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Background: The isolated heart model is widely used for the assessment of coronary vascular response under various experimental conditions. As medium perfusate influences oxygenation conditions, coronary vascular response and myocardial consumption performance may differ between isolated hearts perfused with from with Krebs-Henseleit solution or Krebs-Henseleit mixed with red blood cells (KH-RBC)., Methods: Coronary vascular response to endothelium-dependent and independent vasodilators as well as myocardial performance and oxygen consumption to isoproterenol infusion were compared in isolated rabbit hearts perfused with Krebs-Henseleit or KH-RBC. Krebs-Henseleit perfusate was equilibrated with 95% oxygen and 5% carbon dioxide, KH-RBC (haemoglobin 8.0 +/- 1.1 g.dl) with 20% oxygen, 5% carbon dioxide, and 75% nitrogen. The perfusion pressure was kept constant so that coronary blood flow (CBF) varied with coronary resistance. Data are mean +/- SD., Results: Bradykinin induced a greater increase in CBF in KH-RBC-perfused hearts than in Krebs-Henseleit-perfused hearts (263 +/- 78 versus 134 +/- 35% of baseline, P < 0.001). Sodium nitroprusside induced a greater increase in CBF in KH-RBC-perfused than in Krebs-Henseleit-perfused hearts (257 +/- 70 versus 174 +/- 31% of baseline, P < 0.001). The increases in myocardial performance and in oxygen consumption induced by isoproterenol were greater with KH-RBC-perfused hearts than in Krebs-Henseleit-perfused hearts. A greater myoglobin release was observed in Krebs-Henseleit-perfused hearts., Conclusion: Endothelium-dependent and independent coronary flow responses are increased in KH-RBC-perfused hearts. Moreover, metabolic control of CBF is altered in Krebs-Henseleit-perfused hearts. Such differences should be taken into account when pharmacologic responses of anaesthetic agents are studied.

Unlabelled: We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10-300 microM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (PaO(2) = 137 +/- 16 mm Hg, n = 12) or in the presence (PaO(2) = 541 +/- 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (-13% +/- 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 microM) and cromakalim (0.5 microM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (-16% +/- 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 micro M both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia., Implications: Propofol induced a coronary vasodilation that was amplified in the presence of hyperoxia. This phenomenon does not seem to be related to previous coronary vasoconstriction. The myocardial effects of propofol were not significantly modified in the presence of hyperoxia.

Unlabelled: Major surgery evokes a stress response that can produce deleterious consequences, especially in a population at high risk for those complications. We tested the hypothesis that decreasing or eliminating one of the sources of stress by providing intense analgesia in the immediate postoperative period via application of neuraxial opioids would decrease major nonsurgical complications. Two-hundred-seventeen patients scheduled to undergo abdominal aortic surgery were randomly allocated to receive either general anesthesia alone (control) or general anesthesia combined with intrathecal opioid (1 micro g/kg sufentanil with 8 micro g/kg preservative-free morphine injected at the L4-5 interspace). Postoperative care was identical in the two groups, including patient-controlled analgesia. Each patient provided an assessment of postoperative pain using a visual analog scale. Postopera-tive complications were recorded according to criteria established a priori. The administration of intrathecal opioid provided more intense analgesia than patient-controlled analgesia during the first 24 h postoperatively (P < 0.05). There was no difference between groups for the incidence of combined major cardiovascular, respiratory, and renal complications (P > 0.05) or mortality (P > 0.05). The incidence of myocardial damage or infarction, as defined by abnormal plasma concentration of troponin I, did not differ between the two groups (P > 0.05). In patients undergoing major abdominal vascular surgery, decrease of one contributor to postoperative stress, by provision of intense analgesia for the intraoperative and initial postoperative period, via application of neuraxial opioid, does not alter the combined major cardiovascular, respiratory, and renal complication rate., Implications: Provision of intense analgesia for the initial postoperative period after major abdominal vascular surgery, via the administration of neuraxial opioid, does not alter the combined incidence of major cardiovascular, respiratory, and renal complications.

Unlabelled: In patients chronically treated with angiotensin converting-enzyme inhibitors (ACEI), typically selected doses of ephedrine do not always restore arterial blood pressure when anesthesia-induced hypotension occurs. We postulated that the administration of terlipressin, an agonist of the vasopressin system, with ephedrine more effectively restores pressure in this setting than the administration of ephedrine alone. This prospective, randomized, cross-over, double-blinded study compared terlipressin combined with ephedrine (n = 19) with ephedrine alone (n = 21) in treating hypotension at the induction of anesthesia in 40 ACEI-treated patients undergoing hypotension (mean arterial blood pressure [MAP] <65 mm Hg or <30% of baseline value) after standardized anesthetic protocol (target-controlled IV anesthesia with propofol). Data are mean +/- SD. Patient characteristics, MAP, and heart rate before and after the induction of anesthesia during hypotensive episodes were not significantly different between the two groups. After the first bolus, MAP was significantly greater in the Terlipressin-Ephedrine group (72 +/- 12 mm Hg versus 65 +/- 8 mm Hg, P < 0.05). The occurrence of a second hypotensive episode (5% versus 71%, P < 0.001), the duration (2 +/- 1 min versus 3 +/- 1 min, P < 0.01) of hypotensive episodes, and the median dose of ephedrine (3 versus 6 mg, P < 0.05) were significantly less in the Terlipressin-Ephedrine group. In conclusion, terlipressin combined with ephedrine is more effective than ephedrine alone for treating anesthesia-induced hypotension in ACEI-treated patients. We conclude that this patient population with a partially blocked endogenous response to hypotension may be good candidates for successful use of a vasopressin analog to counteract intraoperative refractory hypotension., Implications: Vascular surgical patients chronically treated with drugs that inhibit the functioning of the renin-angiotensin system may experience hypotension unresponsive to conventional therapy. This double-blinded, cross-over study demonstrated that in these patients the use of a vasopressin analog, terlipressin given with ephedrine, was effective in reversing intraoperative systemic hypotension refractory to ephedrine.

Unlabelled: We compared the hemodynamic stability during carotid endarterectomy of remifentanil with that of sufentanil anesthesia. Fifty-six patients were randomly assigned into Remifentanil (n = 27) or Sufentanil (n = 29) groups. In the Remifentanil group, IV propacetamol (2 g) and morphine (0.1 mg/kg) were infused 30 min before skin closure. In the Sufentanil group, patients received 2 g propacetamol. Beat-to-beat recordings of systolic arterial blood pressure (SBP) and heart rate (HR) were stored on a computer. The maximum and minimum values of BP and HR after induction, at intubation, during the surgical procedure, and after the operation and the coefficients of variation of SBP and HR were used as indices of hemodynamic stability. The coefficients of variation of SBP and HR were similar in both groups during and after surgery. However, at intubation, maximal SBP was higher in the Sufentanil group (P < 0.05). Decreased propofol doses and isoflurane end-tidal concentrations were used in the Remifentanil group. At recovery, a similar profile of SBP and HR was found in both groups. We conclude that intra- and posthemodynamic stability was similar with remifentanil or sufentanil in patients undergoing carotid endarterectomy. However, remifentanil was more effective for blunting the increase in SBP at intubation without increasing the blood pressure-decreasing effect of induction. Intraoperative remifentanil use was associated with a decreased amount of hypnotic drug administered., Implications: Beat-to-beat recordings of heart rate and blood pressure in patients undergoing carotid surgery revealed that hemodynamic stability was similar with remifentanil or sufentanil anesthesia both during and after surgery. Remifentanil was more effective in limiting the increase in blood pressure associated with intubation without increasing the blood pressure-lowering effect of induction or the blood pressure response to recovery.

Unlabelled: Although angiotensin II bolus administration may be used to increase blood pressure in patients chronically treated with angiotensin-converting enzyme inhibitors (ACEI) who have severe hypotension on anesthetic induction, no data are available describing its time course and its effects on the left ventricular function. Fourteen patients chronically treated with ACEI for hypertension and scheduled for vascular surgery were prospectively studied. Patients with cardiac insufficiency were excluded. A transesophageal echocardiography probe was inserted to assess systolic left ventricular function. When hypotension was observed (systolic arterial pressure [SAP] <85 mm Hg), an I.V. bolus of 2.5 microg of angiotensin II (AII) was given, and hemodynamic variables were recorded each 30 s over 5.5 min. Results are expressed as mean +/- SEM. Sixty seconds after the AII bolus injection, the SAP increased from 78 +/- 3 to 152 +/- 6 mm Hg. SAP remained higher than control until the 5th min. This was associated with significant increases in end-diastolic area (from 15.1 +/- 0.6 to 19.3 +/- 1.0 cm2, P < or = 0.001), end-systolic area (from 6.6 +/- 0.4 to 10.7 +/- 0.7 cm2, P < or = 0.001), end-systolic wall stress (from 32 +/- 0.05 to 82 +/- 7 kdynes/cm2, P < or = 0.001). In addition, a decrease in fiber-shortening velocity (from 1.1 +/- 0.05 to 0.76 +/- 0.04 circ/s, P < or = 0.05) and in fractional area change (from 0.57 +/- 0.02 to 0.44 +/- 0.02, P < or = 0.05) was observed. Heart rate did not significantly change during the study. Increases in preload and afterload were observed. However, the administration of AII causes a transient impairment in left ventricular function. We conclude that AII, given as an I.V. bolus of 2.5 microg, is effective in restoring arterial blood pressure within 60 s in patients chronically treated with ACEI., Implications: Severe hypotension on anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors for hypertension could be treated with an I.V. bolus of 2.5 microg of angiotensin II.

Background: Experimental studies suggest that the new short-acting intravenous anesthetic agent eltanolone does not markedly alter hemodynamics or cardiac function. However, because its intrinsic effects on myocardial performance and coronary blood flow are not yet known, they were examined in isolated blood-perfused rabbit hearts., Methods: Coronary blood flow, myocardial contractility, relaxation, and oxygen consumption were measured during perfusion of hearts with 0.1 to 10 micrograms/ml eltanolone (n = 7) or its vehicle (n = 7). To determine whether the cardiac effects of eltanolone are mediated by indirect sympathetic activation, the same dose-response curve was studied in another group of five hearts depleted of catecholamine with reserpine treatment., Results: Coronary blood flow significantly increased with 10 micrograms/ml eltanolone and significantly decreased with 10 micrograms/ ml eltanolone vehicle. At eltanolone concentrations less than 10 micrograms/ml, myocardial contractility and relaxation remained unchanged but decreased at 10 micrograms/ml. Myocardial contractility and relaxation were not affected by perfusion of eltanolone vehicle alone. In eltanolone-perfused hearts, unchanged myocardial oxygen consumption was associated with significant increases in coronary venous oxygen content and tension, but in vehicle-perfused hearts, it was associated with reduced coronary venous oxygen content and tension. In catecholamine-depleted hearts, the variations in myocardial performance and coronary blood flow induced by eltanolone were similar to those observed in intact hearts., Conclusions: Eltanolone (0.1 to 3 micrograms/ml) did not alter myocardial performance or coronary blood flow in isolated blood-perfused rabbit hearts. These effects were not due to an eltanolone-induced indirect sympathetic activation. Cardiac depression and coronary vasodilatation were only observed at concentrations of eltanolone far greater than those in clinical range.

Hypertonic saline improves organ perfusion and animal survival during hemorrhagic shock because it expands plasma volume and increases tissue oxygenation. Because both decreased and increased myocardial performance have been reported with hypertonic saline, the effects of hyperosmolarity and the mechanism accounting for it were investigated in isolated blood-perfused rabbit hearts. Coronary blood flow (CBF), myocardial contractility, relaxation, and oxygen consumption were measured during administration of blood perfusates containing 140-180 mmol sodium concentrations ([Na+]). In two other series of experiments, the role of Na(+)-Ca2+ exchange in the inotropic effect of hyperosmolarity (160 mmol sodium concentration) and hypertonicity (sucrose) were also investigated. Hypertonic [Na+] induced a significant increase in contractility and relaxation, combined with a coronary vasodilation. Myocardial oxygen consumption (MVO2) increased at all hypertonic [Na+] without significant change in coronary venous oxygen tension (PVO2) and content (CVO2). Amiloride (0.3 mmol) inhibited the improved contractility observed with 160 mmol sodium. Similar Na(+)-Ca2+ exchanger blockade did not inhibit the inotropic effect of sucrose. These results confirm the positive inotropic effect of hypertonic [Na+]. The inhibition of this improvement by amiloride suggests that calcium influx through the sarcolemna could be the major mechanism of this effect.

Background: Some clinical and experimental studies suggest that propofol decreases myocardial contractility and relaxation, whereas others report preserved cardiac function. To investigate the effects of propofol on intrinsic contractility and relaxation, increasing concentrations of propofol were infused in isolated blood-perfused rabbit hearts. Equimolar concentrations of thiopental were infused as a reference group., Methods: Coronary blood flow, left ventricular contractility and relaxation (as maximal positive and negative left ventricular pressure derivatives [dP/dtmax and dP/dtmin], respectively), and myocardial oxygen consumption (MvO2) were measured during infusion of 10-1,000 microM propofol in blood-perfused hearts. To determine whether the effects of propofol depend on the heart's perfusate, propofol also was infused in isolated buffer-perfused rabbit hearts. In addition, the effects of propofol solvent were investigated in blood- and buffer-perfused preparations., Results: In blood-perfused preparations, coronary blood flow increased with propofol concentrations greater than 30 microM and with 300 and 1,000 microM thiopental. Left ventricular dP/dtmax and dP/dtmin remained unchanged with propofol and decreased with concentrations of thiopental equal to or greater than 30 microM. MvO2 increased with 1,000 microM propofol, whereas coronary venous oxygen tension and content remained unchanged. MvO2 decreased with thiopental associated with a significant increase in coronary venous oxygen tension and content. In six buffer-perfused hearts, basal coronary blood flow was much greater and MvO2 less than in blood-perfused hearts. Left ventricular dP/dtmax and dP/dtmin decreased with 30, 100, and 300 microM propofol. Propofol vehicle did not change coronary blood flow, myocardial performance, or MvO2 of blood- or buffer-perfused hearts., Conclusions: When compared to a reference drug such as thiopental, propofol did not depress the myocardial performance of blood-perfused rabbit hearts. The type of the perfusate (blood vs. buffer), however, had a major influence on the myocardial effects of propofol.

We studied the effects of moderate changes in red blood cell RBC aggregation on blood flow in the vasodilated vascular bed of an isolated rat heart. We compared a non-aggregating RBC suspension (in Krebs-albumin medium) with RBC suspensions in 1% and 2% Dextran 70 (MW 70000), exhibiting two different degrees of moderate aggregation. Degrees of aggregation were precisely estimated by in vitro laser aggregometry. Each heart was perfused by the non-aggregating RBC suspension and by one aggregating RBC suspensions. Blood flow was measured in a range of perfusion pressure from 40 to 80 mm Hg. For the three RBC suspensions, linear pressure/flow relationships were found. From the comparison between the pressure/flow relationships obtained with Krebs albumin medium and either 1% or 2% Dextran, it was possible to compare in vivo the contribution of RBC to the viscosity (i.e., the relative apparent viscosity) in the 2 aggregating RBC suspensions with that of the non-aggregating RBC suspension. The contribution of RBC to the viscosity was found to be 20% to 25% lower in the 1% RBC suspension than in the non-aggregating RBC suspension. With 2% Dextran which induced a higher degree of aggregation no differences were found between the relative apparent viscosities of the aggregating and the non-aggregating suspension. From the comparison between RBC in 1% Dextran and Krebs-albumin, we concluded that in vivo a moderate RBC aggregation reduces viscous resistance due to the presence of blood in a vascular network. Since no more effect of RBC aggregation per se was found when the degree of aggregation was higher (with RBC in 2% Dextran), this suggests that, in this case, aggregation induces opposite effects along the myocardial vascular network which cancel each other out, thus inducing a nil net balance.

The aims of this randomized study were (1) to determine if isoflurane is effective in controlling blood pressure during thoracic aortic cross-clamping, and (2) to compare its effects on hemodynamics and oxygen transport to those of sodium nitroprusside. Sodium nitroprusside (SNP group, n = 10) or isoflurane (ISO group, n = 10) was started 2 minutes before cross-clamping and was adjusted to maintain systolic arterial pressure as near as possible to preinduction values. The duration of thoracic aortic cross-clamping was 26 +/- 4 minutes in the SNP group and 30 +/- 4 minutes in the ISO group. Administration of isoflurance and sodium nitroprusside was stopped 2 minutes before unclamping. The same anesthetic technique using fentanyl, 6 micrograms/kg, flunitrazepam, 0.02 mg/kg, pancuronium, 0.1 mg/kg, and 50% N2O was used for all patients. At the time of clamping, either isoflurance (maximal expired concentration, 2.5% +/- 0.3%) or sodium nitroprusside (cumulative dose, 11.1 +/- 1.0 mg) was effective in maintaining the systolic blood pressure below 160 mm Hg, whereas the pulmonary capillary wedge pressure did not change. However, only SNP was able to bring the arterial pressure above the cross-clamp back to postinduction levels. During clamping, stroke index values were similar in both groups, but cardiac index increased only in patients receiving SNP. In both groups, at clamping and unclamping, PvO2 was higher than postinduction values, indicating that throughout the study the oxygen needs of the perfused area were adequately met. There was no evidence of acute left ventricular decompensation because pulmonary capillary wedge pressures did not abruptly increase, nor did pulmonary edema occur.(ABSTRACT TRUNCATED AT 250 WORDS)

This randomized study was designed to determine the cardiovascular effects of normovolemic hemodilution and lumbar epidural anesthesia in patients scheduled for vascular surgery. The patients were randomly assigned to three different groups: group 1 (N = 10) included patients undergoing lumbar epidural anesthesia without hemodilution; group 2 (N = 10) consisted of patients with normovolemic hemodilution without epidural anesthesia; and in group 3 (N = 10) normovolemic hemodilution was produced during lumbar epidural anesthesia. The three groups included several patients with a history of either myocardial infarction or stable mild angina or treated and controlled hypertension. In group 1, the level of epidural anesthesia reached T-9 +/- 1. After lumbar epidural anesthesia and 7 mL/kg colloid infusion, pulmonary capillary wedge pressure increased slightly but significantly above baseline, without significant changes either in mean arterial pressure or in cardiac index. In group 2, the same colloid infusion as in group 1 when infused before normovolemic hemodilution increased pulmonary capillary wedge pressure and cardiac index without significant effects on arterial blood pressure. Normovolemic hemodilution using a colloid solution decreased hemoglobin concentration (18%) and increased cardiac index significantly (9%). No significant change in systemic oxygen transport or in total body oxygen consumption was observed. In group 3, with anesthesia to T-9 +/- 1, hemodynamic changes were as observed in group 1. After normovolemic hemodilution, hemoglobin concentration decreased significantly (15%), whereas cardiac index increased significantly (15%) without significant changes either in mean arterial pressure or in heart rate. Systemic oxygen transport and total body oxygen consumption did not change significantly. No patient experienced chest pain or electrocardiographic evidence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)