Crystalloid versus red blood cell-containing medium in the Langendorff-perfused isolated heart preparation.

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.

Amplification by hyperoxia of coronary vasodilation induced by propofol.

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.

A comparison of intrathecal opioid and intravenous analgesia for the incidence of cardiovascular, respiratory, and renal complications after abdominal aortic surgery.

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.

Terlipressin-ephedrine versus ephedrine to treat hypotension at the induction of anesthesia in patients chronically treated with angiotensin converting-enzyme inhibitors: a prospective, randomized, double-blinded, crossover study.

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.