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P N Samuelson

Publications and source records attributed to P N Samuelson.

At least 19 recordsLinked to original sources
PubMed1995

Xanthine oxidase inactivation attenuates postocclusion shock after descending thoracic aorta occlusion and reperfusion in rabbits.

"Declamping shock" is observed after aortic crossclamping, with hypovolemia, hypotension, and metabolic acidemia invariably present. We hypothesized that oxidants derived from xanthine oxidase influence the resuscitative interventions required to maintain baseline hemodynamic and acid-base status after aortic occlusion and reperfusion in rabbits. We also hypothesized that inactivation of xanthine oxidase with sodium tungstate could reduce systemic injury as assessed by the release of lactate dehydrogenase and alkaline phosphatase. To test these hypotheses, we established aortic occlusion in rabbits (n = 10, standard diet; n = 8, tungstate diet) for 40 minutes by inflation of a 4F Fogarty catheter in the descending thoracic aorta followed by 2 hours of reperfusion. Sham-operated rabbits (n = 10, standard diet; n = 9, tungstate diet) served as controls. Tungstate-pretreated rabbits required significantly less Ringer's solution (28%), phenylephrine (68%), and sodium bicarbonate (30%) during reperfusion (p < 0.005). Lactate dehydrogenase and alkaline phosphatase release during reperfusion was significantly attenuated by tungstate pretreatment (p < 0.05). Tungstate pretreatment resulted in plasma xanthine oxidase activities significantly lower than those in the sham group administered a standard diet (p = 0.007). Resuscitation requirements and systemic injury were reduced by inactivation of xanthine oxidase in a rabbit model that simulates the situation of human thoracic aorta operations.

Acid-Base Equilibrium↗
PubMed1994

Xanthine oxidoreductase release after descending thoracic aorta occlusion and reperfusion in rabbits.

Cardiopulmonary and other organ dysfunction often occurs after operation on the descending thoracic aorta. Though there are multiple causes of organ dysfunction in this setting, free radical injury may play a prominent role. Xanthine oxidoreductase, an enzyme that generates oxidants after exposure to ischemia, could be released from ischemic liver and intestine during reperfusion. To test this hypothesis, we created aortic occlusion in eight rabbits for 40 minutes by inflation of a 4F Fogarty balloon catheter in the descending thoracic aorta. Eight sham-operated rabbits served as a control group. Two hours of reperfusion followed removal of the balloon catheter. Hemodynamic and acid-base status were maintained near baseline values during reperfusion. Plasma samples were obtained for determination of the activity of the hepatocellular enzymes xanthine oxidoreductase, aspartate aminotransferase, alanine transferase, and lactate dehydrogenase. Plasma xanthine oxidoreductase activity increased significantly (p < 0.001) during reperfusion (729 +/- 140 microU/ml, mean +/- standard error of the mean) compared with baseline (132 +/- 18 microM/mL). The other enzymes followed a similar pattern of release. We report the release of xanthine oxidoreductase in an animal model that simulates the situation of human thoracic aorta operations. The oxidants produced by the circulating xanthine oxidoreductase observed during reperfusion would likely be toxic to vascular endothelium, potentially contributing to multiple organ dysfunction.

Alanine Transaminase↗
PubMed1988

Coronary and systemic vascular resistance during reperfusion after global myocardial ischemia.

During controlled aortic root reperfusion after global myocardial ischemia for the performance of coronary artery bypass grafting (N = 16), coronary blood flow was the highest during the first 1 minute to 2 minutes even though the aortic root pressure was controlled at about 40 mm Hg. Even during the period of controlled low pressure, flow began to decline, and the decline continued during the period in which the pressure was controlled at 75 mm Hg. Calculated coronary vascular resistance rose steadily from an initially low value to one well above the normal value for beating hearts. A transient fall in resistance resulted from the administration of a bolus of nitroglycerin into the aortic root. When the initial reperfusate was normokalemic, coronary flow was less and coronary vascular resistance higher during the initial phase of reperfusion. The systemic arterial pressure and resistance fell during the first 1 minute to 3 minutes of reperfusion and in 25% of patients, remained low. The greater the potassium load delivered during the initially hyperkalemic phase, the longer the interval between the beginning of reperfusion and the resumption of cardiac systole.

Blood Pressure↗
PubMed1986

Effects of protamine administration after cardiopulmonary bypass on complement, blood elements, and the hemodynamic state.

Nineteen patients were prospectively selected and studied before and after the administration of protamine sulfate following cardiopulmonary bypass (CPB). After protamine administration, C3a, C4a, and C4d were elevated; the peak levels of C3a and C4a were in samples taken 10 minutes after protamine administration while those of C4d were in those obtained at 5 hours. Only C3a was elevated after CPB and before protamine administration. In vitro, only the combination of protamine sulfate and heparin, and neither alone, resulted in increased C3a and C4a. Administration of protamine was associated with small and transient decreases in total white blood cells, granulocytes, and platelets, and with small and transient reductions in systemic and pulmonary arterial and left and right atrial pressures. Systemic vascular resistance fell (p = 0.07), and pulmonary vascular resistance rose but the change could be due to chance (p = 0.29). These data and those reported by others support the inference that complement activation occurs during CPB by the alternative pathway and again during protamine administration by the classic pathway; and that this accompanies a whole-body inflammatory reaction with blood cell and hemodynamic changes which, when extreme, could result in a severe hemodynamic derangement.

Blood Cell Count↗
PubMed1986

Comparison of sufentanil and enflurane-nitrous oxide anesthesia for myocardial revascularization.

This study compared the stress response in patients with coronary artery disease undergoing myocardial revascularization anesthetized with either sufentanil and oxygen or enflurane-nitrous oxide and oxygen. Throughout induction and maintenance of anesthesia, and while the patients were in the intensive care unit, hemodynamics plus plasma catecholamine, sufentanil, and enflurane concentrations were recorded and compared. Three groups were studied: sufentanil, 15 micrograms/kg at induction; sufentanil, 15 micrograms/kg at induction plus 10 micrograms/kg on initiation of cardiopulmonary bypass (CPB); and enflurane anesthesia. Hemodynamics were remarkably stable in all groups but required considerable fine tuning when enflurane was administered. The "stress" of CPB was blunted by the additional dose of sufentanil, as well as by enflurane. This was reflected in those patients receiving the extra sufentanil or enflurane by less severe increases in their epinephrine or norepinephrine concentrations and by less frequent use of sodium nitroprusside to control mean arterial pressure compared to the group of patients given the lower-dose sufentanil. This study suggests that higher blood levels of sufentanil can attenuate, but not eliminate, the stress response to CPB, as can enflurane, and that both the narcotic and inhalation anesthetic techniques for patients with coronary artery disease were quite satisfactory.

Anesthesia↗
PubMed1985

Cardiovascular effects of esmolol in anesthetized humans.

We studied the cardiovascular effects of esmolol, a newly synthesized beta-adrenocepter antagonist, in anesthetized humans. Forty patients (four groups of 10 each) with ischemic heart disease and normal ventricular function were anesthetized with diazepam, pancuronium, and N2O in O2. Esmolol was given by continuous infusion in cumulative doses of 1100 micrograms/kg (group 1), 2000 micrograms/kg (group 2), and 2700 micrograms/kg (group 3); a control group received no esmolol. Infusion of esmolol was begun 3 min prior to and ended 4 min after tracheal intubation. All three doses of esmolol significantly (P less than 0.001) attenuated the heart rate responses to intubation. Rate-pressure products were significantly (P less than 0.001) lower in esmolol-treated patients than in controls after intubation, but ST-segment changes compatible with ischemia occurred in one patient in each group. Increases in heart rate were associated with significant increases in plasma norepinephrine levels (r = 0.45, P = 0.02) in the control group, but not in esmolol-treated patients, a demonstration that esmolol antagonizes the beta-adrenergic effects of norepinephrine. The effect of esmolol on heart rate was absent 5 min after cessation of infusion, and plasma levels of esmolol were undetectable in 26 of 30 treated patients 15 min after the termination of esmolol infusion. Esmolol has a rapid onset and short duration of effect. It can be used safely during anesthesia in patients with normal ventricular function to attenuate cardiac response to sympathetic stimulation.

Adrenergic beta-Antagonists↗
PubMed1983

Regional blood flow during cross-clamping of the thoracic aorta and infusion of sodium nitroprusside.

Labeled microspheres, 15 microns in diameter, were used to determine cardiac output and regional blood flow response to cross-clamping of the midthoracic aorta and subsequent sodium nitroprusside (SNP) infusion in 11 dogs. During aortic cross-clamping, mean arterial pressure above the occlusion (MAPa) increased 30% to 35%, mean arterial pressure below the occlusion (MAPb) decreased 87%, cardiac index decreased 12% to 14%, left atrial pressure (LAP) doubled, and renal and spinal cord (lower part) blood flows decreased substantially (85% to 94%). SNP infusion returned MAPa to baseline values, decreased MAPb by half, and substantially and further decreased renal blood flow (to 3% to 5% of baseline values). Myocardial and cerebral blood flows increased substantially (up to 250% to 400%). An increase in preload (fluid load) was accompanied by an increase in LAP, cardiac index, and myocardial blood flow only but not in renal or spinal cord flow. There was a strong association between cortical renal blood flow and MAPb (r2 = 0.92; p less than 0.0001), which suggests that blood flow through organs and tissues below the occlusion is pressure dependent. The data show that SNP infusion during thoracic aortic cross-clamping improves systemic and regional circulation above the occlusion but decreases MAPb and therefore blood flow below the occlusion. SNP infusion should be used with caution during aortic cross-clamping, since arterial hypotension of any degree may be deleterious to organs below the cross-clamp.

Animals↗
PubMed1983

Midazolam.

Explore the source record for details and available documents.

Anesthetics↗
PubMed1982

Detection of myocardial injury after coronary artery bypass grafting using a hypothermic, cardioplegic technique.

Fifty patients undergoing isolated coronary artery bypass grafting procedures using a clear, cold cardioplegic solution, topical hypothermia, and reduced systemic flow for intraoperative myocardial protection were evaluated for myocardial injury by serial plasma creatine kinase-MB isoenzyme (CK-MB) measurements and electrocardiograms. Forty-one (82%) of the patients had three-vessel disease. Preoperative left ventricular contractility determined angiographically was normal in 13 patients (26%), mildly abnormal in 26 (52%), and moderately or severely abnormal in 11 (22%). The number of arteries grafted ranged from 2 to 6 (mean, 3.5). The mean duration of aortic clamping was 38.6 +/- 1.6 minutes. There were no hospital deaths. Enzymatic and electrocardiographic (ECG) evidence of myocardial infarction occurred in 1 patient. Nonspecific ECG changes occurred in 16 patients (32%), and th electrocardiograms were unchanged in the remaining 33 patients (66%). In the 49 patients without ECG evidence of infarction, the mean peak plasma CK-MB value, which occurred 6 hours after the onset of cardiopulmonary bypass, was 7.9 +/- 0.8 IU/L (standard error of the mean) and the mean integrated area 158 +/- 19.5 IU/L X hours. There was no correlation between these CK-MB values and the extent of disease, number of arteries grafted, or the duration of myocardial ischemia. These data document a low incidence of perioperative myocardial injury with this technique, and can serve as a baseline for comparison with other techniques for intraoperative myocardial protection in this setting.

Adult↗
PubMed1982

Neuronal and adrenomedullary catecholamine release in response to cardiopulmonary bypass in man.

Cardiopulmonary bypass (CPB) alters systemic hemodynamics and affects several biochemical systems involved in cardiovascular regulation. We investigated the changes in levels of circulating epinephrine (E) and norepinephrine (NE) and related them to events during CPB. Twenty-eight patients undergoing various surgical procedures were studied. Plasma E and NE were determined by radioenzymatic assay at eight stages of the operation. A ninefold increase in arterial E (from 75 +/- 13 to 708 +/- 117.3 pg/ml) occurred from prebypass (stage 1) measurements to the end of aortic cross-clamping (stage 4). The values at stage 4 were significantly higher (p less than 0.05) than at all other stages. E decreased rapidly, to 360 +/- 84.3 pg/ml, after myocardial and pulmonary reperfusion (stage 5). Arterial NE increased twofold from stage 1 to stage 4 (from 426 +/- 66.9 to 825 +/- 84.2, p less than 0.05). The increase in NE from initial CPB values (stage 2) to 30 minutes of aortic cross-clamping (stage 3) was associated with an increase in mean blood pressure (r = 0.51, p = 0.02). The peak increases in catecholamines occurred when the heart and lungs were excluded from the circulation, which suggests that either or both contributed to the increase. Because the increase in E was markedly greater than that in NE, the predominant humoral response to CPB appears to be adrenomedullary release of E. This significant increase in catecholamines could jeopardize myocardial protective measures during CPB.

Adrenal Medulla↗
PubMed1982

Relationship of whole body oxygen consumption to perfusion flow rate during hypothermic cardiopulmonary bypass.

Whole body oxygen consumption (Vo2) and its relationship to randomly selected arterial perfusion flow rates (Q) during profoundly hypothermic (20 degrees C) cardiopulmonary bypass were determined in 17 adult patients undergoing routine coronary artery bypass operations. Vo2 falls progressively as Q decreases, from 33 +/- 8.2 ml . min(-1) . m(-2) at Q of 2.0 L . min(-1) . m(-2) to 28 +/- 5.8 at Q of 1.5, 25 +/- 5.7 at Q of 1.0, 20 +/- 4.1 at Q of 0.5, and 14 +/- 5.4 at Q of 0.25. This progressive decrease suggests shutdown of areas of the microcirculation. The upper 70% confidence limit overlaps the asymptote at Qs above 1.2. Percent oxygen extraction increases progressively as Q decreases, from 11 +/- 3.3% at Q of 2.0 to 45 +/- 9.6% at Q of 0.25, suggesting reduced reserves. Mixed venous Po2 and oxygen saturation fall linearly with decreasing Q below 1.2 (r = 0.78 and r = 0.89, p less than 0.0001, respectively), suggesting decreasing flow to perfused areas. Internal jugular venous Po2 and oxygen saturation (measured in 10 patients) fall linearly with decreasing Q below 1.8 (r = 0.72 and r = 0.88, p less than 0.0001, respectively), suggesting decreasing flow to perfused areas of the brain and a difference from the rest of the body in its behavior with decreasing Q. Thus, during cardiopulmonary bypass cerebral blood flow, autoregulation seems present at 20 degrees C. The data set indicates that flows of about 1.2 may be adequate despite limited reserves.

Aged↗
PubMed1981

Hemodynamic responses to anesthetic induction with midazolam or diazepam in patients with ischemic heart disease.

Hemodynamic responses to induction of anesthesia with midazolam maleate and diazepam were compared in patients with ischemic heart disease. While breathing 100% oxygen, 10 patients (group M) received midazolam maleate, 0.2 mg/kg, and 10 patients (group D) received diazepam, 0.5 mg/kg. In addition, 10 patients (group MN) breathing 50% nitrous oxide in oxygen received midazolam, 0.2 mg/kg. Patients in group M had a small but statistically significant (p less than 0.05) decrease (vs awake control values) in systemic and pulmonary arterial blood pressure, pulmonary arterial occluded pressure, stroke index, and left and right ventricular stroke work indices. Patients in group D experienced statistically significant decreases in systemic blood pressure. The only statistically significant differences between groups M and D occurred 5 minutes followed drug administration: heart rates were higher and systemic pressures and left ventricular stroke work indices were lower following midazolam. Hemodynamic changes following midazolam and nitrous oxide were similar to those observed in patients given midazolam and 100% oxygen. Patients in all three groups responded to endotracheal intubation with transient increases in blood pressure, heart rate, and systemic vascular resistance, but the hemodynamic values spontaneously returned toward control levels within 2 to 5 minutes. Although differing somewhat, midazolam, like diazepam, provided rapid, hemodynamically stable induction of anesthesia in patients with ischemic heart disease.

Anesthetics↗
PubMed1981

Midazolam versus diazepam: different effects on systemic vascular resistance. A randomized study utilizing cardiopulmonary bypass constant flow.

In 43 patients electively scheduled for myocardial revascularization surgery, a hemodynamic comparison of 8-chloro-6-(2-fluorophenyl)-1-methyl-4H-imidazo[1,5-a][1,4] benzodiazepine (midazolam, Ro 21-3981, Dormicum) and 7-chloro-1,3-dihydro-1-methyl-5-phenyl-(2H)1,4-benzodiazepin-2-one (diazepam) was made during cardiopulmonary bypass. Midazolam and diazepam were compared in patients with ischemic heart disease to determine the effects of the drugs on systemic vascular resistance at constant flow (cardiac output) and temperature. Diazepam (0.3 mg/kg) produced significantly greater decreases in perfusion pressure, systemic vascular resistance, and venous reservoir volume than did midazolam (0.2 mg/kg). It was concluded that there are subtle differences in the pharmacologic actions of both midazolam and diazepam. When used with constant flow on cardiopulmonary bypass, diazepam causes more pronounced arterial and venous dilation. These data are at variance with the findings in intact man.

Anesthetics↗
PubMed1980

Hemodynamics during diazepam induction of anesthesia for coronary artery bypass grafting.

The hemodynamics during induction of anesthesia were studied in ten patients with ischemic heart disease about to have coronary artery bypass grafting. Intravenous diazepam, 0.5 mg/kg (with 50% N2O in oxygen inspired and pancuronium IV), was used to induce anesthesia. Compared to awake baseline, induction caused statistically significant decreases in the mean arterial pressure, rate pressure product, stroke index, and left and right ventricular stroke work indexed. Although statistically significant, the hemodynamic changes were small and transient and required no modifying treatment. This anesthetic induction technic is safe, efficient, and well tolerated by patients having myocardial revascularization surgery.

Anesthesia, General↗
PubMed1979

Duration of intubation and ICU stay after open heart surgery.

One hundred four consecutive patients undergoing open heart surgery were studied to determine the duration of intubation and ICU stay associated with an anesthetic management protocol designed to avoid prolonged postoperative respiratory depression. The results document the feasibility and safety of early extubation and shortened ICU stay in patients having operations for ischemic and acquired valvular heart disease. Patients with complex congenital heart defects require significantly longer periods of respiratory support and intensive care.

Adult↗