Anesthesia and analgesia
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Anesthesia and analgesia · May 2004
Electrocerebral silence by intracarotid anesthetics does not affect early hyperemia after transient cerebral ischemia in rabbits.
Evidence suggests that early postischemic hyperemia is mediated by both neurological and vascular mechanisms. We hypothesized that if neuronal activity were primarily responsible for reperfusion hyperemia, then electrocerebral silence induced by intracarotid anesthetics (propofol and pentothal) would attenuate the hyperemic response. New Zealand white rabbits were subjected to 10 min of cerebral ischemia using bilateral carotid occlusion and systemic hypotension. Subsequently, carotid occlusion was released, and the mean arterial blood pressure was increased to baseline values. In the control group, intracarotid saline was periodically injected during reperfusion. In the treatment groups, intracarotid propofol or thiopental was administered to maintain electrocerebral silence for 10 min. Physiological data were measured at baseline, during ischemia, and at reperfusion. Satisfactory data were available for 16 of 19 rabbits. Mean arterial blood pressure, end-tidal CO(2), and cerebral blood flows decreased significantly in both groups during carotid occlusion. During early reperfusion, a similar percent increase in cerebral blood flow from baseline values was observed in all 3 groups (192% +/- 76%, 218% +/- 84%, and 185% +/- 101% for saline, propofol, and pentothal, respectively). These results suggest that suppression of neuronal activity during reperfusion does not affect early hyperemia after transient cerebral ischemia. ⋯ Intracarotid injection of anesthetic drugs in doses that are sufficient to produce electrocerebral silence do not obtund early cerebral hyperemia after transient cerebral ischemia. This suggests that vascular, not neuronal mechanisms, are primarily responsible for early postischemic cerebral hyperperfusion.
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Anesthesia and analgesia · May 2004
Comparative StudyA comparison of epinephrine and vasopressin in a porcine model of cardiac arrest after rapid intravenous injection of bupivacaine.
In a porcine model, we compared the efficacy of epinephrine, vasopressin, or the combination of epinephrine and vasopressin with that of saline placebo on the survival rate after bupivacaine-induced cardiac arrest. After the administration of 5 mg/kg of a 0.5% bupivacaine solution i.v., ventilation was interrupted for 3 +/- 1 min (mean +/- SD) until asystole occurred. Cardiopulmonary resuscitation (CPR) was initiated after 1 min of cardiac arrest. After 2 min of CPR, 28 animals received, every 5 min, epinephrine; vasopressin; epinephrine combined with vasopressin; or placebo i.v.. Three minutes after each drug administration, up to 3 countershocks (3, 4, and 6 J/kg) were administered; all subsequent shocks were 6 J/kg. Blood was drawn throughout the experiment for the determination of plasma bupivacaine concentration. In the vasopressin/epinephrine combination group, all pigs survived (P < 0.01 versus placebo); in the vasopressin group 5 of 7, in the epinephrine group 4 of 7, and in the placebo group none of 7 swine survived. The plasma concentration of total bupivacaine showed no significant difference among groups. In this model of bupivacaine-induced cardiac arrest, CPR with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group. ⋯ Although cardiovascular collapse occurs mostly immediately after rapid injection of a local anesthetic in the presence of anesthesiologists, resuscitation may be difficult, and the outcome is usually poor. In this model of bupivacaine-induced cardiac arrest, cardiopulmonary resuscitation with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group.
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In this study we sought to determine the factors influencing red blood cell (RBC) transfusions and to study the transfusion practice of anesthesiologists during liver transplants. A retrospective study of 206 successive liver transplants was undertaken during a period of 52 mo. Transfused blood products were identified. Twenty variables were analyzed in a univariate fashion. For the multivariate analysis, the cases were divided in 2 subgroups: more than 4 RBC units transfused and 4 or less RBC units transfused. The average number of RBC units transfused during a liver transplant was 2.8 (+/- 3.5) per patient, 32.0% did not receive any RBC, and 19.4% did not receive any blood products during the transplant. Three variables were related to the number of RBC units transfused: the starting International Normalized Ratio value, the starting platelet count, and the duration of surgery. We found that there was a wide difference in the transfusion practice of the anesthesiologists involved in this series of liver transplants. It was difficult to identify predictive factors for RBC transfusions when the transfusion rate was small and because of the variability in human factors. Plasma transfusion did not decrease the rate of RBC transfusions; sometimes it was the contrary. ⋯ This is a retrospective study of 206 liver transplants over 52 mo to identify the predictive factors of red blood cell transfusions and the anesthesiologists' transfusion strategies. We conclude that there is a wide difference in transfusion practices among anesthesiologists.
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Anesthesia and analgesia · May 2004
The monoamine reuptake inhibitor milnacipran does not affect nociception to acute visceral distension in rats.
The role of antidepressants in the treatment of visceral pain has not been extensively examined. Milnacipran, an antidepressant that inhibits monoamine reuptake, is widely used in the treatment of depression and fibromyalgia. In this study, we sought to determine the activity of milnacipran against acute visceral nociception. Female virgin rats were studied 7 days after bilateral ovariectomy. For uterine cervical distension (UCD), two metal rods were inserted into the cervical osses under general anesthesia for manual distension. Colorectal distension (CRD) was performed by insertion of a balloon catheter into the descending colon and rectum, followed by manual inflation. Two electrodes were inserted into the rectus abdominus muscle for recording UCD- or CRD-induced reflex contraction, which was quantified by electromyography (EMG). A dose response for milnacipran, administered intrathecally or i.v., was obtained for UCD and CRD stimulation. Milnacipran failed to inhibit the UCD-induced EMG response, whether administered i.v. or intrathecally. Similarly, i.v. milnacipran, administered either acutely or chronically, failed to inhibit the CRD-induced EMG response. CRD and UCD are well established animal models for the study of acute visceral pain. Milnacipran, although it provides some unique advantages compared with other antidepressants, is unlikely to produce analgesia after acute administration in the setting of acute visceral pain. ⋯ Neither intrathecal nor i.v. milnacipran, a monoamine reuptake inhibitor, inhibits an acute visceral pain response induced by colorectal or uterine cervical distension.