A comparison of two techniques for cervical plexus blockade: evaluation of efficacy and systemic toxicity

We compared two techniques of cervical plexus blockade (CPB) for carotid endarterectomy. Cervical plexus nerve block was performed with a combination of bupivacaine and lidocaine, with injections at the C2-C3, C3-C4, and C4-C5 transverse processes in 11 patients (classical CPB) or with a single injection after localization of the cervical plexus with a nerve stimulator in 12 patients (interscalene CPB). Pain scores were obtained during block placement and at predetermined phases of the operation. Arterial blood was sampled before and 3, 5, 8, 10, 15, 25, 40, and 60 min after CPB for measurement of bupivacaine and lidocaine concentrations. Interscalene CPB was less painful than classical CPB. The techniques appeared equally effective. Patients in both groups required equivalent supplementation with IV fentanyl and additional local infiltration with lidocaine during the most painful stages of surgery. The maximal concentration of bupivacaine was lower in interscalene CPB compared with classical CPB (1.0 microg/mL versus 1.5 microg/mL, P < 0.01). The time required to reach the maximal concentration of bupivacaine was 15 (10-40) min in interscalene CPB and 10 (5-17) min in classical CPB (P < 0.05). Lidocaine maximal concentration was similar in both groups, however the time required to reach the maximal concentration was longer (P < 0.05) in interscalene CPB (15 [10-60] min) than in classical CPB (10 [8-20] min). We conclude that the interscalene CPB is as effective as the classical CPB as a regional technique for carotid endarterectomy and may be associated with a lower systemic absorption of bupivacaine. IMPLICATIONS: Cervical plexus blockade for carotid endarterectomy can be effectively performed with a single injection after localization of the cervical plexus with a nerve stimulator. This technique is simple and was associated with less systemic absorption of local anesthetic than the multiple-injection technique.     

LPS-Induced NF-kappaB activation and TNF-alpha release in human monocytes are protein tyrosine kinase dependent and protein kinase C independent

BACKGROUND: Tumor necrosis factor alpha (TNF-alpha) is an important mediator of septic shock. Endotoxin (LPS) signal transduction in human monocytes leads to activation of nuclear factor-kappa B (NF-kappaB) and TNF-alpha release. Previous studies have implicated activation of both protein kinase C (PKC) and protein tyrosine kinases (PTK) in LPS-induced NF-kappaB activation and TNF-alpha production. We hypothesized that inhibition of either PKC or PTK would decrease LPS-induced NF-kappaB DNA binding and TNF-alpha release in human monocytes. MATERIALS AND METHODS: Human monocytes were stimulated with PMA (50 ng/ml) alone or LPS (100 ng/ml) with and without a nonspecific serine/threonine protein kinase inhibitor staurosporine (Stauro), a specific pan-PKC inhibitor bisindolylmaleimide (Bis), or an inhibitor of PTK genistein (Gen). TNF-alpha release in culture supernatants was measured by an ELISA. NF-kappaB DNA binding was evaluated by electrophoretic mobility shift assay. RESULTS: LPS increased NF-kappaB DNA binding and TNF-alpha release in human monocytes. Nonspecific protein kinase inhibition inhibited NF-kappaB activation and TNF-alpha release, while specific PKC inhibition with Bis had no effect on LPS-induced NF-kappaB DNA binding or TNF-alpha release. PTK inhibition with Gen attenuated both LPS-induced NF-kappaB DNA binding and TNF-alpha production in human monocytes. Direct activation of PKC with PMA induced both NF-kappaB activation and TNF-alpha production by human monocytes. CONCLUSIONS: These results suggest that LPS-induced NF-kappaB activation and TNF-alpha release in human monocytes are independent of PKC activity. Furthermore, our results provide evidence that PTK plays a role in LPS-induced NF-kappaB activation and TNF-alpha release in human monocytes and thus could be a potential therapeutic target in inflammatory states.     

Recent developments in SWL physics research

Two projects in our laboratory highlight some recent developments in shockwave lithotripsy (SWL) physics research. In the first project, we developed a prototype of a piezoelectric annular array (PEAA) shockwave generator that can be retrofitted on a Dornier HM-3 lithotripter for active control of cavitation during SWL. The PEAA generator, operating at 15 kV, produces a peak positive pressure of approximately 8 MPa with a -6-dB beam diameter of 5 mm. The shockwave generated by the PEAA was used to control and force the collapse of cavitation bubbles induced by a laboratory electrohydraulic shockwave lithotripter with a truncated HM-3 reflector. With optimal time delay between the lithotripter pulse and the PEAA-generated shockwave, the collapse of cavitation bubbles near the stone surface could be intensified, and the resultant stone fragmentation in vitro could be significantly improved. In the second project, high-speed shadowgraph imaging was used to visualize the dynamics of lithotripter-induced bubble oscillation in a vascular phantom. Compared with the free bubble oscillation in water, the expansion of cavitation bubble(s) produced in silicone tubes and a 200-microm cellulose hollow fiber by either a Nortech EHL or a Dornier XL-1 lithotripter was found to be significantly constrained. Rupture of the cellulose hollow fiber was observed consistently after about 20 shocks from the XL-1 lithotripter at an output voltage of 20 kV. These results confirm experimentally that SWL-induced cavitation in vivo can be significantly constrained by the surrounding tissue, and large intraluminal bubble expansions could cause rupture of capillaries and small blood vessels.     

Fluid percussion brain injury exacerbates glutamate-induced focal damage in the rat

The role of glutamate-mediated neuronal damage in neurotrauma remains controversial. The cerebral levels measured in patients by microdialysis are sufficient to kill neurons in culture, but not in the intact brain of the normal rat. A synergistic effect between excitatory amino acid-mediated damage and other posttrauma mechanisms must therefore be proposed, if glutamate is indeed a significant cause of posttraumatic brain damage. The presence of such a synergistic mechanism was therefore investigated by combining in vivo glutamate perfusion and fluid percussion injury (FPI). Twenty-four adult male Sprague Dawley rats were randomly assigned to three groups: (1) vehicle (n = 9): mock cerebrospinal fluid (CSF) perfusion plus FPI; (2) glutamate + FPI (n = 9): 0.1 M glutamate intracortical perfusion plus FPI; and (3) glutamate without FPI (n = 6). After preparation for central FPI, at a moderate level of injury (2 +/- 0.5 atm), glutamate or mock CSF perfusion was performed via a CMA/12 microdialysis probe (3 mm). Animals were then perfusion fixed, under deep anesthesia, after 3-h survival, for volumetric histopathology. The glutamate perfusion + FPI group (2.42 +/- 1.63 mm3) produced a significantly bigger lesion than mock CSF perfusion + FPI (0.063 +/- 0.41 mm3) and glutamate perfusion alone (1.00 +/- 0.47 mm3). Traumatic brain injury thus seems to enhance glutamate-mediated brain damage, and this may be due to qualitative changes induced in ion channels and receptors, such as the N-methyl-D-aspartate channel, after shear injury.     

内皮素及NO在严重烧伤早期胃肠粘膜缺血中的应用

OBJECTIVE: Inadequate perfusion in splanchnic organs and especially in the gut during acute burn period has been reported in many conventionally "successfully" resuscitated patients, but the mechanisms still remain unclear and its early preventive measures need to be further studied. The aim of this study is to evaluate the role of endothelin and nitric oxide in gut ischemia. METHODS: Eighteen male pigs were randomly assigned to one of the three groups: group C, a sham burn group that was subjected to all surgical procedures except burn; group B, sustained 30% TBSA cutaneous thermal burn; Group N, NO donor (C87-3754) was given intravenously (0.0125 mg.kg-1.min-1) at the beginning of resuscitation. RESULTS: In group B, PVF decreased rapidly after burn, and did not recover in the observation period (72 h), ET levels in portal blood and intestinal tissue elevated contrary to the changes in NO. In group N, PVF was higher than in group B. CONCLUSION: 1. Changes in ET and NO may influence the protal blood flow. 2. NO donor was proved to be beneficial in improving GI tissue perfusion by releasing NO.     

Regeneration of neuronal nitric oxide synthase (nNOS)-containing nerve fibers in rat corpus cavernosum

Aim: To investigate the effect of cavernous nerve injury on the nNOS-containing nerve fibers in rat corpus cavernosum.Methods: Thirty-three male SD rats were randomized into 3 groups: 5 rats underwent pelvic exploration without tran-section of cavernous nerve as the sham-operated controls, the unilateral injury group (14 rats) had the cavernous nerve cuton one side, and the bilateral injury group (14 rats) had the nerves cut on both sides. Corpora cavernosa were harvestedat the 3rd week and 6th month after surgery, nNOS-positive nerve fibers were examined with strepavidin peroxidase im-munohistochemistry techniques (SP method). Results: After bilateral ablation, the nNOS-positive nerve fibers weresignificantly decreased at both the 3rd week ( 17 ± 4) and the 6th month (16 ± 4). For the unilateral injury group, thenNOS-positive nerve fibers were similarly decreased on the side of the neurotomy at the 3rd week (18 ± 6), but by the 6thmonth, the number increased significantly (61±9) and approximated th     

Studies on plasma endothelin changes in varicocele patients

Aim: To investigate the possible role endothelin may play in the pathogenesis of varicocele and varicocele-induced infer-tility. Methods: In varicocele patients, radioimmunoassay is used to determine the blood endothelin concentration inthe spermatic vein and the antecubital vein separately. Results: The blood endothelin concentration of the spermaticvein (66.8±23.5 pg/mL) was significantly higher (P <0.05) than that of the antecubital vein (55.3±25.3 pg/mL).The endothelin concentration in the spermatic vein in Grade Ⅱ varicocele patients was not significantly different from thatin Grade Ⅲ patients ( P = 0.87). Conclusion: The higher blood endothelin level in the spermatic vein may indicate theinvolvement of endothelin in the pathophysiology of varicocele and varicocele-induced infertility. (Asian J Androl 1999Sep ; 1: 159 - 160)     

Nodular glomerulosclerosis with deposition of monoclonal immunoglobulin heavy chains lacking C(H)1

The objective of this study was to further characterize the clinical and immunopathologic features of heavy chain deposition disease (HCDD), a recently described entity. Four patients were diagnosed as having HCDD on a kidney biopsy. All presented with nodular glomerulosclerosis with deposition of gamma1 heavy chains lacking CH1 epitopes, but without light chains. Two different patterns were observed in the serum. First, patients 1 and 2 had a circulating monoclonal IgGlambda containing a short gamma1 heavy chain lacking CH1 epitopes, with an apparent molecular weight of 40 kD consistent with a complete CH1 deletion. Biosynthetic experiments also showed that the deleted heavy chain was produced in excess compared with light chains, and was secreted in vitro together with half Ig molecules, although these abnormal components were not detected by Western blot analysis of whole serum. Second, patients 3 and 4 had a circulating monoclonal IgG1lambda with an apparently normal, nondeleted heavy chain subunit, but serum fractionation followed by immunoblotting revealed an isolated monoclonal gamma1 chain lacking CH1 epitopes. These data strongly suggest that renal deposition of a CH1-deleted heavy chain circulating in low amounts in the serum as a free unassembled subunit is a major feature of HCDD. The CH1 deletion is most likely responsible for the premature secretion in blood of the heavy chain by a clone of plasma cells.