The Journal of surgical research最新文献

{"title":"Immune-enhancing enteral diet selectively augments ileal blood flow in the rat.","authors":"D. Rhoden, P. Matheson, N. D. Carricato, D. Spain, R. Garrison","doi":"10.1006/JSRE.2002.6424","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6424","url":null,"abstract":"BACKGROUND\u0000Clinical studies show that immune-enhancing enteral diets (IED; with L-arginine, fish oil, and RNA fragments) decrease the rate of sepsis and shorten the length of hospital stay after the start of enteral feeding. These beneficial effects are dependent on the route of administration (enteral vs parenteral) and on the nutrient composition (IED vs standard diets). Gut exposure to an IED seems to preserve and/or augment intestinal mucosal immunity. However, nutrient absorption stimulates gut blood flow in a nutrient-specific manner (i.e., postprandial hyperemia). We hypothesized that an IED would initiate a different pattern of whole organ blood flow compared to a standard diet. This suggests that a mechanism for the protective effect of IED might be the preferential augmentation of gut blood flow to gut-associated lymphoid tissue (GALT) or mucosa-associated lymphoid tissue (MALT).\u0000\u0000\u0000METHODS\u0000Male Sprague-Dawley rats (200-225 g) were anesthetized and cannulated for colorimetric microsphere determination of blood flow distribution (with the phantom organ technique). Animals received gastric gavage (2 ml) of an IED (Impact; Novartis) or an isocaloric, isonitrogenous control diet (Boost; Mead-Johnson). Blood flow to the antrum, duodenum, jejunum, ileum, colon, liver, kidneys, and spleen was determined at baseline and 30, 60, 90, and 120 min after gavage.\u0000\u0000\u0000RESULTS\u0000Baseline blood flows to the left and right kidneys were within 10%, indicating the technical integrity of the microsphere technique and assay. Control diet augmented blood flow compared to IED in the antrum, duodenum, jejunum, and spleen. Conversely, IED gavage stimulated a delayed and sustained hyperemic response in the ileum. IED also increased hepatic blood flow early (30 min). IED increased blood glucose levels compared to control diet at 30, 60, and 90 min, suggesting enhanced nutrient absorption.\u0000\u0000\u0000CONCLUSIONS\u0000These data show that blood flow distribution depends on nutrient composition and that IED preferentially augments blood flow to the ileum. Since the terminal jejunum and ileum contain much of the GALT, our data suggest that a mechanism for enterally stimulated mucosal immunity involves selective perfusion of the terminal ileum during IED nutrient absorption.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"125 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124604767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic endosomal trafficking of lipoprotein-bound endotoxin in rats.","authors":"H. Harris, S. Brady, J. Rapp","doi":"10.1006/JSRE.2002.6413","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6413","url":null,"abstract":"Triglyceride-rich lipoproteins (chylomicrons (CM), VLDL) can bind and protect against endotoxin (LPS)-induced shock and mortality in rodents. The protective effect of lipoproteins is in part due to the increased plasma clearance and biliary excretion of LPS. Specifically, CM-LPS complexes are principally removed from the circulation by the liver with a rapid plasma half-life approximating that for CM alone. Thus, we hypothesized that hepatocytes clear CM-bound LPS via known lipoprotein receptors and traffic the toxic macromolecule through the same endosomal pathway employed for the catabolism of triglyceride-rich lipoproteins. To examine the endosomal uptake and biliary excretion of LPS, we isolated early and late hepatic endosomal fractions and hepatic bile from rats following the injection of radiolabeled CM-bound LPS. The uptake of (125)I-LPS was compared in animals that overexpressed either the LDL receptor or the LDL receptor-related protein (LRP) versus untreated control with normal lipoprotein levels. Herein we present data indicating that both the LDL receptor and the LRP participate in the rapid internalization of CM-bound LPS by hepatocytes. Upregulation of the LDL receptor increased the accumulation of (125)I-LPS in late endosomes (P < 0.03). In contrast, increased levels of the LRP were associated with negligible movement of LPS into late endosomes but a trend toward the increased biliary excretion of the radiolabeled macromolecule. Taken together these data further elucidate the role of the liver in the host innate immune response to infection and potentially implicate distinct roles for the LDL receptor and LRP in the catabolism of CM-bound LPS.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"71 4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128011472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of PKC in the late phase of microvascular protection induced by preconditioning.","authors":"Wei Z. Wang, Linda L. Stepheson, G. Anderson, F. Miller, K. Khiabani, W. A. Zamboni","doi":"10.1006/JSRE.2002.6427","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6427","url":null,"abstract":"INTRODUCTION\u0000We hypothesized that the late phase of microvascular protection induced by ischemic preconditioning or by adenosine is protein kinase C (PKC) dependent.\u0000\u0000\u0000MATERIALS AND METHODS\u0000The cremaster muscle of male Sprague-Dawley rats underwent 45 min of ischemic preconditioning and, 24 h later, 4 h of warm ischemia followed by 60 min of reperfusion. To mimic the effects of IPC, adenosine (ADO; an adenosine receptor agonist) or 4-phorbol 12-myristate 13-acetate (PMA; a PKC activator) was delivered to the vascular network of the cremaster 24 h before the prolonged ischemia via local intra-arterial infusion. To block the microvascular protection induced by ADO or IPC, chelerythrine (CHE; a PKC blocker) was given by local intra-arterial infusion prior to the administration of ADO or the initiation of IPC. Microvascular responses in the cremaster muscle to ischemic preconditioning or pharmacological preconditioning were determined by measuring terminal arteriole diameter and capillary perfusion using intravital microscopy and by the evaluation of the endothelium-dependent nitric oxide system in terminal arterioles.\u0000\u0000\u0000RESULTS\u0000Blockade of PKC using CHE on day 1 eliminated both ADO- and IPC-induced microvascular protections seen on day 2. However, the microvascular protection induced by the administration of PMA (without IPC) that was given 24 h before the 4 h of warm ischemia/reperfusion was significantly better than the control group response (sham IPC), but was not as good as the protection induced by IPC or ADO alone.\u0000\u0000\u0000CONCLUSION\u0000The overall results from these studies suggest that ischemic or ADO preconditioning induces late-phase microvascular protection in skeletal muscle by a PKC-dependent mechanism.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"62 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126549317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of nitric oxide in ischemia/reperfusion of the pancreas.","authors":"S. Benz, R. Obermaier, R. Wiessner, P. Breitenbuch, D. Burska, H. Weber, R. Schnabel, J. Mayer, F. Pfeffer, H. Nizze, U. Hopt","doi":"10.1006/JSRE.2002.6457","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6457","url":null,"abstract":"BACKGROUND\u0000Ischemia/reperfusion injury, and thus graft pancreatitis, remains a major problem in pancreas transplantation. Contradictory results about the role of nitric oxide (NO) in pancreatic ischemia/reperfusion have been reported; however, in none of the reports has a detailed comparison between inhibition of NO synthase and NO supplementation been carried out.\u0000\u0000\u0000METHODS\u0000Vascular isolation of the pancreatic tail was performed in landrace pigs. After splenectomy catheters placed in the distal part of the splenic vessels allowed collection of the venous effluent and perfusion of the pancreatic tail. Three hours of complete warm ischemia was followed by 6 h of reperfusion. The effect of the NO donor sodium nitroprusside (SNP) and L-arginine was compared to a control group and NO synthase inhibition with L-NAME.\u0000\u0000\u0000RESULTS\u0000Lipase in the venous effluent of the pancreas was significantly decreased in the SNP and the L-arginine groups. Vascular resistance was markedly elevated in the L-NAME group and reduced in the NO donor groups. Tissue pO2 after reperfusion was only significantly elevated in the SNP group. Granulocyte infiltration and also overall histological tissue injury were most severe in the control group followed by the L-NAME group, the SNP group, and the L-ARG group.\u0000\u0000\u0000CONCLUSION\u0000The data show that supplementation of nitric oxide is clearly protective in pancreatic ischemia/reperfusion. However, inhibition of NO synthesis does not lead to an equally clear aggravation of tissue injury.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"9 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124004196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulmonary hypoplasia and congenital diaphragmatic hernia: advances in the pathogenetics and regulation of lung development.","authors":"M. R. Chinoy","doi":"10.1006/JSRE.2002.6390","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6390","url":null,"abstract":"","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120239153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impairment of activation of hepatocyte growth factor precursor into its mature form in rats with liver cirrhosis.","authors":"M. Kaibori, Tomohisa Inoue, Y. Sakakura, M. Oda, T. Nagahama, A. Kwon, Y. Kamiyama, K. Miyazawa, T. Okumura","doi":"10.1006/JSRE.2002.6438","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6438","url":null,"abstract":"BACKGROUND\u0000Hepatocyte growth factor (HGF) has a crucial role in liver regeneration following injury. The conversion of an inactive precursor form of HGF (proHGF) into a biologically active form (mature HGF) is essential, as HGF is involved in the recovery of liver damage. Liver regeneration is markedly poor in patients with liver cirrhosis after resection. We hypothesized that impairment of liver regeneration in cirrhosis is in part because of the absence of activation of proHGF to mature HGF. Studies were performed to clarify the molecular form of HGF in the liver of rats with fibrosis/cirrhosis before and after liver resection.\u0000\u0000\u0000METHODS\u0000Rat models of liver fibrosis/cirrhosis were induced by intraperitoneal administration of dimethylnitrosamine, followed by 45% partial hepatectomy or sham operation. HGF was purified from the liver and plasma on a SP-Sepharose column and was analyzed by Western blotting.\u0000\u0000\u0000RESULTS\u0000Production of proHGF in the liver increased in the following order: rats with normal liver, rats with fibrosis, and rats with cirrhosis. However, the levels of proHGF were similar after liver resection in the liver of these groups. A small but significant level of mature HGF was detected before resection in the fibrosis group, but not in the normal and cirrhosis groups. Liver resection increased the levels of mature HGF in the normal and fibrosis groups, but marginally in the cirrhosis group.\u0000\u0000\u0000CONCLUSIONS\u0000These results demonstrate that the conversion of proHGF into mature HGF is impaired after liver resection in liver cirrhosis, while proHGF production is similar in the livers of normal, fibrosis, and cirrhosis groups. Acceleration of the processing of the HGF molecule may contribute to the improvement of liver dysfunction in cirrhosis.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"79 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124308126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional heterogeneity of the kupffer cell population is involved in the mechanism of gadolinium chloride in rats administered endotoxin.","authors":"H. Kono, H. Fujii, M. Asakawa, Masayuki Yamamoto, A. Maki, M. Matsuda, I. Rusyn, Y. Matsumoto","doi":"10.1006/JSRE.2002.6434","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6434","url":null,"abstract":"BACKGROUND\u0000The purpose of this study was to determine if evidence of functional heterogeneity between subtypes of the Kupffer cell (KC) may be involved in the mechanism of the protective effect of gadolinium chloride (GdCl3) in endotoxemia.\u0000\u0000\u0000METHODS\u0000Rats pretreated with or without GdCl3 were administered lipopolysaccharide (LPS) or vehicle. Serum and liver tissues were collected after LPS administration for cytokine measurements and pathological and immunohistochemical evaluation.\u0000\u0000\u0000RESULTS\u0000After LPS administration, increases in expression of TNF-alpha and IL-6 mRNA in the liver were blunted significantly by GdCl3. In control liver tissue, ED2-positive cells were a predominant fraction, with a few ED1-positive cells, and GdCl3 eliminated only ED2-positive cells. Further, ED2-positive cells were larger in size than ED1-positive ones. Importantly, the number of ED1-positive cells in the liver was increased about threefold in the control group but not in the GdCl3 group after LPS injection. Intermediate or large KCs isolated by counterflow centrifugal elutriation showed greater capacity for phagocytosis and production of superoxide and TNF-alpha than small ones. In contrast, IL-6 production was increased to a greater extent in small than in intermediate or large cells. GdCl3 eliminated the intermediate or large KC subpopulation predominantly.\u0000\u0000\u0000CONCLUSION\u0000Collectively, functional heterogeneity of the KC population was involved in the mechanism of the protective effects of GdCl3 in endotoxemia. TNF-alpha derived from activated intermediate or large KCs may activate small KCs and the latter may be recruited to other organs, such as lungs and kidneys, and produce a large amount of IL-6, leading to multiple organ failure.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128530401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk factors for conversion of laparoscopic to open cholecystectomy.","authors":"S. Kanaan, K. Murayama, L. Merriam, L. Dawes, J. Prystowsky, R. Rege, R. Joehl","doi":"10.1006/JSRE.2002.6393","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6393","url":null,"abstract":"BACKGROUND\u0000Laparoscopic cholecystectomy (LC) has become the treatment of choice for symptomatic gallstones; however conversion to open cholecystectomy (OC) remains a possibility. Unfortunately, preoperative factors indicating risk of conversion are unclear. Therefore, we aimed to identify risk factors associated with conversion of LC to OC.\u0000\u0000\u0000PATIENTS AND MATERIALS\u0000Records of 564 patients undergoing LC in 1995 and 1996 were reviewed. Patients were assigned to one of two groups: (1) acute cholecystitis defined by the presence of gallstones, fever, leukocyte count >10(4), and inflammation on ultrasound or histology; (2) chronic cholecystitis that included all other symptomatic patients. Demographics, history, and physical, laboratory, and radiology data, operative note, and the pathology report were reviewed.\u0000\u0000\u0000RESULTS\u0000161 of 564 patients, had acute and 403 patients had chronic cholecystitis; 16 acute cholecystitis patients (10%) were converted from LC to OC and 17 chronic cholecystitis patients (4%) had LC converted to OC. Patients having open conversion were significantly older, had greater prevalence of cardiovascular disease, and were more likely to be males. LC conversion to OC in acute cholecystitis patients was associated with a greater leukocyte count; in gangrenous cholecystitis patients, 29% had open conversion.\u0000\u0000\u0000CONCLUSIONS\u0000Importantly, these risk factors-older men, presence of cardiovascular disease, male gender, acute cholecystitis, and severe inflammation-are determined preoperatively, permitting the surgeon to better inform patients about the conversion risk from LC to OC. While acute cholecystitis was associated with more than a twofold increased conversion rate, only 10% of these patients could not be completed laparoscopically. Therefore, acute cholecystitis alone should not preclude an attempt at laparoscopic cholecystectomy.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"31 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124784716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Significance of altered bilirubin subfractions in bile following hepatectomy.","authors":"K. Suto, A. Fuse, Y. Igarashi, W. Kimura","doi":"10.1006/JSRE.2002.6437","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6437","url":null,"abstract":"BACKGROUND\u0000Hyperbilirubinemia occurs as a sign of hepatic failure after hepatectomy. The pathogenesis of this event has not been elucidated. In cases complicated with postoperative infection, hyperbilirubinemia is prolonged and the composition of bilirubin subfractions in bile changes markedly. A reduction in the proportion of bilirubin diglucuronide (BDG) is especially notable. This study was aimed at clarifying the relationship between infection and biliary bilirubin subfractions, with a view to shedding light on the mechanisms of change.\u0000\u0000\u0000MATERIALS AND METHODS\u0000Rats underwent either laparotomy or partial hepatectomy (Hx). Daily intraperitoneal injections of lipopolysaccharide (LPS) or natural saline were administered for 3 days following surgery. Total serum bilirubin levels and proportions of BDG and bilirubin in bile were measured until Day 5 after the operation. Hepatic levels of UDP-glucuronic acid (UDP-GA), UDP-glucose, NAD(+), and total adenine nucleotides (TAN) and activities of UDP-glucuronyltransferase (UDP-GT) and UDP-glucose dehydrogenase were measured on Day 4.\u0000\u0000\u0000RESULTS\u0000In hepatectomized rats treated with LPS (Hx-LPS), total serum bilirubin levels were elevated, biliary bilirubin levels were decreased, and the proportion of biliary BDG was decreased on Day 4. Hepatic levels of UDP-GA, NAD(+), and TAN and activities of UDP-GT in Hx-LPS were reduced. In all groups tested, a significant linear correlation between BDG and UDP-GA and between UDP-GA and NAD(+) was found.\u0000\u0000\u0000CONCLUSIONS\u0000The reduction of UDP-GA might be effected by reduced hepatic levels of NAD(+) in endotoxemia following hepatectomy. It is therefore suggested that alterations in biliary bilirubin subfractions might accurately reflect the energy state of the remnant liver following hepatectomy.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"34 5 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127981498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of nitric oxide on the contractile function of rat reperfused skeletal muscle.","authors":"K. Ikebe, Teiji Kato, M. Yamaga, T. Tsuchida, H. Irie, Y. Oniki, K. Takagi","doi":"10.1006/JSRE.2002.6395","DOIUrl":"https://doi.org/10.1006/JSRE.2002.6395","url":null,"abstract":"BACKGROUND\u0000The involvement of nitric oxide (NO) in ischemia-reperfusion injury remains controversial and has been reported to be both beneficial and deleterious. The purpose of this study was to examine the contribution of NO and superoxide to skeletal muscle function using an ischemic revascularized hind limb model in rats.\u0000\u0000\u0000PATIENTS AND MATERIALS\u0000Warm ischemia produced by vascular pedicle clamping was sustained for 3 h. The animals were divided into four groups according to the solution administrated: (1) saline, (2) N-methyl-L-arginine acetate (L-NMMA), (3) L-NMMA + N-(N-L-g-glutamyl-S-nitroso-l-cysteinyl)glycine (S-nitrosoglutathione), or (4) superoxide dismutase (SOD). Saline, L-NMMA, or L-NMMA + S-nitrosoglutathione was infused for the first 2 h of reperfusion. The SOD was administered as an intravenous bolus 5 min before the onset of reperfusion. Postischemic blood flow was measured by a Doppler flow meter. Muscle contractile function was determined after 24 h of reperfusion.\u0000\u0000\u0000RESULTS\u0000Postischemic blood flow was significantly decreased by the L-NMMA infusion compared with that in the saline-treated group. No significant difference in postischemic blood flow was noted in the saline-, L-NMMA + S-nitrosoglutathione-, and SOD-treated groups. Contractile function of the gastrocnemius muscle in the L-NMMA-and SOD-treated groups, but not in the L-NMMA + S-nitrosoglutathione group, was significantly better than that in the saline-treated group.\u0000\u0000\u0000CONCLUSION\u0000Limiting postischemic blood flow and SOD infusion are both beneficial in decreasing the ischemia-reperfusion injury of skeletal muscle. S-Nitrosoglutathione infusion following suppression of endogenous NO production does not reduce ischemia-reperfusion injury.","PeriodicalId":191568,"journal":{"name":"The Journal of surgical research","volume":"60 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125510960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}