[Biliobiliary fistula (Corlette type I): a case report with preoperative diagnosis by magnetic resonance cholangio-pancreatography].
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Biomedical subjects
Publications and source records attributed to I Takeyoshi.
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BACKGROUND: Ischemia-reperfusion injury may result in the local release of proinflammatory cytokines. A newly synthesized organic compound, FR167653, has been characterized as a potent suppressant of interleukin-1beta and tumor necrosis factor-alpha. We investigated the effects of FR 167653 on ischemia-reperfusion injury of canine hearts during preservation and transplantation. METHODS: Seventeen pairs of adult mongrel dogs were used. The donor heart was removed, stored in University of Wisconsin solution at 4 degrees C for 12 hours, and then transplanted orthotopically. Recipients were divided into the FR-treated group (FR167653 1 mg/kg/hr, 8 dogs) and the control group (9 dogs). Hemodynamic parameters, including cardiac output, left ventricular pressure (LVP), and the maximum rate of increase of LVP, were assessed after 120 minutes of reperfusion. The heart specimen was then harvested for histopathologic examination. RESULTS: The values of LVP (mm Hg) of the FR-treated and the control groups were 120+/-10 and 79+/-9, respectively. The values of LV dp/dt (mm Hg/sec) in the FR-treated and control groups were 4944+/-414 and 2292+/-380, respectively. There were significant differences in LVP (P < .05) and the maximum rate of increase of LVP (P < .01) between the two groups. The values of cardiac output (L/min) of the FR-treated and control groups were 1.27+/-0.12 and 0.71+/-0.11 of the baseline, respectively, showing a significant difference (P < .05) between the two groups. Histopathologic findings included irregular glycogen distribution in myocardial cells of the control group, although this change was less frequent in the FR-treated group. CONCLUSION: FR 167653 seems to have a protective effect on tissue subjected to ischemia-reperfusion injury during the acute phase after heart transplantation.
BACKGROUND: Ischemia-reperfusion injury may result in the local release of proinflammatory cytokines. A newly synthesized organic compound, FR167653, has been characterized as a potent suppressant of interleukin-1 beta and tumor necrosis factor-alpha. We investigated the effects of FR167653 on ischemia-reperfusion injury of the lung by using an in situ warm lung ischemia model in dogs. METHODS: Thirteen dogs were divided into two groups; seven dogs were assigned to the control group, and six were assigned to the FR167653-treated group. The latter group was administered FR167653 (1 mg/kg/hr) continuously beginning 30 minutes before induced ischemia and ending 2 hours after reperfusion. Warm ischemia was induced for 3 hours by clamping the pulmonary artery and veins. The left main bronchus was bisected and anastomosed 3 hours later. Arterial oxygen saturation, left pulmonary vascular resistance, and cardiac output were measured. Blood was collected to measure interleukin-1 beta level, and the lung specimen was harvested for histologic study. RESULTS: Arterial oxygen saturation levels after 30 minutes and 2 hours of reperfusion were significantly (p < 0.05) higher in the FR167653-treated group than in the control group. After 30 minutes of reperfusion, cardiac output deterioration was significantly (p < 0.05) greater in the control group than in the FR167653-treated group, and left pulmonary vascular resistance was significantly (p < 0.05) lower in the FR167653-treated group than in the control group. The 3-day survival rate was 67% in the FR167653-treated group and 14% in the control group. There were statistically significant differences (p < 0.05) between the survival rates of the two groups. Alveolar damage with interstitial edema and hyaline membranes localized along the alveolar duct were observed in the control group; whereas reduced interstitial edema was observed in the FR167653-treated group. Blood levels of IL-1 beta were lower in the FR167653-treated group than in the control group. CONCLUSION: FR167653 seems to generate a protective effect relative to ischemia-reperfusion injury of the lung in the early stage of tissue damage.
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Lazaroids have been reported to attenuate preservation and reperfusion injury. In this study, we examined whether lazaroids can improve the outcome after 48-hr canine liver preservation and transplantation. Adult female beagle dogs were randomized into 4 dosage groups (5 animals each). Lazaroid U-74389G was intravenously administered at a dose of 0 mg/kg, 6 mg/kg, 10 mg/kg, or 15 mg/kg to donors 30 min before harvesting and also to recipients 30 min before revascularization. Control animals (0 mg/kg) were given the lazaroid vehicle. The liver grafts were orthotopically transplanted after 48 hr of hypothermic preservation in UW solution. Lazaroid treatment significantly improved outcome after transplantation. Five-day animal survival increased from 0% in the control to 60% in the 6 mg/kg group, 100% in the 10 mg/kg group, and 80% in the 15 mg/kg group. Lazaroid protected the hepatocytes from damage during preservation, and enhanced energy charge and hepatic blood flow after reperfusion. Histological alterations were significantly less severe in the lazaroid-treated groups. The area of necrotic hepatocytes decreased from 43.7 +/- 17.7 in the control to 13.5 +/- 3.0 in the lazaroid 10 mg/kg group. These results indicate that lazaroid U-74389G has potential for improvement of clinical liver preservation.
Mucosal injury caused by ischemia and reperfusion has been well documented with the small intestine, but little is known about the colon. In the present study, the effect of warm and cold ischemia on the canine colon was studied and compared to that on the small intestine. After in situ flushing, the small intestine and the colon from six beagle dogs were removed and stored for 0.5, 1.5, and 3 hr at 37 degrees C (warm ischemia) or for 1, 6, 12, 24, 36, and 48 hr at 4 degrees C (cold ischemia). Electrophysiology, permeability, biochemistry, and histopathology of the specimens at each ischemic period and after reperfusion in the Ussing chamber were determined. Warm and cold ischemia induced duration-dependent suppression of electrophysiology in both organs, but the colonic mucosa retained higher activity of absorptive enterocytes and cryptic cells than the small intestine. Only the colon showed increased permeability of FITC-conjugated Dextran from the mucosal surface to the submucosal layer after prolonged ischemia. Changes in adenine nucleotides and purine catabolites were not markedly different between the organs. Histopathologic abnormalities during ischemia and after reperfusion were more serious with the small intestine than with the colon. Compared to warm ischemia, hypothermia lessened or delayed these morphofunctional derangements in both organs, which became universally worsened after reperfusion. Colonic mucosa receives morphofunctional derangements from ischemia and reperfusion, but the severity of the damage was much less severe in the colon than in the small intestine.
While machine preservation reduces the incidence of delayed graft function in renal transplant recipients, it is only used in 10% of kidney transplantations. The performance of our portable, low-flow-pulsatile organ perfusion system was examined in a canine kidney autotransplantation model. Grafts were stored for 72 h by simple cold preservation in University of Wisconsin (UW) solution, or by high or low-flow machine preservation After preservation, the grafts were autotransplanted and the animals were followed for 15 days. Graft function was better in machine-preserved kidneys. Tissue biochemistry indicated that machine preservation resulted in higher levels of adenine nucleotides and better histological integrity than the cold storage. While histology and biochemistry of machine-preserved groups were similar, electromicroscopy of high-flow grafts showed mild accumulation of intravenous debris and endothelial swelling. This study shows that a simplified machine perfusion technique is effective for organ preservation.
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The demand for glutamine increased only in the preserved intestine in the early postoperative period (3 days after transplantation). Glutamine demand of the preserved grafts returned to control and immediate levels 7 and 14 days after transplantation. Three days after intestinal transplantation, when the intestinal mucosa was actively regenerating, the demand for glutamine was markedly enhanced. The enhanced demand for glutamine was met by increased output of glutamine by the liver and skeletal muscle. Glutamine uptake by the intestinal graft was enhanced by a brief infusion of glutamine. Thus, we believe exogenous glutamine supplementation may be beneficial for the recovery of intestinal grafts with severe mucosal injury.
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A 76-year-old Japanese woman with hepatic encephalopathy was successfully treated for congenital splenorenal shunts by surgical intervention. The flow volume of the splenorenal shunts was 800 ml/min with a shunt pressure of 9.8 mmHg. The portal pressures before and after the shunt resection were 9 mmHg and 12 mmHg, respectively. The portal flows before and after the shunt resection were 230 ml/min and 470 ml/min, respectively. Therefore, both the hepatic sinusoid and the portal vein might provide good compliance for an increased portal flow volume load after shunt resection.
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