Anesthesia and analgesia
-
Anesthesia and analgesia · Mar 2004
The effects of a polymerized bovine-derived hemoglobin solution in a rabbit model of arterial thrombosis and bleeding.
Hemoglobin-based oxygen carriers (HBOCs) have been developed primarily for their oxygenating function and possible use as an alternative to red blood cells during surgery or after major trauma. However, their effect on hemostasis has not been studied extensively. We compared the effects on hemostasis of bovine-derived hemoglobin solution (HBOC-201) with gelatin solution and saline infusion in an experimental model of arterial thrombosis and bleeding. After anesthesia, the Folts model was constructed in 30 rabbits. The common carotid artery was exposed, and a 60% stenosis was induced. A compression injury of the artery was then produced, which triggered a series of cyclic episodes of thrombosis (cyclic flow reductions [CFRs]). After the number of baseline CFRs was counted, animals were assigned randomly to one of three groups (n = 10 each): saline (control), gelatin, or HBOC-201 solution. The effect of studied solutions was observed by recording the number of CFRs during another period and was compared with that of saline. Ear immersion bleeding time was recorded after each CFR period. Gelatin and HBOC-201 had similar effects, manifested by significantly decreased CFRs (from median of 7 to 1 and 6 to 1, respectively) and significantly lengthened bleeding time (from 88 to 98 s and 81 to 102 s, respectively; P < 0.05). Saline infusion had no significant effect on CFRs or bleeding time. HBOC-201 and gelatin had similar effects marked by a reduction in the arterial thrombosis rate and increased bleeding time in rabbits. ⋯ In a rabbit thrombosis and hemorrhagic model, a polymerized bovine-derived hemoglobin solution and a gelatin solution infusion decreased arterial thrombosis and lengthened bleeding time.
-
Anesthesia and analgesia · Mar 2004
Amplification by hyperoxia of coronary vasodilation induced by propofol.
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. ⋯ 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.
-
Anesthesia and analgesia · Mar 2004
Vasodilation increases the threshold for bupivacaine-induced convulsions in rats.
Bupivacaine affects the vascular resistance by peripheral and central nervous system (CNS) mechanisms. As vasoconstrictors increase the CNS toxicity of IV bupivacaine, vasodilators may decrease its CNS toxicity. We examined the hypothesis that vasodilators decrease the CNS toxicity of bupivacaine in awake, spontaneously breathing rats. Male Sprague-Dawley rats were randomly divided into control (C), nicardipine (N), and phentolamine (P) groups (n = 12 in each group). Racemic bupivacaine was administered IV at 1 mg/kg/min until tonic/clonic convulsions occurred. Saline, nicardipine (0.4 microg/min), and phentolamine (10 microg/min within 5 min, 50 microg/min thereafter) were simultaneously administered with bupivacaine in groups C, N, and P, respectively. Mean arterial blood pressure was significantly increased by infusion of bupivacaine in group C and was maintained at baseline levels before the onset of convulsions in groups N and P. The convulsive dose of bupivacaine in group C was 5.8 +/- 1.5 mg/kg, but was significantly larger in groups N and P (7.6 +/- 1.5 and 8.1 +/- 1.1 mg/kg, P = 0.02 and 0.001, respectively). However, there were no differences in total or protein-unbound plasma concentration of bupivacaine or in concentration of bupivacaine in the brain at the onset of convulsions among the 3 groups. We conclude that nicardipine and phentolamine increase the cumulative dose but do not affect the threshold plasma or brain concentrations required for bupivacaine-induced convulsions. ⋯ Bupivacaine, a long-acting local anesthetic, induces central nervous system toxicity when its plasma concentration is increased. Nicardipine and phentolamine increased the cumulative dose but did not affect the threshold plasma concentrations, required for bupivacaine-induced convulsions, suggesting that both nicardipine and phentolamine inhibited the increase in the plasma concentration of bupivacaine by inducing peripheral vasodilation.
-
Anesthesia and analgesia · Mar 2004
Clinical TrialAnalgesia after total knee arthroplasty: is continuous sciatic blockade needed in addition to continuous femoral blockade?
Continuous femoral "3-in-1" nerve blocks are commonly used for analgesia after total knee arthroplasty (TKA). There are conflicting data as to whether additional sciatic blockade is needed. Our routine use of both continuous femoral (CFI) and sciatic (CSI) peripheral nerve blocks was changed because of concerns that sciatic blockade, and its motor consequences in particular, might obscure diagnosis of perioperative sciatic nerve injury. ⋯ Within 1 h of a 5-10 mL CSI bolus of 0.2% ropivacaine and beginning an infusion of the same drug at 5 mL/h, patients' median pain by verbal analog scale decreased from 7.5 to 2.0 (mean scores from 7.3 to 2.4). It was possible to maintain this level of analgesia until the third postoperative day when catheters were discontinued. Our experience suggests that, in most patients, adequate analgesia after TKA cannot be achieved with CFI alone and that the addition of CSI renders a significant improvement in analgesia.
-
Anesthesia and analgesia · Mar 2004
Effect of isoflurane on neuronal apoptosis in rats subjected to focal cerebral ischemia.
Although isoflurane can reduce ischemic neuronal injury after short postischemic recovery intervals, this neuroprotective efficacy is not sustained. Neuronal apoptosis can contribute to the gradual increase in infarct size after ischemia. This suggests that isoflurane, although capable of reducing early neuronal death, may not inhibit ischemia-induced apoptosis. We investigated the effects of isoflurane on markers of apoptosis in rats subjected to focal ischemia. Fasted Wistar-Kyoto rats were anesthetized with isoflurane and randomly allocated to awake (n = 40) or isoflurane (n = 40) groups. Animals in both groups were subjected to focal ischemia by filament occlusion of the middle cerebral artery for 70 min. Pericranial temperature was servo-controlled at 37 degrees C +/- 0.2 degrees C throughout the experiment. In the awake group, isoflurane was discontinued and the animals were allowed to awaken. In the isoflurane group, isoflurane anesthesia was maintained at 1.5 MAC (minimum alveolar anesthetic concentration). Animals were killed 7 h, 1 day, 4 days, or 7 days after reperfusion (n = 10/group/time point). The area of cerebral infarction was measured by image analysis in a hematoxylin and eosin stained section. In three adjacent sections, apoptotic neurons were identified by TUNEL staining and immunostaining for active caspase-9 and caspase-3. Infarct size was smaller in the isoflurane group than the awake group 7 h, 1 day, and 4 days after reperfusion (P < 0.05). However, this difference was absent 7 days after reperfusion. The number of apoptotic (TUNEL, caspase-3, and caspase-9 positive) cells 1 day after ischemia was significantly more in the awake versus isoflurane group. After a recovery period of 4 or 7 days, the number of apoptotic cells in the isoflurane group was more than in the awake group. After 7 days, the number of caspase-3 and -9 positive neurons was more in the isoflurane group (P < 0.05). The data indicate that isoflurane delays but does not prevent the development of cerebral infarction caused by ischemia. Isoflurane reduced the development of apoptosis early after ischemia but did not prevent it at later stages of postischemic recovery. ⋯ The effect of isoflurane on neuronal apoptosis was investigated in rats subjected to focal cerebral ischemia. In isoflurane-anesthetized animals, ischemia-induced apoptosis occurred during the later stages of postischemic recovery. Isoflurane did not inhibit postischemic neuronal apoptosis.