The purpose of this study was to investigate the effect of propofol on cerebral blood flow, cerebral metabolism, and cerebrovascular autoregulatory capability. Seven anesthetized baboons were given propofol at three different infusion rates. An infusion of 3 mg.kg-1.h-1 caused minimal changes, but infusion rates of 6 and 12 mg.kg-1.h-1 decreased cerebral blood flow by 28% and 39%, respectively. The changes in cerebral metabolic rate of oxygen were not statistically significant. However, with the two higher infusion rates, there was a trend toward decrease, by 5% and 22%, respectively, for the cerebral metabolic rate of oxygen, and by 18% and 36% for the cerebral metabolic rate of glucose. A 25-30 mm Hg increase in arterial blood pressure had no influence on cerebral blood flow. Replacement of nitrous oxide by nitrogen had no significant influence on cerebral blood flow or metabolism. It is concluded that propofol causes a dose-dependent decrease in cerebral blood flow. However, the study does not prove that this decrease in cerebral blood flow is accompanied by the same degree of decrease in cerebral metabolism. Further studies are clearly needed to clarify propofol's influence on the coupling between cerebral metabolism and blood flow. The physiologic responsiveness of the cerebral circulation to alterations in arterial pressure is well preserved. Propofol appears to prevent the metabolic stimulation and increased cerebral blood flow that has been associated with the administration of nitrous oxide.

SummaryThe primary goal of' this study was to assess the influence of clonidine administered after induction on postoperative shivering after elective peripheral surgery. The effect of clonidine on intra-operative haemodynamics (blood pressure and heart rate) during thejirst 30min after induction and on the postoperative sedation of the patient was also investigated. Two hundred and eighty male ASA 1 and 2 patients, undergoing elective peripheral surgery were randomly administered either placebo or clonidine 2 pg.kg-' intravenously over 10 min after induction of anaesthesia. Clonidine was found to reduce the total incidence (p = 0.024, the severity (p = 0.005) and the duration (p = 0.01) of postoperative shivering. Clonidine did not increase postoperative sedation or diminish overall consciousness. We conclude that administration of clonidine 2 pg.kg-' intravenously after induction of anaesthesia is safe and reduces postoperative shivering in this group of patients. Key wordsComplications; shivering. Pharmacology; clonidineRecovery from anaesthesia and surgery is frequently accompanied by involuntary muscular activity. Besides the discomfort for the patient, shivering can exacerbate postoperative pain and induce complications in patients with coronary artery disease or heart failure by increasing oxygen consumption [I] To date, no unequivocal direct evidence has been published to show that preventive pre-or postoperative administration of clonidine reduces postanaesthetic shivering after peripheral surgery. This large, randomly administered, double-blind study was performed to evaluate the influence of clonidine administered at induction on postoperative shivering after elective peripheral surgery. The effect of clonidine on intra-operative haemodynamics (blood pressure and heart rate) during the first 30 min after

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To investigate the mechanism underlying postischemic cardiac dysfunction (myocardial stunning), contractility and adenine nucleotide metabolism were studied in three groups of isolated perfused rabbit hearts (control, ischemic, and reperfused), whereas Ca2`uptake by the sarcoplasmic reticulum (SR) was measured in homogenates obtained from them. The hearts were Langendorff-perfused as being the major mechanism underlying postischemic myocardial dysfunction. The hypothesis that a decrease of ATP levels underlies stunning has been tested in a number of studies, and the conclusion has been reached that the ATP levels and the available free energy during reperfusion after short ischemia are sufficient to sustain the energetic needs of contraction.12 It is found that ATP levels can recover to near normal values without improvement in contractility. Conversely, contractility can be made to increase during stunning,13 even in the presence of decreased ATP levels. Finally, recent studies of mitochondrial function, including one from this laboratory,14 suggest that mitochondria isolated from stunned hearts retain normal function. Thus, research efforts on the mechanisms of myocardial stunning now focus on a possible abnormality of the excitation-contraction coupling. Among the cellular organelles whose altered functions might account for the contractile deficiency in stunned hearts are the sarcoplasmic reticulum (SR), the contractile myofilaments, and the cell surface membrane. The discovery of a Ca21 overload during ischemia and/or reperfusion suggests that a deficient cellular Ca2' homeostasis may be the major characteristic of an abnormal excitationcontraction coupling in stunned myocardium.15"6 Because of its role in intracellular Ca2+ regulation and in excitation-contraction coupling, the SR has been sug-