Comparative study of different concentrations of prilocaine and ropivacaine for intraoperative axillary brachial plexus block.

BACKGROUND AND OBJECTIVE: To compare the anaesthetic characteristics in terms of onset and offset times of the sensory and motor blocks of prilocaine 1% and ropivacaine 0.75% alone and in different combinations when used for brachial plexus anaesthesia in axillary perivascular blocks. METHODS: After informed consent 96 ASA I-III patients undergoing forearm or hand surgery participated in this prospective, randomized, double-blind study. Patients received either prilocaine 1% 40 mL (G1), prilocaine 1% 30 mL and ropivacaine 0.75% 10 mL (G2), prilocaine 1% 20 mL and ropivacaine 0.75% 20 mL (G3) or ropivacaine 0.75% 40 mL (G4) for axillary perivascular brachial plexus anaesthesia. Onset and duration of sensory and motor blocks in the distribution of the musculocutaneous, radial, median and ulnar nerves were assessed. RESULTS: The onset time of the sensory and motor blocks of the whole brachial plexus differed only between patients in G4 with ropivacaine 0.75% 40 mL demonstrating a later motor onset in comparison to all other groups and a later sensory onset in comparison to G1 and G2 (P < 0.01). The addition of ropivacaine resulted in longer offset times of the sensory and motor blocks. The median offset time of the motor block was 179.5 min in G1, 262 min in G2, 389.5 min in G3 and 745 min in G4 (P < 0.01). The median offset time of the sensory block was 163.5 min in G1, 277 min in G2, 383.5 min in G3 and 784 min in G4 (P < 0.01). There was no difference in onset and offset times between sensory and motor blocks within the groups. CONCLUSIONS: For axillary perivascular brachial plexus block prilocaine 1% alone and in combination with ropivacaine 0.75% was similar in terms of onset of sensory and motor blocks but different in duration of sensory and motor blocks without a differential sensory and motor offset.

Recovery from myocardial stunning is faster with desflurane compared with propofol in chronically instrumented dogs.

Volatile anesthetics exert a protective role in myocardial ischemia. An increase in sympathetic tone might exert deleterious effects on the ischemic myocardium. The use of the volatile anesthetic desflurane in myocardial ischemia is controversial because of its sympathetic activation. We compared propofol and desflurane on myocardial stunning in chronically instrumented dogs. Mongrel dogs (n = 8) were chronically instrumented for measurement of heart rate, left atrial, aortic, and left ventricular pressure, rate of rise of left ventricular pressure, and myocardial wall-thickening fraction (WTF). An occluder around the left anterior descending artery (LAD) allowed the induction of reversible LAD-ischemia. Two experiments were performed in a cross-over fashion on separate days: 1) Induction of 10 min of LAD-ischemia during desflurane anesthesia and 2) Induction of 10 min of LAD-ischemia during propofol anesthesia. Both anesthetics were discontinued immediately after completion of ischemia. WTF was measured at predetermined time points until complete recovery from ischemic dysfunction occurred. Both anesthetics caused a significant decrease of WTF in the LAD-perfused myocardium. LAD-ischemia led to a further significant decrease of LAD-WTF in both groups. During the first 3 h of reperfusion, WTF was significantly larger in the desflurane group. Mean arterial pressure and heart rate were greater during ischemia and the first 10 min of reperfusion in the desflurane group compared with the propofol group. Recovery from myocardial stunning in dogs was faster when desflurane was used at the time of ischemia as compared with propofol anesthesia. The mechanism for this difference is unclear, but sympathetic activation by desflurane was not a limiting factor for ischemic tolerance in chronically instrumented dogs.

Clonidine improves recovery from myocardial stunning in conscious chronically instrumented dogs.

UNLABELLED: Clonidine, an alpha2-adrenergic agonist, has been widely used in anesthesia because of its sedative, analgesic, sympatholytic, and specific hemodynamic effects. The use of clonidine in myocardial ischemia is controversial because of its bradycardic and hypotensive effects. In the present study, we tested the hypothesis that clonidine improves recovery from myocardial stunning in conscious dogs. Seven dogs were chronically instrumented to allow measurement of left atrial pressure (LAP), aortic blood pressure (ABP), left ventricular pressure (LVP), maximal rate of increase of LVP (LVdP/dtmax), and myocardial wall thickening fraction (WTF). The myocardial blood flow was measured using colored microspheres. To compensate for any potential interaction between the two ischemic episodes, experiments were performed on separate days in a cross-over fashion (four animals underwent Condition 1, and three underwent Condition 2 as their first experiment). The ischemic episodes involved 1) 10 min of ischemia of the left anterior descending (LAD) coronary artery without any intervention, and 2) 10 min of LAD ischemia 30 min after 10 microg/kg iv clonidine. WTF was measured before the induction of ischemia or the application of clonidine (baseline) and at predetermined time points until complete recovery of myocardial function. WTF recovered faster during the first 2 h of reperfusion when clonidine was administered. The increase in plasma epinephrine was attenuated by clonidine during ischemia, but there was no change during reperfusion. The increase of plasma norepinephrine levels was attenuated during ischemia and reperfusion. The hemodynamic effects of clonidine did not depress myocardial perfusion or impair myocardial function. IMPLICATIONS: In this study, we investigated the effects of IV clonidine on myocardial stunning in chronically instrumented dogs. Clonidine improved the recovery from myocardial stunning and attenuated increases in catecholamine plasma levels.