- 22.9 mmHg)] or hyperoxic (PaO2 = 554.8 +/- 61.7 mmHg) blood. In the hyperoxic group only, PaO2 was adjusted 10 s before the onset of reperfusion by raising inspired oxygen concentration to 100%. The area of infarction (AI) was defined by triphenyltetrazolium staining, and the area at risk (AR) by fluorescent microspheres. These areas were measured by planimetry. Heart rates and blood pressures did not differ between the two groups during occlusion or reperfusion. Infarct size (AI/AR) was 49.1 +/- 16.5% in the normoxic group (n = 17) and 40.8 +/- 16.1% in the hyperoxic group (n = 18). From these data, 90% confidence limits establish that the maximal true increase in AI/AR caused by hyperoxia would be 0%-1%. Hyperoxic reperfusion of ischemic myocardium compared with normoxic reperfusion does not significantly increase myocardial infarct size.

Animals↗
PubMed1991

Effects of nitrous oxide on coronary pressure and regional contractile function in experimental myocardial ischemia.

To determine whether nitrous oxide (N2O) worsens myocardial ischemia by diminishing coronary pressure, we performed two sets of experiments using an acutely instrumented swine model of regional coronary ischemia. In constant pressure experiments (n = 11), coronary pressure and heart rate were kept constant as N2O (77%-79%) was substituted for N2 in the inspired gas. Nitrous oxide decreased systolic shortening, measured by sonomicrometry, from 68.0% to 63.6% (P less than 0.05) of preischemic control values in the ischemic zone and from 116.2% to 103.2% (P less than 0.05) of control values in the adjacent normal myocardium. There was no disproportionate effect of N2O on ischemic myocardium, and the N2O-induced depression of contractile function was fully reversible. In a series of constant external stenosis experiments (n = 13), the effects of N2O on heart rate, mean arterial pressure, and the coronary stenosis itself were not controlled. In these experiments, substitution of N2O for N2 induced deterioration in both the ischemic zone (systolic shortening decreased from 68.7% to 58.4% of preischemic control values, P less than 0.05) and in the adjacent normal myocardium (systolic shortening decreased from 113% to 102.9% of preischemic control, P less than 0.05). Nitrous-oxide-induced ischemic zone contractile dysfunction was often not reversible. The pressure gradient across the coronary stenosis did not increase and peripheral coronary pressure did not decrease because of N2O. Diffusion hypoxia was also excluded. This study confirms that N2O has a significant but mild depressant effect on the performance of both normal and ischemic myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Myocardial metabolism during hypoxia: maintained lactate oxidation during increased glycolysis.

In the intact animal, myocardial lactate utilization and oxidation during hypoxia are not well understood. Nine dogs were chronically instrumented with flow probes on the left anterior descending coronary artery and with a coronary sinus sampling catheter. [14C]lactate and [13C]glucose tracers, or [13C]lactate and [14C]glucose were administered to quantitate lactate and glucose oxidation, lactate conversion to glucose, and simultaneous lactate extraction and release. The animals were anesthetized and exposed to 90 minutes of severe hypoxia (PO2 = 25 +/- 4 torr). Hypoxia resulted in significant increases in heart rate, cardiac output and myocardial blood flow, but no significant change in myocardial oxygen consumption. The arterial/coronary sinus differences for glucose and lactate did not change from normoxia to hypoxia; however, the rate of glucose uptake increased significantly due to the increase in myocardial blood flow. Tracer-measured lactate extraction did not decrease with hypoxia, despite a 250% increase in lactate release. During hypoxia, 90% +/- 4% of the extracted 14C-lactate was accounted for by the appearance of 14CO2 in the coronary sinus, compared with 88% +/- 4% during normoxia. Thus, in addition to the expected increase in glucose uptake and lactate production, we observed an increase in lactate oxidation during hypoxia.

Acetates↗
PubMed1990

Increased lactate appearance and reduced clearance during hypoxia in dogs.

In order to assess the effects of severe hypoxia on whole body glucose and lactate kinetics, nine experiments were performed on anesthetized, ventilated mongrel dogs. [U-13C]glucose and [1-14C]lactate (n = 5), or [6-14C]glucose and [U-13C]lactate (n = 4) were infused using the primed-continuous infusion method. Cardiac output was measured by thermodilution. After a control period with 21% O2, inspired O2 was reduced for 90 minutes. Three of the experiments resulted in unstable hemodynamics and lactate levels, and are excluded from the mean data. Arterial PO2 fell from a control level of 106.8 +/- 11.9 to 24.2 +/- 3.5 mmHg during the last 45 minutes of hypoxia, and O2 transport fell to 52% of normoxic values. Arterial lactate concentration and the rate of appearance increased by 428% and 182%, respectively, from control to hypoxia. The metabolic clearance rate for lactate fell by 34%. Arterial glucose levels did not change significantly with hypoxia, but the rate of glucose disappearance rose by 70%, and the rate of glucose conversion to lactate increased 3-fold. It is concluded that acute severe hypoxia in anesthetized dogs causes 1) a large increase in arterial lactate levels, but no significant change in glycemia, 2) a large increase in the rate of lactate disappearance and only a small increase in the rate of glucose disappearance and 3) a fall in the metabolic clearance rate of lactate.

Animals↗
PubMed1990

Cardiovascular and neuromuscular effects of three steroidal neuromuscular blocking drugs in dogs (ORG 9616, ORG 9426, ORG 9991).

Developmental research has been directed toward creating nondepolarizing muscle relaxants with an onset time and duration of actions shorter than that of vecuronium or atracurium. We determined the cardiovascular and neuromuscular effects of three new and promising nondepolarizing muscle relaxants in six dogs anesthetized with halothane. Each dog was anesthetized four times (each time separated from the others by at least 1 wk); one muscle relaxant was studied each time. Three doses (one, three, and five times the ED90) were given as intravenous bolus injections. ORG 9616 and ORG 9991 had shorter durations of action than ORG 9426. The duration of action of the doses that were five times the ED90 was 18 +/- 5.88 and 15.8 +/- 4.41 min (mean +/- SD) with ORG 9616 and ORG 9991, respectively, as compared with 39.7 +/- 17.15 min with ORG 9426 (P less than 0.05). ORG 9426 was virtually free of cardiovascular effects. The ED90 doses of ORG 9616 and ORG 9991 did not cause cardiovascular effects; the doses of three and five times the ED90 caused small decreases in mean arterial blood pressure and increases in heart rate. Mean arterial blood pressure decreased from 99 +/- 10.2 to 88 +/- 13.1 mm Hg and from 98 +/- 11.7 to 77 +/- 8.1 mm Hg with five times the ED90 dose of ORG 9616 and ORG 9991, respectively. The authors conclude that ORG 9426 has a duration of neuromuscular blockade that is probably similar to vecuronium, and one that is free of cardiovascular effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Androstanols↗
PubMed1988

Surface-induced hypothermia: effects on coronary blood flow autoregulation and vascular reserve.

Surface-induced hypothermia has been shown to exert a protective effect in canine models of myocardial infarction. However, its effects on coronary blood flow (CBF) autoregulation and coronary vascular reserve (CVR) have not been investigated. The effects of mild (32 degrees C) and moderate (27 degrees C) hypothermia on CBF autoregulation and CVR (at 60 mm Hg diastolic pressure) were studied using a chronically instrumented canine preparation. Coronary artery pressure-flow relations were obtained over a wide range of coronary diastolic pressures (10 to 106 mm Hg) with autoregulation intact and during adenosine-induced maximal coronary conductance (MCC) at 37, 32, 27 degrees C (n = 7 dogs), and after rewarming (n = 5 dogs). Halothane (1 MAC end-tidal concentration, temperature adjusted) was the anesthetic. Autoregulation remained intact during hypothermia. CBF remained relatively constant between diastolic pressures of 43.1 +/- 9.0 and 84.0 +/- 14.4 mm Hg (mean +/- SD). No significant differences were observed between temperatures in the autoregulated pressure range. CBF correlated well with myocardial oxygen consumption (MVO2) (r2 = 0.81, P less than 0.0001). There were no significant changes in MVO2, CBF, MCC, or CVR at 32 degrees C. At 27 degrees C, MVO2 (3.65 +/- 1.3 at 37 degrees C vs 2.35 +/- 1.4 ml O2.min-1 at 27 degrees C), autoregulated CBF (34.9 +/- 15.1 vs 19.5 +/- 10.8 ml.min-1), the slope of the line of MCC (4.31 +/- 0.7 vs 2.7 +/- 0.4 ml.mm-1.min-1), and CVR (147.1 +/- 24.6 vs 90.1 +/- 27.3 ml.min-1) were all less than control (P less than 0.05). After rewarming to 37 degrees C, no significant changes from control were noted. The authors conclude that coronary autoregulation remains intact at both 32 and 27 degrees C, although MCC and CVR are significantly decreased at 27 degrees C.

Animals↗
PubMed1988

Effects of halothane, enflurane, and isoflurane on coronary blood flow autoregulation and coronary vascular reserve in the canine heart.

To investigate the effects of volatile anesthetics on coronary blood flow (CBF) autoregulation and coronary vascular reserve, studies were performed on chronically instrumented dogs, awake and during the administration of 1.0 MAC halothane, enflurane, and isoflurane. Coronary pressure-flow plots were generated by measuring left anterior descending coronary artery blood flow while varying coronary inflow pressure with a hydraulic occluder. Autoregulation was quantitated by two measures: the slope of the horizontal "autoregulated" portion of the pressure-flow relationship and the autoregulation index (ArI) of Norris. Slope values (ml.min-1.mmHg-1 +/- SD) were: awake, 0.243 +/- 0.043; halothane, 0.414 +/- 0.044; enflurane, 0.587 +/- 0.187; and isoflurane, 0.795 +/- 0.246. The increase in slope was statistically significant only for halothane and isoflurane (P less than .05). The ArI approaches 1.0 when autoregulation is perfect, and approaches zero or is a negative number when autoregulation is absent. The authors found ArI values of: awake, 0.55; halothane, -0.08; enflurane, -0.01; isoflurane, -0.02. These values indicate good autoregulation while awake, but impaired autoregulation with all three anesthetics (P less than .05). Coronary vascular reserve was calculated, at a diastolic coronary pressure of 40 mmHg, as the difference between resting flow and flow during maximal coronary vasodilation induced by intracoronary adenosine. Coronary vascular reserve, maximal coronary conductance, and coronary zero-flow pressure were not significantly altered by these anesthetics. The authors conclude that 1.0 MAC enflurane, halothane, and isoflurane mildly disrupt CBF autoregulation, increasing CBF out of proportion to myocardial demands. Under the conditions of this study, these anesthetics do not affect maximal CBF or coronary vascular reserve.

Animals↗
PubMed1987

Effects of isoflurane and halothane on coronary vascular resistance and collateral myocardial blood flow: their capacity to induce coronary steal.

Some coronary vasodilators, paradoxically, may endanger patients with coronary artery disease by causing "coronary steal." To determine the capacity of isoflurane and halothane to cause coronary steal, the authors studied their effects on coronary vascular resistance (CVR), diastolic coronary artery pressure, and collateral myocardial blood flow. Using ameroid constrictors, chronic occlusions of the left anterior descending (LAD) coronary artery were created in ten dogs. Six to eight weeks after implantation, the dogs were anesthetized with fentanyl and pentobarbital, and a stenosis was created on the circumflex (Cx) coronary artery. Isoflurane and halothane were each administered in doses of 0.5 and 1.5 MAC. Diastolic aortic pressure was held constant. Using small catheters in the circumflex and LAD coronary arteries, the authors measured diastolic coronary artery pressures. Collateral myocardial blood flow was measured by the microsphere method. In this model, halothane and isoflurane minimally affect CVR. The maximum change in CVR, which was found during 1.5 MAC isoflurane, was -8% (not significant). Diastolic coronary pressures distal to the Cx stenosis (54.5 +/- 11.5 mmHg) and distal to the LAD occlusion (44.5 +/- 5.2 mmHg) did not change significantly with either isoflurane or halothane. Transmural collateral blood flow distal to the LAD occlusion (0.51 +/- 0.11 cc.g-1.min-1) was unaltered by either drug. There was no evidence of coronary steal. Epicardial ECG S-T segments showed no evidence of ischemia. The finding of minimal direct effects of halothane and isoflurane on CVR, diastolic coronary pressure, and collateral myocardial blood flow suggest that, under the conditions of this study, neither agent, when used as an adjuvant to high-dose narcotic anesthesia, is likely to cause myocardial ischemia by a coronary "steal" mechanism.

Animals↗
PubMed1985

Significance of the pericardium in human subjects: effects on left ventricular volume, pressure and ejection.

To assess the effect of the pericardium, left ventricular systolic function and diastolic compliance were studied in 15 patients before and after pericardiotomy during coronary artery surgery. Using first pass radionuclide angiography, curves for left ventricular systolic function (stroke work versus end-diastolic volume) and a measure of diastolic compliance (pulmonary capillary wedge pressure versus end-diastolic volume) were generated by changing body position to alter venous return. Left ventricular end-diastolic volume ranged from 41 to 111 ml/m2 and pulmonary capillary wedge pressure from 0 to 24 mm Hg. No significant changes were found in blood pressure (150/83 to 148/82 mm Hg), heart rate (66.7 to 67.1 beats/min), cardiac index (2.38 to 2.41 liters/min per m2), ejection fraction (0.56 to 0.54), end-systolic volume index (31.4 to 32.2 ml/m2), end-diastolic volume index (65.9 to 69.5 ml/m2) or pulmonary capillary wedge pressure (7.5 to 7.3 mm Hg). The pericardium did not affect the curves relating stroke work and end-diastolic volume or those relating pulmonary capillary wedge pressure and end-diastolic volume. Thus, when filling pressure and volume are normal or only moderately elevated, the pericardium does not appear to affect left ventricular systolic function or diastolic compliance in patients.

Adult↗
PubMed1983

Whole-body oxygen consumption during low-flow hypothermic cardiopulmonary bypass.

To assess the adequacy of tissue perfusion during low-flow, moderately hypothermic cardiopulmonary bypass (CPB), we measured whole-body oxygen consumption (VO2), serum lactate concentrations, and acid-base balance in 12 men undergoing myocardial revascularization. When perfusion flow rate was kept at control levels (2.1 L/min/m2), decreasing the patient's body temperature to 25.4 +/- 1.8 degrees C (mean +/- SD) was associated with a reduction in VO2 of almost 50% (from 83.3 +/- 14.6 ml/min/m2 to 45.6 +/- 9.6 ml/min/m2, p less than 0.001). Subsequent lowering of flow rate by nearly half (from 2.1 to 1.2 L/min/m2) under these moderately hypothermic conditions failed to alter VO2, which was measured several times over a 40 minute period. Although small increases in base deficit occurred during hypothermia, acidosis did not occur after reductions in flow rate. Serum lactate levels were not affected by changes in either temperature or flow rate. We conclude that a perfusion flow rate as low as 1.2 L/min/m2 does not compromise tissue perfusion during CPB with moderate systemic hypothermia and cardioplegic arrest.

Body Temperature↗
PubMed1983

MAC values of thiopental and fentanyl in rats.

A comparison of the effects of thiopental or fentanyl with those of inhaled anesthetics requires the establishment of a comparable level of anesthetic potency. Accordingly, using the response of male Sprague-Dawley rats to tail-clamping, we determined the ED50S for thiopental and fentanyl. Half of the rats were pretreated with phenobarbital. After subcutaneous injection of various doses of thiopental or fentanyl, each rat was tested for movement in response to tail-clamping at 15-min intervals for 2 h. In untreated rats, the maximal effect of thiopental (i.e., the lowest ED50 value was 107 +/- 10 mg/kg, mean +/- SEM) occurred 75 min after injection. Although higher values were found at other times, differences from the nadir were relatively small. In rats pretreated with phenobarbital, the lowest value (130 +/- 8 mg/kg) occurred at 60 min. The lowest ED50S for fentanyl (52 +/- 7 micrograms/kg for control rats, and 73 +/- 14 micrograms/kg for pretreated rats) were found at 15 min.

Anesthesia, Intravenous↗