K Kawata

Gunma University, Maebashi, Gunma Prefecture, Japan

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Publications (13)27.2 Total impact

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    ABSTRACT: Abstract Small bowel transplantation (SBT) has become an increasingly promising treatment for short bowel syndrome. The evaluation of graft viability after SBT, however, has not been established, except by mucosal biopsy. We monitored intestinal mucosal acidity in order to detect small intestinal ischemia-reperfusion injury. Mongrel dogs were used in this study. After laparotomy, the small bowel was isolated with a vascular pedicle. A tonometer to measure intramucosal pH (pHi) was then positioned in the terminal ileum. The superior mesenteric artery was occluded with or without concomitant superior mesenteric vein occlusion for 60 or 120 min. The value of pHi was determined from laparotomy (baseline) to 12 h after reperfusion. Whole-thickness specimens of the ileum were taken before ischemia, just before reperfusion, and 1 h afterward. Mucosal injury was graded histopathologically. pHi decreased from baseline in relation to the degree of histopathological mucosal injury. There was a significant correlation between histological findings and the change in pHi. We conclude that monitoring intestinal mucosal acidity is a reliable way of determining graft viability after SBT.
    Transplant International 06/2008; 11(6):401 - 407. · 3.16 Impact Factor
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    ABSTRACT: Nitric oxide (NO) appears to play an important role in tissue injury during reperfusion. FK409 is the first spontaneous NO donor that increases plasma guanosine 3',5'-cyclic monophosphate. We investigated the effects of the NO donor FK409 (FK) on ischemia-reperfusion injury in a canine warm ischemia model. Fourteen adult mongrel dogs were divided into two groups: the control group and the FK group, which received FK. The superior mesenteric artery and vein were both clamped for 2 h and then reperfused for 12 h. Arterial and intramucosal pH were well maintained in the FK group in comparison with the control group. Histologically, ischemia-reperfusion injury was significantly more severe in the control group than in the FK group. The serum NO levels were significantly higher in the FK group than in the control group during FK administration. FK409 has protective effects on ischemia-reperfusion injury of the small intestine due to NO release.
    Digestive Diseases and Sciences 09/2001; 46(8):1748-56. · 2.26 Impact Factor
  • Transplantation Proceedings 02/2001; 33(1-2):862. · 0.95 Impact Factor
  • Transplantation Proceedings 02/2001; 33(1-2):883. · 0.95 Impact Factor
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    ABSTRACT: This study investigated the effects of a selective COX-2 inhibitor, FK3311, on warm ischemia-reperfusion (I/R) injury in the canine lung. Sixteen adult mongrel dogs were used in this study. In the FK group (n = 8), FK (1 mg/kg) was administered intravenously 15 min before ischemia and 15 min before reperfusion. In the control group (n = 8), a vehicle was injected in the same manner. Warm ischemia was induced for 3 h by clamping the left pulmonary artery, veins, and bronchus. Five-minute clamping tests of the right pulmonary artery were performed before ischemia and 30 min after reperfusion. During the test, left pulmonary vascular resistance (L-PVR), cardiac output (CO), and arterial oxygen pressure (PaO(2)) were measured. The lung specimens were simultaneously harvested for wet-to-dry weight ratio (WDR) measurements, histopathological studies, and polymorphonuclear neutrophil (PMN) counts. Serum thromboxane (Tx) B(2) and 6-keto-prostaglandin (PG) F(1alpha) (stable metabolites of TxA(2) and PGI(2), respectively) were also measured 30 min after reperfusion. L-PVR, CO, PaO(2), and WDR were significantly (P < 0.05) better in the FK group than in the control group. Histological tissue edema was mild, and PMN infiltration was significantly (P < 0.05) reduced in the FK group compared to the control group. The serum TxB(2) levels were significantly (P < 0.05) lower in the FK group than in the control group, while 6-keto-PGF(1alpha) levels were not significantly (P < 0.05) reduced. Two-day survival rate was significantly (P < 0.05) better in the FK group than in the control group. FK has protective effects on pulmonary I/R injury stemming from marked inhibition of TxA(2).
    Journal of Surgical Research 02/2001; 95(2):167-73. · 2.02 Impact Factor
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    ABSTRACT: BACKGROUND:Liver grafts from non-heart-beating donors inevitably suffer from warm ischemic injury. In these grafts, large quantities of inflammatory cytokines and arachidonic acid metabolites are induced, further aggravating injury. Cyclooxygenase (COX) is an intracellular enzyme that converts arachidonic acid into prostaglandin (PG)G2 and PGH2. COX has two isoforms: constitutive COX-1 and inducible COX-2. The aim of this study was to evaluate the effects of COX-2 inhibition by FK3311 (FK) on warm ischemic injury in a canine total hepatic vascular exclusion (THVE) model.STUDY DESIGN:Sixteen mongrel adult dogs were studied. The portal triad of the hilum and the inferior vena cava above and below the liver was clamped for 1 hour. Splanchnic decompression was achieved by active splenofemorojugular bypass. The animals were divided into two groups. FK (1 mg/kg) was administered in the FK group (n = 8), and saline was administered in the control group (n = 8). Hepatic venous blood was collected to measure serum alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase (LDH), and hyaluronic acid levels. Serum thromboxane (Tx)B2 and 6-keto-PGF1α levels were also measured. Hepatic tissue blood flow was estimated simultaneously. Liver specimens were harvested for histologic study and polymorphonuclear neutrophils were counted.RESULTS:Alanine aminotransferase, aspartate aminotransferase, and hyaluronic acid 2 and 6 hours after reperfusion and LDH 30 minutes and 2 and 6 hours after reperfusion were significantly (p < 0.05) lower in the FK group than in the control group. Hepatic tissue blood flow remained significantly (p < 0.05) higher in the FK group than in the control group 1, 2, and 6 hours after reperfusion. Histologic tissue damage was mild and polymorphonuclear neutrophil infiltration was significantly lower (p < 0.05) in the FK group than in the control group 1 and 6 hours after reperfusion. Thirty minutes after reperfusion, TxB2 was significantly reduced (p < 0.05) in the FK group, and 6-keto-PGF1α was not significantly lower.CONCLUSIONS:FK protected against hepatic warm ischemia-reperfusion injury by marked inhibition of TxA2.
    Journal of the American College of Surgeons 01/2001; 192(1):54-62. · 4.50 Impact Factor
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    ABSTRACT: BACKGROUND:Liver grafts from non-heart-beating donors inevitably suffer from warm ischemic injury. In these grafts, large quantities of inflammatory cytokines and arachidonic acid metabolites are induced, further aggravating injury. Cyclooxygenase (COX) is an intracellular enzyme that converts arachidonic acid into prostaglandin (PG)G2 and PGH2. COX has two isoforms: constitutive COX-1 and inducible COX-2. The aim of this study was to evaluate the effects of COX-2 inhibition by FK3311 (FK) on warm ischemic injury in a canine total hepatic vascular exclusion (THVE) model.STUDY DESIGN:Sixteen mongrel adult dogs were studied. The portal triad of the hilum and the inferior vena cava above and below the liver was clamped for 1 hour. Splanchnic decompression was achieved by active splenofemorojugular bypass. The animals were divided into two groups. FK (1 mg/kg) was administered in the FK group (n = 8), and saline was administered in the control group (n = 8). Hepatic venous blood was collected to measure serum alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase (LDH), and hyaluronic acid levels. Serum thromboxane (Tx)B2 and 6-keto-PGF1α levels were also measured. Hepatic tissue blood flow was estimated simultaneously. Liver specimens were harvested for histologic study and polymorphonuclear neutrophils were counted.RESULTS:Alanine aminotransferase, aspartate aminotransferase, and hyaluronic acid 2 and 6 hours after reperfusion and LDH 30 minutes and 2 and 6 hours after reperfusion were significantly (p < 0.05) lower in the FK group than in the control group. Hepatic tissue blood flow remained significantly (p < 0.05) higher in the FK group than in the control group 1, 2, and 6 hours after reperfusion. Histologic tissue damage was mild and polymorphonuclear neutrophil infiltration was significantly lower (p < 0.05) in the FK group than in the control group 1 and 6 hours after reperfusion. Thirty minutes after reperfusion, TxB2 was significantly reduced (p < 0.05) in the FK group, and 6-keto-PGF1α was not significantly lower.CONCLUSIONS:FK protected against hepatic warm ischemia-reperfusion injury by marked inhibition of TxA2.
    Journal of the American College of Surgeons 01/2001; · 4.50 Impact Factor
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    ABSTRACT: IL-1 and TNF-alpha are known to be pleiotropic cytokines associated with various inflammatory conditions such as small intestinal injury after ischemia-reperfusion. FR167653 has been characterized as a potent suppressant of IL-1 and TNF-alpha production. The effect of FR167653 on intestinal reperfusion injury was investigated in a warm ischemia model of the canine gut. Sixteen mongrel dogs were divided into two groups: a control group and a FR group to which FR167653 was administered. Both the superior mesenteric artery and vein were clamped for 2 hr. Arterial pH, hepatic venous hemoglobin oxygen saturation, intramucosal pH, and the survival rate were well maintained in the FR group in comparison with the control group after reperfusion. FR167653 inhibited the expression of IL-1beta mRNA. Histologically, ischemia-reperfusion injury was more severe in the control group than the FR group. This study suggests that FR167653 inhibits proinflammatory cytokines and ameliorates ischemia-reperfusion injury of the small intestine.
    Digestive Diseases and Sciences 12/1999; 44(11):2334-43. · 2.26 Impact Factor
  • Transplantation Proceedings 12/1998; 30(7):3467-8. · 0.95 Impact Factor
  • Source
    Transplantation Proceedings 12/1998; 30(7):3703-4. · 0.95 Impact Factor
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    ABSTRACT: Small bowel transplantation (SBT) has become an increasingly promising treatment for short bowel syndrome. The evaluation of graft viability after SBT, however, has not been established, except by mucosal biopsy. We monitored intestinal mucosal acidity in order to detect small intestinal ischemia-reperfusion injury. Mongrel dogs were used in this study. After laparotomy, the small bowel was isolated with a vascular pedicle. A tonometer to measure intramucosal pH (pHi) was then positioned in the terminal ileum. The superior mesenteric artery was occluded with or without concomitant superior mesenteric vein occlusion for 60 or 120 min. The value of pHi was determined from laparotomy (baseline) to 12 h after reperfusion. Whole-thickness specimens of the ileum were taken before ischemia, just before reperfusion, and 1 h afterward. Mucosal injury was graded histopathologically. pHi decreased from baseline in relation to the degree of histopathological mucosal injury. There was a significant correlation between histological findings and the change in pHi. We conclude that monitoring intestinal mucosal acidity is a reliable way of determining graft viability after SBT.
    Transplant International 02/1998; 11(6):401-7. · 3.16 Impact Factor
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    ABSTRACT: Though liver grafts from non-heart-beating donors are now attracting much attention, these grafts inevitably suffer from severe warm ischemia. The aim of this study was to evaluate the effect of TNF-alpha and IL-1 suppression on warm ischemia-reperfusion injury in a canine total hepatic vascular exclusion model. Warm ischemia was induced by 1-h total hepatic vascular exclusion with active splenofemuro-juglar bypass. Animals were divided into two groups. FR167653 (1 mg/kg/hr) was administered via the portal vein from 30 min prior to ischemia until 2 h after reperfusion to the FR group (n = 7), and a vehicle was administered to the control group (n = 7). The serum alanine aminotransferase, aspartate amino-transferase, lactate dehydrogenase, and hyaluronic acid levels were measured. Hepatic tissue blood flow was also measured. Liver specimens were harvested for histological study, and polymorphonuclear neutrophils were counted. Serum liver enzymes were significantly (p < 0.05) lower, and hepatic tissue blood flow was kept significantly (p < 0.05) better in the FR group than in the control. Histological tissue damage was mild, and polymorphonuclear neutrophil infiltration was significantly (p < 0.05) lower in the FR group than in the control group. FR167653 provides protective effects on hepatic warm ischemic injury in a canine total hepatic vascular exclusion model.
    Hepato-gastroenterology 50(49):161-4. · 0.77 Impact Factor
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    ABSTRACT: The purpose of this study was to investigate the effects of a selective COX-2 inhibitor, FK3311, on warm ischemia-reperfusion injury of the canine small intestine. Ten adult mongrel dogs were used. FK (1 mg/kg) was administered intravenously 15 minutes prior to ischemia and 15 minutes prior to reperfusion in the FK group (n = 5), and only an inert vehicle was injected in the control group (n = 5). The superior mesenteric artery and vein were clamped closed for 2 hours and then unclamped for 12 hours of reperfusion. Arterial and intramucosal pH were measured, and samples were taken for histological examination at 1, 3, 6, and 12 hours after the start of reperfusion. Serum thromboxane B2 and 6-keto-prostaglandin F1 alpha (stable metabolites of TxA2 and PGI2) were measured 30 minutes after reperfusion began. Arterial and intramucosal pH changes were significantly (p < 0.05) smaller in the FK group than in the control group. Histological ischemia-reperfusion injury was significantly (p < 0.05) more severe in the control group than in the FK group. Serum thromboxane B2 and 6-keto-prostaglandin F1 alpha levels were significantly (p < 0.05) lower in the FK group compared to the control group. FK protects the small bowel from ischemia-reperfusion injury by suppression of prostanoid production.
    Hepato-gastroenterology 50(54):1970-4. · 0.77 Impact Factor