RESUMO
Objective To compare the anesthetic effects of interscalene brachial plexus combined with ulnar nerve and axillary brachial plexus block guided by nerve stimulator. Methods Eighty patients belonging to ASA ⅠorⅡ and undergoing replantation of severed palm or wrist were divided randomly into 2 groups, Each group had 40 patients. Nerve stimulator guided nerve block. Patients in groupⅠreceived interscalene brachial plexus combined with ulnar nerve block, and those in groupⅡreceived axillary brachial plexus block. The onset time, hold time, tourniquet tolerance of radial nerve, median nerve and ulnar nerve of two groups was recorded. The phrenic nerve block, Horner′s syndrome and recurrent laryngeal nerve block was compared between two groups. Results The onset time of radial nerve, median nerve and ulnar nerve in group Ⅰwas (5.13 ± 0.76), (7.13 ± 1.04), (3.23 ± 0.62) min , in group Ⅱ was (9.23 ± 1.61), (12.35 ± 1.76), (8.83 ± 1.13) min, and there were significant differences (P<0.05). The excellent rates of sensory block of radial nerve, median nerve and ulnar nerve in group Ⅰ were 90.0%(36/40), 85.0%(34/40), 97.5%(39/40), in group Ⅱ were 72.5%(29/40), 65.0%(26/40), 70.0%(28/40), and there were significant differences (P<0.05). The full rates of motor block of radial nerve, median nerve and ulnar nerve in groupⅠwere 75.0%(30/40), 37.5%(27/40), 80.0%(32/40), in groupⅡ were 47.5%(19/40), 40.0%(16/40), 45.0%(18/40), and there were significant differences (P < 0.05). The tourniquet tolerance rate in group Ⅰwas significantly higher than that in groupⅡ:90.0%(36/40) vs. 62.5%(25/40) , P<0.05. In groupⅠ, phrenic nerve block occurred in 2 patients, and Horner syndrome occurred in 1 patient. None had laryngeal recurrent nerve block in both group. Conclusions The interscalene brachial plexus combined with ulnar nerve block guided by nerve stimulator is more suitable for a long time microsurgery of the palm or wrist, because it takes action faster, has better sensory and motor block effects, improves the rate of tourniquet tolerance without increasing untoward reaction.
RESUMO
Objective To evaluate the role of c?Jun N?terminal kinase ( JNK) and p38 mitogen?ac?tivated protein kinase ( p38MAPK) signaling pathways in attenuation of myocardial ischemia?reperfusion ( I∕R) injury by morphine postconditioning. Methods Healthy adult male Sprague?Dawley rats, weighing 180-240 g, were used in the study. Their hearts were excised and retrogradely perfused in a Langendorff apparatus with Krebs?Ringer ( K?R) buffer saturated with 95% O2?5% O2 at 37℃. After 15 min of equili?bration, 52 isolated hearts were divided into 4 groups ( n=13 each) using a random number table: control group (group C), I∕R group, morphine postconditioning group (group MP), and morphine postcondition?ing plus anisomycin group ( group MP+A) . The hearts were continuously perfused with K?R buffer for 105 min in group C. In group I∕R, the hearts were subjected to 45 min of global ischemia by stopping perfusion with K?R buffer, followed by 60 min of reperfusion by restoration of perfusion with K?R buffer. In group MP, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and then by 50 min of reperfusion with K?R buffer. In group MP+A, the hearts were subjected to 45 min of global ischemia, followed by 10 min of reperfusion with K?R buffer containing 3?0 μmol∕L morphine and 1?0 μmol∕L anisomycin ( an activator of JNK and p38MAPK) and then by 50 min of reperfusion with K?R buffer. At 60 min of reperfusion, 8 hearts in each group were selected for measurement of the myocardial infarction and amount of creatine kinase?MB ( CK?MB) released from the myocardium, and the myocardial infarct size was calculated. At 20 min of reperfusion, 5 hearts in each group were selected to detect the expression of phosphorylated JNK ( p?JNK ) , phosphorylated p38MAPK ( p?p38MAPK) and cytochrome c ( Cyt c) in myocardial tissues ( by Western blot) and content of nicotinamide adenine dinucleotide ( NAD+) in myocardial tissues ( by spectrophotometry ) . Results Compared to group C, the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regulated, and the content of NAD+ was significantly decreased in I∕R, MP and MP+A groups ( P<0?05) . Compared to group I∕R, the myocardial infarct size and amount of CK?MB released from the myocardium were signifi?cantly decreased in MP and MP+A groups, and the expression of p?JNK, p?p38MAPK and Cyt c was sig?nificantly down?regulated, and the content of NAD+ was significantly increased in group MP (P<0?05). Compared to group MP , the myocardial infarct size and amount of CK?MB released from the myocardium were significantly increased, the expression of p?JNK, p?p38MAPK and Cyt c was significantly up?regula?ted, and the content of NAD+ was significantly decreased in group MP+A (P<0?05). Conclusion The mechanism by which morphine postconditioning attenuates myocardial I∕R injury is related to inhibition of activation of JNK and p38MAPK signaling pathways in rats.