Mouse complement: the effect of sex hormones and castration on two of the late-acting components.

The titer of late-acting complement components in sera from male mice is 8-10 times higher than the titer of sera from female mice. Using assays developed to measure the serum content of two of the late-acting components, we have shown that this difference is due to the effect of androgen and estrogen on these two late-acting complement components. These two components have been tentatively identified as C'5 and C'6. Androgen and estrogen have greater effect on C'6 than on C'5. The possibility has not been excluded that still other of the late-acting complement components are affected by androgens and estrogens. The course of homograft rejection was unchanged in mice deficient in C'5 and C'6.

Mouse complement: influence of sex hormones on its activity.

Sex hormones influence the hemolytic of one or more of the late-acting components of complement measured in the presence of trisodium ethylenediaminetetraacetate. The titers of the serums of male mice, normally tenfold higher than those of females, fell after castration, becoming about the same as those of females. The titers of the serums from females rose after these mice were castrated, but castration did not affect the activities of the first, second, and fourth components of complement. Serums of normal and castrated mice of both sexes treated with testosterone showed increased late-acting component activity, whereas the estrogen caused decreased activity. Treatment in vitro of mouse serum with these hormones had no effect on the activity of late-acting components.

Forssman antigen content of guinea pig hepatomas induced by diethylnitrosamine: a quantitative approach to the search for tumor-specific antibodies.

The Forssman antigen content of diethylnitrosamine-induced guinea pig hepatomas was found to be greater than that of either autogenous or allogeneic guinea pig liver. The autogenous normal liver was obtained from guinea pigs before tumor induction, and comparison of normal and neoplastic tissues was based on the capacity of these tissues to inhibit (absorb) the hemolytic activity of rabbit antitumor serum. A method is presented for distinguishing quantitative from qualitative antigenic differences in the search for tumor-specific antigens. The results of these experiments indicate that, in the absence of strict quantitation, quantitative differences may be mistaken for qualitative differences.

Two-dimensional and Doppler echocardiographic diagnosis of an aortic to right atrial fistula complicating aortic dissection.

A 60 year old woman presented with massive aortic root dilation and sudden cardiovascular collapse 10 years after aortic valve replacement. An aortic to right atrial fistula was diagnosed by echocardiographic imaging and Doppler ultrasound. At operation, the patient was found to have chronic aortic dissection with aneurysm formation. Rupture of the aneurysm into the right atrium was confirmed.

Economics of elective coronary revascularization. Comparison of costs and charges for conventional angioplasty, directional atherectomy, stenting and bypass surgery.

OBJECTIVES: This study was designed to evaluate more closely the true in-hospital costs of elective revascularization by directional coronary atherectomy and intracoronary stenting and to compare these costs with those of the traditional revascularization alternatives (i.e., conventional balloon angioplasty and coronary artery bypass surgery). BACKGROUND: Previous studies have suggested that total hospital charges for directional coronary atherectomy or intracoronary stenting are significantly higher than those for conventional angioplasty. However, hospital charges do not necessarily reflect true economic costs, and their use may provide misleading data with regard to cost-effectiveness. METHODS: We analyzed in-hospital charges from the itemized hospital accounts of 300 patients undergoing elective angioplasty, directional atherectomy, Palmaz-Schatz coronary stenting or bypass surgery between January 1, 1990 and December 31, 1991. Costs were then derived by adjusting itemized patient accounts for department-specific cost/charge ratios. Catheterization laboratory costs were based on actual resource consumption, and daily room costs were adjusted for the intensity of nursing services provided. RESULTS: Length of hospital stay was similar for atherectomy (2.3 +/- 1.5 days) and conventional angioplasty (2.6 +/- 1.7 days) but significantly longer for stenting (5.5 +/- 2.6 days, p < 0.05). Total costs were also significantly higher for coronary stenting ($7,878 +/- $3,270, median $6,699, p < 0.05) than for angioplasty ($5,396 +/- $2,829, median $4,753) or atherectomy ($5,726 +/- $2,716, median $4,986). However, length of stay, resource consumption (laboratory and radiologic testing, drugs, blood products, for example) and total costs for bypass surgery were still greater than for any of the percutaneous interventional procedures. CONCLUSIONS: In contrast to previous studies utilizing only hospital charges, the in-hospital costs of angioplasty and directional coronary atherectomy were similar. Although the cost of coronary stenting was approximately $2,500 higher than that of conventional angioplasty, the magnitude of this difference was smaller than the $6,300 increment previously suggested on the basis of analysis of hospital charges. These findings reflect the inherent discrepancies between cost-based and charge-based methodologies and may have important implications for future studies evaluating the relative cost-effectiveness of newer coronary interventions.

Mechanisms causing coronary microvascular dysfunction following crystalloid cardioplegia and reperfusion.

OBJECTIVE: The aim was to examine the mechanisms of coronary microvascular dysfunction during cardiopulmonary bypass and ischaemic arrest using a crystalloid cardioplegic solution. METHODS: Porcine hearts were arrested with cold hyperkalaemic (K+ = 25 mmol.litre-1) cardioplegic solution for 1 h during cardiopulmonary bypass and then reperfused for 1 h. Selected hearts were arrested but not reperfused. Coronary vessels of non-instrumented pigs were used as controls. In vitro vascular responses of subepicardial and subendocardial arterioles were examined in a pressurised (40 mm Hg) no flow state with video microscopy. RESULTS: Following 1 h of ischaemic cardioplegia, endothelium dependent relaxations of epicardial arterioles to the receptor mediated agent ADP and the non-receptor-mediated agent calcium ionophore A23187 were moderately reduced, and the contractile responses to KCl or the thromboxane A2 analogue U46619 were reduced compared to responses of vessels from control animals. After 1 h of reperfusion, U46619 caused contraction greater than control values, while contraction to KCl and endothelium dependent relaxations to ADP or A23187 were further reduced. Responses of endocardial microvessels to serotonin were slightly more affected by cardioplegia and reperfusion than were epicardial vessels, while the effect on responses of epicardial and endocardial vessels to bradykinin or A23187 were similar. Endothelium independent relaxation to sodium nitroprusside was not altered in any of the experimental groups. The addition of manganese superoxide dismutase to the cardioplegic solution markedly preserved endothelium dependent responses to ADP and A23187 and contractile response to U46619, compared to the responses of vessels from the plain crystalloid cardioplegia group, but had no effect on relaxation to sodium nitroprusside or on contraction to KCl. Five hours of normokalaemic hypothermia (5-10 degrees C) in Krebs buffer had minimal effect on vasodilator responses. Electron microscopy revealed preserved endothelial and smooth muscle cell structure, and focal mononuclear leucocyte-endothelium adherence following cardioplegic arrest and reperfusion. CONCLUSIONS: Ischaemic cardioplegia-reperfusion induced endothelium dependent and direct smooth muscle microvascular dysfunction is at least partially mediated by prolonged exposure of vessels to hyperkalaemia and to the generation of oxygen derived free radicals. Leucocytes probably mediate injury during reperfusion, while hypothermia has minimal effect on recovery of vasomotor function.

Medically refractory unstable angina pectoris. II. Hemodynamic and angiographic effects of intraaortic balloon counterpulsation.

Of 60 patients receiving intraaortic balloon counterpulsation for angina refractory to maximal medical therapy, a subgroup of 10 patients underwent left ventricular angiography both with and without counterpulsation. Severe stenosis of the left anterior descending coronary artery was present in all 10 patients. Counterpulsation resulted in a significant decrease in systolic and end-diastolic left ventricular pressures and no increase in cardiac index. Left ventricular diastolic and systolic volume, ejection fraction and regional contraction patterns, often abnormal, were unchanged. However, mean normalized systolic ejection rate was improved by the addition of counterpulsation. It is concluded that intraaortic balloon counterpulsation has relatively little effect on the left ventricular volume of patients with medically refractory angina pectoris. The symptomatic improvement that takes place seems to occur mainly through the effect of counterpulsation on preload and afterload.

Medically refractory unstable angina pectoris. I. Long-term follow-up of patients undergoing intraaortic balloon counterpulsation and operation.

Of 82 patients with medically refractory unstable angina pectoris seen between October 1972 and January 1978, 60 patients underwent a combination of intraaortic balloon pump counterpulsation, cardiac catheterization and coronary revascularization. Most patients had atherosclerotic involvement of the vessels of the anterior left ventricular wall, 48 patients (80 percent) had abnormalities of left ventricular wall contraction and 22 patients (36 percent) had evidence of acute myocardial injury. One operative and one late death occurred. The perioperative infarction rate was 5 percent. Survivors, followed up for 3 to 63 months (mean 31 months), have done remarkably well; 77 percent are considered employable,and more than 90 percent are in functional class I or II.

Repair of postinfarction ventricular septal defect in the elderly. Early and long-term results.

We performed 13 operations on 12 elderly patients with ventricular septal defect (VSD) following myocardial infarction. All patients were older than 65 years (range 66 to 82 years) and six were over 70 years of age. Ten underwent operation, with counterpulsation support, within 3 weeks of development of the VSD. Among eight patients with anteriorly located VSDs, there were four survivors. Among four patients with inferior defects, three survived. Overall hospital survival was 58%. Hospital costs were no greater in the elderly than in younger patients. The seven long-term survivors were followed up for from 10 months to 7.5 years (mean 3.9 years). There was one sudden death at 7.5 years in a previously well man. Of the remaining six patients, five are in New York Heart Association Class I, and one is in Class II. One woman, now 84 years old, lives independently over 2 years after repair. Our experience with respect to management suggests that unless medical therapy results in continued improvement rather than stability alone, hemodynamic deterioration is inevitable, and survival for delayed repair is unlikely. Furthermore, undue delay frequently results in renal failure and severely compromises the chances for survival after repair in the acute state.

Impaired endothelium-dependent coronary microvascular relaxation after cold potassium cardioplegia and reperfusion.

Myocardial dysfunction after cardiac operations might be influenced by altered myocardial perfusion in the postoperative period. To investigate possible alterations in vascular reactivity, in vitro coronary microvascular responses were examined after ischemic cardioplegia with use of a porcine model of cardiopulmonary bypass. Since myocardial perfusion is primarily regulated by arteries less than 200 microns in diameter, these vascular segments were examined. After 1 hour of ischemic arrest with cold crystalloid cardioplegia and 1 hour of reperfusion, microvessels (100 to 190 microns in diameter) were pressurized in a no-flow state, preconstricted by 30% to 60% of the baseline diameter with acetylcholine, and examined with video microscopic imaging and electronic dimension analysis. Endothelium-dependent relaxations to bradykinin (55% +/- 13% versus 99% +/- 1% = maximum relaxation of the preconstricted diameter in cardioplegia-reperfusion vessels versus control vessels, respectively; p < 0.05) and the calcium ionophore A 23187 (33% +/- 6% versus 90% +/- 4%; p < 0.05) were markedly impaired while endothelium-independent relaxation to sodium nitroprusside was similar to control value. After 1 hour of ischemic cardioplegia without reperfusion, endothelium-dependent relaxation was only slightly affected. Transmission electron microscopy showed minimal endothelial damage after ischemic cardioplegia and reperfusion. These findings have important implications regarding coronary spasm and cardiac dysfunction after cardiac operations.

Traumatic aortic valve injury sustained despite the deployment of an automobile air bag.

Blunt chest trauma is a rare cause of aortic valve dysfunction. A case of the successful management of traumatic injury to the aortic valve is reported. The aortic valve injury was sustained in an automobile accident despite the use of a seat belt and the deployment of an air bag. The literature is briefly reviewed. Aortic valve injury remains a consideration in cases of automobile-associated chest trauma, even in automobiles equipped with seat belts and air bags.

Altered pulmonary microvascular reactivity after total cardiopulmonary bypass.

Pulmonary vascular resistance is frequently elevated after cardiac operations in which cardiopulmonary bypass is used. In our study of the possible contribution of altered pulmonary microvascular reactivity to this condition, sheep were heparinized, cannulated via the aorta and right atrium, and placed on total cardiopulmonary bypass. After 90 minutes of total cardiopulmonary bypass and pulmonary arterial occlusion, the sheep were removed from cardiopulmonary bypass, and their lungs were perfused normally for 60 minutes. Noninstrumented animals were used as controls. To evaluate the effect of 90 minutes of extracorporeal circulation without reduced pulmonary perfusion, we studied additional sheep after they underwent right heart bypass with a pump-oxygenator. Pulmonary microarterial vessels (130 to 230 microns in diameter) from each group were examined in vitro in a pressurized (20 mm Hg), no-flow state with video microscopic imaging and electronic dimension analysis. After preconstriction of vessels with the thromboxane A2 analog U46619 by 30% to 40% of the baseline diameter, vasoactive drugs were applied extraluminally. Serotonin caused control microvessels to dilate. In the presence of the nitric oxide synthetase inhibitor NG-methyl-L-arginine, this was converted to a significant contractile response. Acetylcholine alone had minimal effect on control vessels. However, in the presence of the cyclooxygenase inhibitor indomethacin, acetylcholine caused a significant relaxation response. After total cardiopulmonary bypass and pulmonary reperfusion, pulmonary microvessels contracted significantly when exposed to acetylcholine and serotonin, compared with respective control responses. Both these contractile responses were inhibited in the presence of indomethacin. Endothelium-independent responses to sodium nitroprusside and U46619 and dilation responses to adenosine were not altered after cardiopulmonary bypass. Extracorporeal circulation with continued pulmonary arterial perfusion (right heart bypass group) had no effect on microvascular responses. In conclusion, total cardiopulmonary bypass with associated reduced pulmonary perfusion causes significant alterations of endothelium-dependent pulmonary microvascular responses because of the increased release of a constrictor prostanoid substance and possibly because of reduced release of endothelium-derived relaxing factor.

Mechanical assistance of the left ventricle: acute effect on cardiac performance and coronary flow of different perfusion patterns.

Mechanical circulatory assistance by ventricular assist devices provides an opportunity to influence the aortic pressure pattern, which may affect ventricular loading and coronary perfusion. The effect of synchronous, pulsatile coronary perfusion of an assist device-supported left ventricle has not been studied. To analyze the effect of different perfusion patterns on left ventricular performance and on coronary flow, independent of pressure and volume loading, we used three different modes of aortic perfusion in an isometric, contracting, isolated canine heart model. The effect of nonpulsatile, counter-pulsatile, and copulsatile coronary perfusion was analyzed in four subgroups to simulate different, clinically relevant situations (using two different ventricular end-diastolic volumes [normal and high] and two mean perfusion pressures [normal and critically low]). Our experiments demonstrated that total coronary flow is optimized by making the perfusion pressure pulsatile and by synchronously timing the pump systole with ventricular diastole (counterpulsation). Under identical conditions of preload and mean perfusion pressure, coronary flow and left ventricular contractility were decreased during non-pulsatile and copulsatile aortic perfusion when compared with counterpulsatile flow. There were no significant differences between the nonpulsatile and copulsatile modes. We conclude from these data that a nonejecting, but contracting, left ventricle will have improved systolic function and coronary blood flow if the coronary perfusion pressure is synchronized in a counterpulsatile manner. This is a significant implication for mechanical left ventricular assist devices when used to promote myocardial recovery.

The "H" graft: an alternative approach for performing minimally invasive direct coronary artery bypass.

OBJECTIVES: Minimally invasive direct coronary artery bypass permits arterial revascularization without cardiopulmonary bypass, potentially decreasing associated morbidity. The procedure is, however, technically challenging and associated with significant postoperative pain resulting from retraction through the small incision. METHODS AND PATIENT SELECTION: From December 1996 to April 1997, eight patients underwent grafting of the left anterior descending coronary artery by use of a short segment of right inferior epigastric artery attached proximally to the side of an in situ left internal thoracic artery. We have termed this procedure the "H" graft MIDCAB. RESULTS: No patients required intraoperative conversion to conventional bypass. No postoperative deaths or myocardial infarctions occurred. Six patients with normal renal function underwent postoperative angiography that demonstrated graft patency with rapid filling of the left anterior descending coronary in each case. Postoperatively clinical signs of acute ischemia were resolved or a normal exercise tolerance test was obtained in all patients. The median postoperative length of stay was 3 days. Rib spreading and chest wall retraction were not required in any procedure. CONCLUSIONS: The "H" graft procedure is an attractive alternative to standard minimally invasive bypass because of greater technical simplicity, the avoidance of internal thoracic artery harvest, and excellent visualization with no chest wall retraction.

Effects of perfusion pressure on myocardial performance, metabolism, wall thickness, and compliance: comparison of the beating and fibrillating heart.

The effects of brief periods of graded reductions in perfusion pressure on normally beating and fibrillating hearts were examined. Mechanical and metabolic parameters were studied in the isolated, isovolumic (balloon in left ventricle), blood-perfused dog heart preparation. Experiments were carried out at perfusion pressures of 100, 75, 50, and 25 mm Hg, and comparisons of performance were made at the same ventricular volumes in the beating and fibrillating heart. A fall in perfusion pressure significantly decreased systolic performance in the beating heart. Diastolic pressure-volume relations were not altered by changes in perfusion pressure in the beating heart, but the fibrillating heart became significantly more compliant as perfusion pressure declined. Coronary blood flow and myocardial oxygen consumption were consistently higher during fibrillation than during sinus rhythm, and both parameters declined significantly at decreasing perfusion pressures. The fibrillating heart produced lactate at a perfusion pressure below 65 mm Hg, while the beating heart produced lactate at a perfusion pressure below 35 mm Hg. These studies demonstrate that brief periods of relatively modest decreases in perfusion pressure during ventricular fibrillation alter myocardial energy demand-supply relationships to result in ischemia of the fibrillating heart.

Cyanosis in uncomplicated atrial septal defect with normal right cardiac and pulmonary arterial pressures.

A patient with cyanosis in an uncomplicated ostium secundum atrial septal defect without pulmonary hypertension is described. There were no anatomic abnormalities in right-sided cardiac valves or venous return and no evidence of right ventricular hypoplasia or hypertrophy; however, the diastolic pressure curve suggested a decreased compliance. We suggest that this unusual finding may be a result of intrinsically abnormal right ventricular compliance.

Effects of vasoactive drugs on flows through left internal mammary artery and saphenous vein grafts in man.

Vasoactive agents are commonly used in the postcardiopulmonary bypass period to elevate the mean arterial pressure of myocardial revascularization patients. Concern exists that administration of vasoactive agents in this setting may affect flow through saphenous vein and internal mammary artery grafts. Twenty-eight patients were randomly assigned to receive one of the six two-drug combinations of phenylephrine, norepinephrine, and epinephrine. After termination of cardiopulmonary bypass baseline, hemodynamic measurements and electromagnetic flow probe measurements of saphenous vein and internal mammary artery graft flow were made. The first agent was then infused to elevate mean arterial pressure 20 mm Hg. After 5 minutes of stability, hemodynamic and graft flow measurements were repeated. The infusion was terminated, 5 minutes of stability were obtained, and baseline measurements were repeated. The second agent was then infused, and measurements were repeated after a 5-minute stabilization period. Phenylephrine induced a nonsignificant increase in saphenous vein graft flow (68 +/- 31 versus 81 +/- 49 ml/min) and a significant decrease in internal mammary artery graft flow (40 +/- 16 versus 32 +/- 12 ml/min). Norepinephrine induced a significant increase in saphenous vein graft flow (80 +/- 39 versus 97 +/- 39 ml/min) and no significant change in internal mammary artery graft flow (44 +/- 20 versus 45 +/- 20 ml/min). Epinephrine induced a significant increase in both saphenous vein (82 +/- 38 versus 96 +/- 40 ml/min) and internal mammary artery (38 +/- 12 versus 55 +/- 24 ml/min) graft flows. We conclude that administration of vasoactive agents in the postcardiopulmonary bypass period may significantly affect saphenous vein and internal mammary artery graft flows.

Pulmonary microvascular responses to protamine and histamine. Effects of cardiopulmonary bypass.

Total cardiopulmonary bypass with associated reduced pulmonary blood flow causes significant alterations of endothelium-dependent pulmonary microvascular responses after resumption of normal perfusion. To determine if this change in pulmonary vascular reactivity may influence the responses of pulmonary arterioles to protamine and histamine, we examined isolated pulmonary microvessels after cardiopulmonary bypass. Sheep were heparinized, cannulated, and placed on either total bypass without ventilation or partial bypass (70% of baseline pulmonary arterial flow) with continued ventilation. After 90 minutes, sheep were separated from cardiopulmonary bypass and the lungs were perfused normally for 60 minutes. Vessels from noninstrumented sheep were used as controls. Peripheral pulmonary arterioles (90 to 190 microns) were cannulated, pressurized (20 mm Hg) in a no-flow state, and examined with video microscopy. After precontraction of vessels with the thromboxane A2 analog U46619 by 18% to 25% of the baseline diameter, vasoactive agents were applied. Protamine sulfate, histamine, heparin, and the protamine-heparin complex caused significant dose-dependent relaxations of control pulmonary microvessels. These relaxation responses were substantially reduced or converted to contractile responses in endothelium-denuded vessels, which suggests that these relaxations are mediated through endothelium-dependent mechanisms. After partial bypass, responses to protamine and histamine were slightly reduced compared with the respective responses of control vessels, whereas the relaxation to protamine-heparin complex was not significantly altered. After total bypass, relaxation responses to protamine and protamine-heparin complex were markedly reduced, whereas histamine induced contraction of pulmonary microvessels. Endothelium-independent relaxation to sodium nitroprusside was not affected by partial cardiopulmonary bypass and was slightly reduced after total bypass. A reduced direct vascular relaxation response to protamine and increased contractile response to histamine (or other humoral substances released during the systemic administration of protamine sulfate) may contribute to the elevation of pulmonary vascular resistance during infusion of protamine after cardiopulmonary bypass.

Comparison of two transfusion strategies after elective operations for myocardial revascularization.

We performed a prospective, randomized trial of two different strategies for postoperative packed red blood cell replacement in 39 autologous blood donors undergoing elective myocardial revascularization. The "liberal" group received blood to achieve a hematocrit value of 32%, and the "conservative" group received transfusions for a hematocrit value less than 25%. Although the groups had significantly different mean hematocrit values from the fourth postoperative hour (28.7% versus 31.2%) through the fifth postoperative day (28.4% versus 31.3%), there were no significant differences in fluid requirement, hemodynamic parameters, or hospital complications. Significantly fewer units of packed cells were required in the conservatively transfused group (20 units/20 patients) compared with the liberally transfused group (37 units/18 patients) (p = 0.012). Exercise tests were performed on the fifth and sixth postoperative days, with a transfusion being given to the conservative group between tests. Although a significant improvement in exercise endurance occurred in the conservative group receiving a transfusion (p = 0.008), no significant difference in duration or degree of exercise was demonstrated between the two groups on either day. In comparing these two groups of profoundly anemic patients, we identified no adverse consequence associated with the greater degree of hemodilution and could identify no correlation between hematocrit value and exercise capacity. We conclude that although the limits of hemodilution are still poorly defined, postoperative blood transfusion in revascularized patients should be guided by clinical indications and not by specific hematocrit values.

Changes in autonomic response of the cerebral circulation after normothermic extracorporeal circulation.

Patients who undergo cardiopulmonary bypass frequently have neuropsychologic dysfunction. This study was undertaken to determine whether altered cerebral perfusion and vascular responses may in part lead to these neuropsychologic changes. Pigs were placed on normothermic cardiopulmonary bypass for 2 hours. Basal cerebral blood flow and in vivo responses to administration by internal carotid artery of neuronally released vasoactive substances were evaluated before and 5 to 15 minutes after termination of cardiopulmonary bypass. Another group of pigs were placed on cardiopulmonary bypass for 2 hours and then perfused off bypass for 1 additional hour. In vitro responses of cerebral arterial microvessels (100 to 175 microns) from both groups were examined in a pressurized (40 mm Hg) no-flow state with videomicroscopy. Vessels from uninstrumented pigs served as control preparations for in vitro studies. Cerebrovascular resistance and cerebral perfusion were maintained constant during cardiopulmonary bypass and after separation from bypass. The internal carotid artery infusion of acetylcholine (cholinergic agonist) caused increased internal carotid artery blood flow before cardiopulmonary bypass but decreased blood flow after cardiopulmonary bypass. After 2 hours of cardiopulmonary bypass, the increase in internal carotid artery blood flow induced by isoproterenol (a beta-adrenoceptor agonist) was reduced, whereas the response to sodium nitroprusside (a guanylate cyclase activator) was unchanged. In vitro acetylcholine-induced microvascular vasodilation was converted to a contractile response and isoproterenol elicited less relaxation after 2 hours of cardiopulmonary bypass. One hour of cerebral perfusion after cardiopulmonary bypass caused a further reduction in isoproterenol-induced relaxation but had no further effect on the cholinergically mediated response. In vitro relaxation responses to sodium nitroprusside and forskolin (an adenylate cyclase activator) were similar in all experimental groups, suggesting that second-messenger mechanisms remain intact after normothermic cardiopulmonary bypass. In conclusion, basal cerebrovascular resistance and internal carotid artery blood flow are maintained if the systemic circulation and pressure are supported with fluid administration after cardiopulmonary bypass. Agonist-induced vasodilation of cerebral microvessels to cholinergic and beta-adrenoceptor stimulation are selectively impaired after normothermic cardiopulmonary bypass, whereas second-messenger mechanisms remain intact.