Y-27632 attenuates IR-induced hepatic microcirculation disruption by inhibiting contraction of HSCs.

Intraoperative NIRS enables quantification of the extent of congestion in the anterior segment after implantation of a right lobe liver graft and even enables prediction of such congestion at the phase of ex vivo perfusion.

Objective The purpose of this study was to determine how calcitonin gene related peptide (CGRP) via axon reflex participates in increasing local muscle blood flow (MBF) following manual acupuncture (MA). Methods Male Sprague-Dawley rats (N=56, 270-350 g) were used. We examined (1) the effects of MA on MBF in the tibialis anterior (TA) muscle in normal rats; (2) the effects of MA on MBF in the TA injected with saline or hCGRP (low: 2×10 −4 mol/litre; high: 2×10 −3 mol/litre), a competitive CGRP receptor antagonist, in rats; and (3) the effects of MA on MBF in the TA in capsaicin-treated rats. The capsaicin-treated rats were injected with capsaicin dissolved in an ethanol solution within 24 h after birth (50 mg/ kg subcutaneously). MA was applied to the right TA for 1 min. 51Cr-labelled microspheres (15 μm in diameter) were used to measure MBF. Results MA significantly increased MBF without changing arterial blood pressure in normal rats ( p<0.05). MA also significantly increased MBF in saline-injected, low hCGRP 8-37 -injected and high hCGRP 8-37 -injected rats ( p<0.001, 005 and 0.05, respectively). The increases in low and high hCGRP 8-37 -injected rats were lower than those in saline-injected rats, but the difference was not significant. However, MA did not significantly increase MBF in capsaicin-treated rats ( p=0.38). Conclusions We obtained conflicting results, suggesting that the participation of CGRP released via axon reflex may be limited to a local increase in MBF following MA.

The findings indicate that dHGF may prevent chronic liver-allograft dysfunction and thus may become a novel treatment for chronic liver-allograft dysfunction.

No abstract

The pathway leading to cell death in clinical liver transplantation is not known. Eight liver transplant recipients and eight donors were enrolled in this study. Postoperative serum levels of alanine transferase had significantly increased in the recipients compared with those in the donors. Mild centri-lobular necrosis was observed in only liver tissues taken from the recipients. Tumor necrosis factor (TNF)-R1 and death receptor 5 expression levels had increased in liver tissues taken from the recipients. There were no changes in the levels of Fas/Fas ligand expression in liver tissues from either the donors or recipients. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) expression was down-regulated in donor liver after hepatectomy and liver allograft after implantation. The results suggest that, although ischemic liver injury was not serious, due to the short ischemia time, TNF and TRAIL signals are associated with liver ischemic injury in live-donor liver transplantation but Fas signal is not.

Graft-versus-host disease (GVHD) after liver transplantation is uncommon but is a serious complication that can be fatal. Hemophagocytic syndrome (HPS), which is caused by activation of autologous T lymphocytes, is also a serious complication that can occur after liver transplantation. Because these complications share the clinical triad of skin rash, marrow failure, and diarrhea, differential diagnosis is difficult. We describe a case of severe GVHD resembling HPS in clinical features that occurred after living-related liver transplantation. The patient who had undergone the transplantation had high fever, pancytopenia, and skin rash 3 wk after the operation. Examination of a bone-marrow biopsy sample revealed the presence of abundant monocytes with phagocytosis, suggesting either GVHD or HPS. Donor human leukocyte antigens were detected in the peripheral blood of the patient by polymerase chain reaction, but this finding is not specific for GVHD. A definitive diagnosis was made by demonstration of remarkable anti-self response and undetectable anti-donor response in a mixed lymphocyte reaction assay using carboxyfluorescein diacetate succinimidyl ester.

Objective To investigate the contributions of nitric oxide (NO) and prostaglandins (PGs) to the increase in local muscle blood flow (MBF) observed following manual acupuncture (MA). Methods Male Sprague-Dawley rats (n=112; 250-310 g) were injected intraperitoneally with a non-selective NO synthase inhibitor (NG-nitro-Larginine methyl ester hydrochloride: L-NAME; 10, 50 or 500 mg/kg), a non-selective cyclooxygenase inhibitor (indomethacin; 10, 50 or 500 mg/kg), a combination of L-NAME and indomethacin (500 mg/kg each) or saline only under urethane anaesthesia (1.2 g/kg). We used the sparrow pecking technique for 1 min with a stainless steel acupuncture needle (0.20×30 mm) as the acupuncture stimulation method. The stimulus point was on the right tibialis anterior muscle. 51Chromium-labelled microspheres were used for MBF measurement. Results MA increased MBF in the saline-injected group ( p<0.001). This increase was partially inhibited by L-NAME in a dose-dependent manner ( p>0.05, p<0.05 and p<0.001 for 10, 50 and 500 mg/kg, respectively). On the other hand, indomethacin did not suppress the increase ( p>0.05 each for 10, 50 and 500 mg/kg). No significant difference was observed between the inhibitory effects of combined administration of L-NAME and indomethacin and single administration of L-NAME ( p>0.05). Conclusions These results suggest that NO is a major factor in the MA-induced increase in MBF, while PGs do not contribute significantly to this increase. As complete inhibition was not achieved by administration of L-NAME±indomethacin, it appears that non-NO and non-PG vasodilators are additionally involved. BACKGROUNDAcupuncture induces analgesia and functional improvement in various types of