The effects of L-NG-nitroarginine in a zymosan-induced multiple organ dysfunction syndrome model.

BACKGROUND: The aim of this study was to investigate the role of nitric oxide in mesenteric ischemia, organ injury and survival in zymosan-induced multiple organ dysfunction syndrome (MODS) by using the nonselective nitric oxide synthase inhibitor L-N(G)-nitroarginine (L-NNA). METHODS: Swiss albino mice (20-40 g) were used in the study. The animals were randomly divided into four groups. The first group was treated intraperitoneally with saline and served as the sham group for L-NNA. The second group was treated with zymosan (500 mg/kg). The mice in the third and fourth group received L-NNA (20 mg/kg), 1 and 6 h after saline or zymosan administration. Six hours after the administration of zymosan, animals were used for mesenteric arterial blood flow (MABF) measurements and then sacrificed for biochemical and histopathological analyses at the 18th hour. RESULTS: In zymosan-treated animals, MABF was significantly lower than that of solvent saline-treated controls (controls: 4.7 +/- 0.8 ml.min(-1); zymosan: 1.7 +/- 0.7 ml.min(-1), p < 0.05). L-NNA did not prevent zymosan-induced MABF decrease (controls: 4.5 +/- 0.8 ml.min(-1); zymosan: 2.5 +/- 1.4 ml.min(-1), p <0.05). Also treatment with L-NNA has no beneficial effect on survival and organ injury in zymosan-induced MODS. CONCLUSION: In this study, inhibition of both inducible and constitutive nitric oxide synthase by L-NNA did not abolish the harmful effects of zymosan. L-NNA remains an agent without any therapeutic potential in this acute experimental model of MODS.

Heterogeneity of damage between segments of rat liver after inflow-outflow obstruction.

BACKGROUND: Total vascular exclusion (TVE) causes warm liver ischemia. The complete explanation of the events during inflow and outflow obstruction of the liver during selective TVE has not yet been studied. The aim of this study was to investigate the liver injury caused by inflow-outflow obstruction in the rat liver. MATERIALS AND METHODS: Forty Wistar-Albino rats were divided into four groups. Liver inflow occlusion (groups A and C) or inflow-outflow occlusion (groups B and D) was applied for 30 minutes. Samples were collected at the end of the ischemia period. We examined oxidative injury in the liver tissue and liver histopathology. RESULTS: Oxidative stress and histopathologic alterations were more prominent with TVE application. Significant alterations were shown in hepatic superoxide dismutase, glutathione, and glutathione S-transferase levels. Central segments of the rat liver were affected significantly from inflow occlusion, whereas dome segments were significantly damaged from inflow-outflow occlusion. CONCLUSIONS: Inflow-outflow occlusion of the liver caused more tissue damage compared with inflow occlusion. The pattern of distribution of the damage due to TVE seemed different from other well-known ischemia-reperfusion injuries.

Evaluation of liver damage after application of TVE in the rat model.

INTRODUCTION: The aim of this study was to investigate the effects of total vascular exclusion (TVE) on the liver during the early period of reperfusion. MATERIALS AND METHODS: Forty Wistar-Albino rats were divided into four groups. Portal pedicle clamping (groups 1 and 2) or TVE (groups 3 and 4) were applied for 10 minutes. Samples were collected at the time of clamp release (groups 1 and 3) and at 30 minutes of reperfusion (groups 2 and 4). We examined oxidative injury to and histopathology of the liver. RESULTS: Oxidative stress was more prominent with TVE application. Significant alterations were shown in hepatic superoxide dismutase, catalase, glutathione, and glutathione S-transferase levels. The levels of malondialdehyde and myeloperoxidase were not altered significantly. CONCLUSION: Inflow-outflow occlusion of the liver causes more oxidative stress compared with inflow occlusion.

The effects of dimethyl sulfoxide on liver damage caused by ischemia-reperfusion.

INTRODUCTION: The aim of this study was to investigate the effects of dimethyl sulfoxide on liver damage caused by ischemia-reperfusion after portal vein clamping. MATERIAL AND METHODS: Forty New Zealand rabbits were divided into three groups with the portal veins of all the rabbits except the sham group clamped for 30 minutes: group I, sham procedure; group II, control group; and group III, 500 mg/kg DMSO. The drug was administered IM in the left inguinal region 30 minutes before the operation. Blood samples (5 mL) were taken from the animals at 15, 30, and 45 minutes. At the end of the experiment 1 g of liver tissue samples were obtained. Malondialdhyde (MDA), nitric oxide (NO), AST, ALT, and LDH plasma levels were measured in the blood samples. Liver tissue samples stained with hematoxylin eosin were examined under light microscopy for histopathological changes. FINDING: The liver enzymes in both clamping groups increased significantly compared with the sham group (P < .01). Enzyme levels of the DMSO group decreased significantly compared to the control clamping group (P < .05). Similar to the enzyme changes, MDA and NO levels increased in the portal vein clamping versus the sham group and decreased in the drug-administered group versus the control clamped group (P < .03). The severity of histopathological changes was less in the DMSO group than in the clamped controls. CONCLUSION: DMSO decreased the severity of liver damage after portal vein clamping.

Effects of diphenhydramine HCl and methylprednisolone in the prevention of abdominal adhesions.

OBJECTIVE: The purpose of this study was to determine the effects of diphenhydramine hydrochloride and methylprednisolone in peritoneal adhesions. MATERIALS AND METHODS: Forty-eight male rats were used in the study. The rats were anesthetized by 5 mg/kg ketamine hydrochloride. After opening the abdomen, 10 longitudinal incisions of 2 to 3 cm in length were made on the right parietal peritoneum, and a 2 cm(2) peritoneal layer was excised from the left abdominal wall. The abdomen was closed with 3/0 silk suture. Group I was the control group, group II was given 10 mg/kg diphenhydramine intravenously, group III was given 20 mg/kg methylprednisolone intravenously, and group IV was administered both of the drugs in the above doses. A blood sample of 2 mL was taken from the rats on the 14th day after the operation. The animals were then sacrificed. The abdomen was opened and abdominal adhesions were examined. A tissue sample of 1 g was taken from the abdominal incision line. Albumin, zinc, and hemoglobin levels and leucocyte counts in the blood were determined as well as hydroxyproline levels in the tissue. RESULTS: Numbers of adhesions were as follows: 9 in group I, 3 in group II, and 2 in group III. No adhesion was observed in group IV. Albumin, zinc, and hemoglobin levels and leucocyte counts were found to be similar in all groups. Hydroxyproline levels in the tissue were significantly lower in groups III and IV than in groups I and II (P <0.05). CONCLUSIONS: Diphenhydramine and methylprednisolone reduced postoperative adhesions significantly in rats. Further investigations are needed in order to use these drugs as antiadhesive agents in humans.

A comparison of the hemodynamic and metabolic effects of extraperitoneal carbon dioxide and nitrous oxide insufflation.

BACKGROUND: The aim of the present study was to compare the hemodynamic and metabolic effects of extraperitoneal carbon dioxide (CO(2)) and nitrous oxide (N(2)O) insufflation. MATERIAL AND METHODS: Fourteen dogs were used in the experiment. All the animals were intubated under general anesthesia. A catheter was placed into the right jugular vein for central venous pressure (CVP), pulmonary artery pressure (PAP), pulmonary wedge pressure (PWP), and heart rate (HR) monitorization. End-tidal CO(2) pressure was measured by a capnometer connected to the endotracheal tube. Another catheter was inserted into the left femoral artery for arterial blood gas analysis and blood pressure monitorization. The preperitoneal dissection was made from a 1.5 cm subumbilical incision by using a preperitoneal dissection balloon. A laparoscope was placed in the preperitoneal space and the gas insufflation was kept at a constant pressure of 12 mm Hg throughout the experiment. All the study parameters were measured at the beginning of the insufflation and at every 15 minutes for 1 hour. RESULTS: Mean artery pressure increased with time in both groups, but the increase was only significant in the CO(2) group. PWP, CVP, PAP, and HR increased slightly in both groups, but there was no significant difference between the groups. The end-tidal CO(2) increased in the CO(2) group but decreased from the baseline in the N(2)O group. A significant acidosis was observed in only the CO(2) group. PaCO(2) significantly increased in the CO(2) group; hence, PaCO(2) slightly decreased in N(2)O group. The difference between the groups was significant. CONCLUSIONS: N(2)O insufflation of the extraperitoneal space in dogs avoided the unwanted metabolic and hemodynamic side effects of CO(2) insufflation. Thus, N(2)O insufflation in the extraperitoneal space is a safer alternative to CO(2) insufflation experimentally, and can be preferred especially in patients with cardiac and pulmonary diseases.