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BackgroundDonor brain death (BD) is an independent risk factor for graft survival in recipients. While in some patients BD results from a fast increase in intracranial pressure, usually associated with trauma, in others, intracranial pressure increases more slowly. The speed of intracranial pressure increase may be a possible risk factor for renal and hepatic graft dysfunction. This study aims to assess the effect of speed of BD induction on renal and hepatic injury markers.MethodsBD induction was performed in 64 mechanically ventilated male Fisher rats by inflating a 4.0F Fogarty catheter in the epidural space. Rats were observed for 0.5, 1, 2 or 4 h following BD induction. Slow induction was achieved by inflating the balloon-catheter at a speed of 0.015 ml/min until confirmation of BD. Fast induction was achieved by inflating the balloon at 0.45 ml/min for 1 min. Plasma, kidney and liver tissue were collected for analysis.ResultsSlow BD induction led to higher plasma creatinine at all time points compared to fast induction. Furthermore, slow induction led to increased renal mRNA expression of IL-6, and renal MDA values after 4 h of BD compared to fast induction. Hepatic mRNA expression of TNF-α, Bax/Bcl-2, and protein expression of caspase-3 was significantly higher due to slow induction after 4 h of BD compared to fast induction. PMN infiltration was not different between fast and slow induction in both renal and hepatic tissue.ConclusionSlow induction of BD leads to poorer renal function compared to fast induction. Renal inflammatory and oxidative stress markers were increased. Liver function was not affected by speed of BD induction but hepatic inflammatory and apoptosis markers increased significantly due to slow induction compared to fast induction. These results provide initial proof that speed of BD induction influences detrimental renal and hepatic processes which could signify different donor management strategies for patients progressing to BD at different speeds.

The therapeutic benefit of extended lymphadenectomy in patients with gastric cancer is not generally accepted. We therefore analyzed the data of 82 patients with total gastrectomy and extended lymphadenectomy (compartment I: lymph nodes 1-6 and compartment II: lymph nodes 7-11) from 1979 to 1986 (GL group) for morbidity, mortality and survival and compared these with the results of a historical control group of 81 patients from 1971 to 1986 (group G), who similarly had undergone total gastrectomy but only compartment-I lymphadenectomy (lymph nodes 1-6). The 30-day operative mortality in the GL group was 6% (5/82), which was no higher than that of the control group (9.5%, 4/42) during the same observation period (1979-1986). The comparison of the actuarial survival according to the old TNM system (UICC 1978) in both groups showed no significant differences: stages I and II P = 0.22, stage III P = 0.29, all curative cases (stages I+II+III) P = 0.12. In addition, the patients of the GL group were restaged according to the new TNM system (UICC 1987). The calculated 5-year survival rate in this group was: stage I, 89%; stage II, 64%; stage III, 21%; curative total (stages I+II+III), 62%; stage IV, 0%. All patients (n = 12) with involvement and dissection of lymph nodes of compartment II died within 38 months. Only two of these patients (17%) had a potentially curative operation. Our results indicate that compartment-II lymph node dissection did not influence the operative mortality or the prognosis compared with compartment-I lymphadenectomy. Since patients with positive lymph nodes in compartment II did not benefit from the extended lymph node dissection of this area, obviously because of systemic spread, the question of the effectiveness of the extended lymphadenectomy remains unresolved.

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