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K Yin

Publications and source records attributed to K Yin.

At least 19 recordsLinked to original sources
PubMed2001

Re-evaluation of cellulose acetate polymer: angiographic findings and histological studies.

BACKGROUND: Cellulose acetate polymer (CAP) is a new liquid embolic material that has been used experimentally in intravascular treatment of intracranial aneurysms. But this compound is still controversial in some aspects such as safety, efficiency, and histological changes. In this study, we re-evaluated the material with regard to intravascular treatment of aneurysms. METHODS: The carotid arteries of rats and experimental aneurysms in canines were embolized with CAP. The effects of CAP were evaluated according to angiographic and histological results. RESULTS: A strong chemo-corrosive effect was observed. This led to severe damage to vessels and rupture of two thrombosed canine aneurysm models. There were significant technical difficulties including out-flow of CAP and a high rate of occlusion of the parent arteries. CONCLUSIONS: We conclude that currently CAP is not an ideal embolic material for intracranial aneurysms. Further tests and improvements are needed before it can be widely used clinically.

Angiography, Digital Subtraction↗
PubMed2001

Pattern of cytokine and adhesion molecule mRNA in hapten-induced relapsing colon inflammation in the rat.

We examined the mRNA expression of cytokines, chemokines, integrins, and selectins in colon lesions of rat colitis with a semi-quantitative RT-PCR assay. Rat colitis was induced by trinitrobenzene sulfonic acid (TNBS) in 50% ethanol. Within 24 h, an acute inflammation occurred with hyperemia, edema, necrosis and an intense infiltration of granulocytes in the mucosa. The lesion proceeded into a T-lymphocyte/monocyte-driven chronic inflammation for two weeks and healed in 6 weeks. An acute inflammation recurred at the same site when the recovered animals were systemically injected with TNBS. We isolated RNA from colon tissue at 24 h, 1, 2, 4, 6 weeks after TNBS treatment and from the relapsed animals. The mRNA for cytokines IL-1beta, IL-6, IL-10 and the chemokines CINC, MIP-1alpha, MCP-1 were significantly (P < 0.05) elevated and persisted for 2 weeks, decreased in 6 weeks and increased again during relapse. IFN-gamma mRNA stayed at control levels initially, but increased dramatically in the second weeks of chronic inflammation as well as in relapse. The mRNA levels of adhesion molecules, ICAM-1, VCAM-1, the mucosal homing integrin beta7 as well as P- and E-selectin were greatly enhanced between 1 and 3 weeks. The data showed that the chronically inflamed tissue expresses a time-dependent changing pattern of TH1 cytokines and adhesion molecules that maintain the infiltration and activation of inflammatory cells and tissue injury.

Animals↗
PubMed2001

Role of IFN-gamma in bacterial containment in a model of intra-abdominal sepsis.

Interferon-gamma (IFN-gamma) is a specific activator of macrophage function and plays a critical role in the host immune defense to bacterial infection. In this study we examined the role of IFN-gamma in the regulation of bacterial load in the cecal ligation and puncture (CLP) model of intra-abdominal sepsis in the rat. In initial studies, levels of IL-12, MCP-1, and IFN-gamma were measured in the peritoneal lavage fluid 24 and 48 h after CLP. IL-12 and MCP-1 levels were both significantly increased at 24 h after CLP compared to sham controls and this difference was maintained at 48 h after CLP. Interestingly, IFN-gamma levels were not significantly increased 24 h after CLP, but were increased at 48 h after CLP. These results clearly suggest that although an inflammatory response had occurred 24 h post-surgery, with increases in the proinflammatory cytokine IL-12 and the potent chemotactic agent MCP-1, levels of IFN-gamma in CLP rats were similar to sham controls. To further investigate the role of IFN-gamma on the development of sepsis we examined the effect(s) of administering anti-IFN-gamma antibody on bacterial load after CLP. We show that use of anti-IFN-gamma antibody can significantly decrease bacterial load in the peritoneum. The mechanism of the effect(s) of anti-IFN-gamma is probably by increasing intestinal adhesions to seal the cecum and reduce bacterial movement into the peritoneum.

Animals↗
PubMed2001

Colon epithelial cell death in 2,4,6-trinitrobenzenesulfonic acid-induced colitis is associated with increased inducible nitric-oxide synthase expression and peroxynitrite production.

Peroxynitrite, derived from the reaction of nitric oxide (NO(.)) with superoxide (O(2)), is a potent nitrating and oxidizing agent that can induce apoptosis in a variety of different cell types. In the present study, we investigated the possible role of peroxynitrite as a mediator of colon epithelial cell death in rat colitis. Rat colon inflammation was induced by intracolonic administration of 2,4,6-trinitrobenzenesulfonic acid (TNBS) and rats were sacrificed 24 h after TNBS administration. Expression of inducible nitric-oxide synthase (iNOS) was detected by reverse transcription-polymerase chain reaction and immunohistochemistry. The enzymatic activities of Ca(2+)-independent iNOS and Ca(2+)-dependent constitutive nitric-oxide synthase were determined biochemically. Evidence of peroxynitrite-mediated cell injury was detected by immunostaining of nitrotyrosine. Apoptosis was examined by in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and DNA gel electrophoresis. To evaluate the specific contribution of peroxynitrite to the observed cell injury, a selective iNOS inhibitor, L-N(G)-[1-iminoethyl]lysine (L-NIL), was administered after TNBS induction. Morphological examination and analysis of TUNEL/cytokeratin double immunofluorescence revealed significant apoptosis in mucosal epithelial cells. Nitrotyrosine was colocalized with TUNEL, strongly demonstrating the association of peroxynitrite with the apoptotic death of colon epithelial cells. The administration of L-NIL reduced iNOS activity in 24-h lesions by 92% and also significantly attenuated both nitrotyrosine staining and apoptotic cell counts in the colon epithelium. These results strongly suggest that local elevated level of peroxynitrite produced from increased iNOS expression and activity is a major contributor to colon epithelial apoptosis during colon inflammation.

Animals↗
PubMed2001

[Aneurysmal model induced by elastase].

OBJECTIVE: To induce the aneurysms by corrosion of aneurysmal wall with elastase, imitating clinical intracranial aneurysms patho-morhologically. METHODS: The elastase-corroded arterial segments were transplanted onto lateral walls of carotid arteries. Follow-up and pathological examination of the aneurysms were made at two weeks and one month after construction. RESULTS: The aneurysms formed by the transplantation of elastase-corroded arterial segments were found persistent or enlarge a little within one month. The aneurysms were purplish red and easy to rupture when exposed. The walls were deprived of elastic layer, and constructed by thin connective tissue. CONCLUSIONS: The aneurysms made by transplanting elastase-corroded arterial segments are simple to built, while morphological and pathological characteristics are demonstrated good clinical mimicry, we believe our aneurysm model may well substitute the most popularly used aneurysms made of venous pouches.

Aneurysm↗
PubMed2000

Regulation of expression of nuclear factor kappa B RelA in oligodendrocytes: effect of hypoxia.

Little is known about the expression of nuclear factor kappa B (NF-kappaB) in oligodendrocytes. We demonstrate that under normal culture conditions only 21% of oligodendrocytes express NF-kappaB p65; exposure to hypoxia increased this to 69%. A similar increase in total p65 was seen with Western blots. Northern blot analysis demonstrated that NF-kappaB p65 mRNA increased during the first few h following hypoxia, suggesting that exposure to hypoxia affects NF-kappaB p65 transcription or p65 mRNA stability. Under normoxic conditions only 2% of the oligodendrocytes exhibited activated NF-kappaB; this was increased to 8% by hypoxia followed by reoxygenation. Despite activation of NF-kappaB, no detectable expression of the pro-inflammatory genes iNOS and ICAM-1 was seen. This is the first demonstration that hypoxia can up-regulate p65.

Animals↗
PubMed2000

Lung compartmentalization of inflammatory cells in sepsis.

Lung injury commonly occurs in the setting of systemic inflammatory response syndrome occurring during bacterial sepsis. There has been little work quantifying different leukocytes within the different compartments of the lung and their association with overt lung injury in sepsis. We examined the pathogenesis of lung injury after cecal ligation and puncture (CLP), a clinically relevant model of sepsis. To assess the sequestration and migration of leukocytes, leukocyte differentials were obtained for the lung vascular compartment and the bronchoalveolar airspace. At 24 h post CLP, there were signs of edema in the lung, while at 48 h after CLP, there were clear indications of alveolar wall thickening with increased cellularity and diffuse alveolar hemorrhage. The number of lymphocytes in the pulmonary vascular compartment dropped by 50% and doubled in the (bronchoalveolar lavage) BAL, 24 h after CLP compared to sham controls suggesting that there was transendothelial migration of lymphocytes. At 48 h after CLP, lymphocyte numbers in the vasculature was similar to controls but BAL lymphocyte numbers were still raised. The number of pulmonary intravascular neutrophils were similar to controls at 24 h post CLP but were greatly elevated 48 h after CLP. The increase in neutrophils was partly due to a substantial increase in the percentage of immature band cells, indicating recruitment of neutrophils from the bone marrow. There were very few neutrophils in the BAL of sham controls and CLP rats. Perfusate monocyte/macrophages were significantly increased 48 h after CLP and a similar increase in macrophages was observed in the BAL. These results strongly suggest a role for lymphocytes and macrophages in the development of overt lung injury as the migration of these cells corresponds to that of the appearance of lung injury 48 h after CLP. Importantly our data also demonstrates the compartmentalization and migration of different inflammatory cell-types during the development of sepsis.

Animals↗
PubMed2000

Chinese-made electrolytic detachable coil in the embolization of a dog aneurysmal model.

OBJECTIVE: To develop a Chinese-made electrolytic detachable coil (CEDC) that would allow patients to enjoy the benefit of electrolytic detachable coil without having to rely on the expensive Guglielmi detachable coil (GDC), and to test the safety and efficiency of CEDC. METHODS: Radiopacity of the marker of the CEDC was tested. The anti-strain force of coils and connection points were measured. In vitro and in vivo electrolyses were conducted. We produced 21 aneurysm models including lateral, bifurcation, and terminal aneurysm models, and embolized 18 models with CEDC. RESULTS: Radiopacity of the marker was satisfactory. Anti-strain of the coil and the connection point have shown the safety and efficiency of CEDC. Electrolysis in vitro and vivo, was similar to that of GDC. 83% of the aneurysm models were completely occluded. Coils were found to induce thrombosis in the aneurysm cavity, and could lead to a new endothelium over the entrance of the aneurysm, with organized tissue replacing thrombosis in 2 months. CONCLUSIONS: CEDC is as efficient and safe as GDC. The marker, the ability to induce thrombosis inside the sac and the growth of new endothelium over the orifice are very satisfactory.

Animals↗
PubMed2000

[Significance of the changes of urinary uric acid, ANP, renin and aldosterone in sleep apnea syndrome patients].

OBJECTIVES: To assess the utility of urinary uric acid excretion and urinary uric acid/creatinine ratio as the marker of nocturnal respiratory disturbance in patient with sleep apnea syndrome (SAS) before and after the institution of nasal continuous positive airway pressure (nCPAP). Another purpose is to explore the relationship between the nocturnal diuresis and atrial natriuretic peptide (ANP), renin-aldosterone in SAS. METHODS: 22 cases diagnosed as SAS by polysomnography (PSG) were selected as trial group, 11 cases excluded from SAS by PSG were as control group, and 13 severe SAS patients were treated by nCPAP and taken as nCPAP therapy group. The markers mentioned above were compared in these groups. RESULTS: The overnight change in urinary uric acid/creatinine ratio in trial group is 0.47 +/- 0.31, which is significantly higher than that in control group (0.01 +/- 0.23), P < 0.05, and in nCPAP therapy group after therapy (0.01 +/- 0.19) significantly lower than that before nCPAP therapy (0.48 +/- 0.27), P < 0.001. The morning urinary uric acid excretion in trial group is (5.4 +/- 2.3) mg/L which is also significantly higher than that in control group (3.2 +/- 1.4) mg/L, P < 0.001, and in nCPAP therapy group (3.3 +/- 1.2) mg/L significantly lower than that before nCPAP (5.9 +/- 2.6) mg/L, P < 0.05. The mean morning blood ANP in trial group is (0.182 +/- 0.004) microgram/L, which is higher than that in control group (0.182 +/- 0.004) microgram/L, P < 0.05, and in nCPAP therapy group (0.122 +/- 0.001) microgram/L is much lower than that before nCPAP therapy (0.180 +/- 0.003) microgram/L, P < 0.001. However there are no statistic significant differences between these groups in blood renin-aldosterone. CONCLUSIONS: The urinary uric acid excretion and overnight change in urinary uric acid/creatinine are good markers to determine the effects of nCPAP on SAS. The nocturnal diuresis in SAS patients is correlated with the increase of ANP in plasma.

Adult↗
PubMed2000

[Re-evaluation of an embolic material for aneurysm cellulose acetate polymer].

OBJECTIVE: To re-evaluate the safety, effect, and pathological reactions of cellulose acetate polymer (CAP). METHODS: 30 right carotid arteries of rats were embolized and got two embolized vessels for histological study in each of the seven stages within four months. Fifteen canine aneurysmal models were created by transplantation of venous pouches. Twelve of them were occluded with CAP. Digital Subtraction Angiography (DSA) follow-ups of occluded aneurysmal models were carried out 1, 2 and 8 weeks after occlusion. One animal was sacrificed randomly at each stage for pathological study. RESULTS: Only five of the 12 aneurysmal models were completely or partially occluded within the patency of parent arteries within two months of observation after embolization with CAP. Stenosis of one branch of aneurysmal parent artery was occurred. The residual cavity of one partially occluded model artery was enlarged. Two models ruptured on four and five days after embolization. Three embolized models and their parent arteries were all occluded. PATHOLOGICAL FINDINGS: acute pathological reaction occurred within vessels embolized with CAP. Endothelial cell and basal membrane were damaged and vanished. Elastic lamina was exposed to arterial lumen and attached by thrombus layer. Fibrous cells and smooth muscle cells showed obvious degeneration. CAP and thrombus were gradually organized in two months after thrombosis. The orifices of aneurysmal models were covered with newly developed fibrous tissue and endothelial cells in two months after thrombosis. CONCLUSIONS: We think that acute chemical erosive effect of CAP was evident. A strong effect could lead to rupture of some of the CAP thrombosed aneurysmal models. Besides, stenosis or occlusion of the parent arteries could be induced in some cases after embolization with CAP. For the above shortcomings and limitations, it should be improved carefully before it is applied in clinic.

Aneurysm↗
PubMed1999

Role of interferon-gamma in lung inflammation following cecal ligation and puncture in rats.

Interferon-gamma (IFN-gamma) has been implicated in the mortality of animal models of endotoxemia. On the other hand, the specific role of IFN-gamma in the development of organ inflammation in a model of polymicrobial sepsis has not been elucidated. In this study, we hypothesized that IFN-gamma plays an important role in lung inflammation after cecal ligation and puncture (CLP). To verify this hypothesis, lung tissue was removed 5 h after CLP or from sham controls. The mRNA expression (by RT-PCR) of IFN-gamma was increased in lung homogenates of CLP rats compared to sham controls. Using immunohistochemistry, we show for the first time the increased presence of IFN-gamma staining cells in the lung following CLP. Only very small amounts of positive staining for IFN-gamma was observed in lungs of sham controls. The presence of IFN-gamma in the lung 5 h after CLP correlated with a twofold increases in lung superoxide generation and MPO activity (index of neutrophil sequestration). Plasma and lung nitrite levels (breakdown product of nitric oxide) were also significantly increased in CLP rats. IFN-gamma antibody (1.2 mg/kg, i.v.) administered immediately after CLP significantly decreased lung superoxide levels to levels similar to the sham controls without affecting MPO activity, or lung or plasma nitrite levels. These results provide evidence that IFN-gamma may contribute to lung inflammation 5 h following CLP via increased production of superoxide.

Animals↗
PubMed1999

Enzyme immunoassays (EIAs) of eicosanoids.

Enzyme immunoassay of eicosanoids is a nonradioactive, highly sensitive method of determining the concentration of eicosanoids in biological samples. Although relatively easy to use, the assays require a high level of precise pipetting technique and familiarity with critical points in the assay procedure. Although assay kits complete with plates, buffers, antibodies, tracers, and color development reagents are available, it is more economical to develop the assay within the laboratory if the assay is to be performed routinely. The only major disadvantage with EIA is that the investigator is limited to measuring eicosanoids with commercially available enzyme-tracers and antibodies. The labeling of particular eicosanoids by enzyme tracers is rarely, if ever, performed outside of industry. Growing of antibodies is conducted in many laboratories but is beyond the scope of this chapter. It requires a significant level of commitment of time and resources to establish the specificity of the antibody (i.e., does the antibody cross-react with eicosanoids of similar structure). Furthermore, this will not solve the problem of availability of eicosanoid-tracer. On the other hand, it must be noted that with the exception of the cytochrome P-450 metabolites of arachidonic acid, most of the major eicosanoids that are biologically active and are known to play regulatory roles in physiology and/or pathology, have commercially available antibodies and enzyme-tracers.

Eicosanoids↗
PubMed1998

Augmentation of nitric oxide, superoxide, and peroxynitrite production during cerebral ischemia and reperfusion in the rat.

The effect of ischemia produced by bilateral occlusion of the common carotid arteries (30 min) followed by 4 hours of reperfusion on total and inducible nitric oxide synthase (NOS) activity and the production of nitric oxide (NO), superoxide and peroxynitrite in the cerebral hemispheres was determined in the rat. Compared to sham-operated controls, cerebral ischemia-reperfusion resulted in a significant increase in total and inducible NOS activity and a significant increase in the production of NO and superoxide in the cerebral hemispheres. The level of NO in the plasma and the peripheral leukocyte count were also significantly increased. Immunohistochemical staining for nitrotyrosine (a marker of peroxynitrite production) showed that ischemia-reperfusion resulted in increased synthesis of cerebral peroxynitrite. Administration of the irreversible NOS inhibitor, Nomega-nitro-L-arginine (L-NA), increased superoxide levels in the brain and significantly reduced plasma NO. Total and inducible NOS activity as well as NO and immunoreactive nitrotyrosine, in the cerebral hemispheres were reduced with L-NA administration. The number of leukocytes in the plasma was unaffected by administration of L-NA. These findings suggest that cerebral ischemia-reperfusion causes increased production of reactive oxygen species in the cerebral hemispheres and that the production of peroxynitrite, and not superoxide, may be dependent upon the availability of NO.

Animals↗
PubMed1998

Time-dependent cardiovascular and inflammatory changes in acute endotoxemia.

The pathophysiology of experimental acute endotoxemia is a complex process involving both cardiovascular dysfunction and an inflammatory response. We have examined the correlation in hemodynamic changes and the pulmonary inflammatory response after lipopolysaccharide (LPS) administration with respect to time. Importantly, we have measured the lung and plasma levels of nitric oxide (NO) over time, as well as rapid generation of lung superoxide after LPS administration. In anesthetized rats given a bolus injection of LPS (10 mg/kg intravenously, from Salmonella enteritidis), mean arterial blood pressure dropped by 63-70% within 15 min, and cardiac output fell by 57-63% within 20 min compared with saline controls. Mean arterial blood pressure recovered slightly but was still 51, 30, and 25% less than that of saline controls 45, 105, and 165 min after LPS administration, respectively. Cardiac output remained depressed throughout the experimental period and was 35% lower than in saline controls 165 min after LPS treatment. There was a small increase in plasma nitrite/nitrate as an index of plasma NO production after 45 min and a 10-fold increase 165 min after LPS addition compared with controls, strongly suggesting that NO mediates the hypotension that occurs 165 min after LPS administration. Lung NO production increased twofold 105 min after LPS administration and remained higher than in saline controls. Histological sections showed that there was fluid accumulation and alveolar collapse in the lung 45 min after LPS, whereas after 165 min, there was extensive tissue damage and increased leukocyte accumulation compared with controls. These results suggest that there was no correlation between early (1 h) tissue damage and NO production. We found an increase in lung superoxide generation 15 min after injection of LPS that coincided with the alterations in cardiovascular function. These results suggest that early lung tissue damage and/or hemodynamic changes may be due to superoxide generation from the lung.

Acute Disease↗
PubMed1998

Effects of mild chronic heat exposure on the concentrations of thiobarbituric acid reactive substances, glutathione, and selenium, and glutathione peroxidase activity in the mouse liver.

To determine whether mild and chronic heat stress leads to oxidative stress and to differentiate such effects of different exposure periods, we kept male ICR-mice at an ambient temperature of either 35 degrees C or 25 degrees C for 6 hours, 3 days, or 7 days and measured the concentrations of thiobarbituric acid reactive substances (TBARS), glutathione (GSH), selenium (Se), and glutathione peroxidase (GSH-Px) activities in the liver. Since the food consumption of the heat-exposed group was only half that of the control, we prepared pair-fed groups, which were kept at 25 degrees C and whose food consumption were limited to those of the heat-exposed group for the 3-day and the 7-day exposure. TBARS concentrations of the liver was significantly higher in the heat group than the control after the 3-day exposure, while there was no significant difference among the groups after the 7-day exposure. There was no significant difference in GSH concentrations between the heat-exposed group and the control after the 7-day exposure, when the GSH concentration of the pair-fed group was significantly lower than that of the control. Hepatic cytosolic Se GSH-Px activity in the heat group was significantly less than that in the control group after the 6-hour exposure and it tended to be lower in the heat group than that of the control group after the 7-day exposure, while there was no difference in the total GSH-Px activity among the three groups. Our results showed that mild and chronic heat exposure may cause oxidative damage to organisms and that GSH-related anti-oxidative systems would play an important role to defensive reaction.

Animals↗
PubMed1998

[Pathophysiology and surgical treatment on Relaxed Pelvic Floor Syndrome].

OBJECTIVE: To study the pathophysiology of the "Relaxed Pelvic Floor Syndrome (RPFS)" and to assess the value of the "Pelvic Cavity Fixation Operation (PCFO)" for the syndrome. METHOD: 11 patients, who were diagnosed as having RPFS, underwent standardized PCFO. All the patients were followed for a mean time of 19 months (5 - 72 months). RESULT: The main syndromes and signs included difficulty in defecation, inability to empty the rectum properly, fullness of perineum, protrusion of perineum at bearing down, back-inclining uterus, relaxation of the rectum on digital examination. The anorectal dynamics showed that the sequence pressure and rest pressure of the anal cannel were lower and the time of contraction of the anal cannel decreased than that of the normal controls. The rectum sensation was damaged slightly. Defeacography showed that there were relaxing changes in several systems in the pelvic cavity. Operatively, it was easy to see the relaxation of the supporting structure of the colon, rectum, uterus and the lower position of the peritoneal cavity. PCFO has achieved good results. Seven patients were free of symptoms completely and 4 improved. CONCLUSION: The relaxing changes of the supporting tissue of many viscus fefer to several systems are the pathophysiologic of the RPFS. "Pelvic Cavity Fixation Operation" is useful in the treatment of the syndrome.

Adult↗
PubMed1998

Inhibition of nitric oxide synthase attenuates peroxynitrite generation, but augments neutrophil accumulation in hepatic ischemia-reperfusion in rats.

The role of nitric oxide (NO) and peroxynitrite in the process of neutrophil adhesion and infiltration was investigated in a model of hepatic ischemia-reperfusion. Male Fischer rats were subjected to 30 min of hepatic no-flow ischemia followed by 4 h of reperfusion (I/R). I/R induced liver injury as evidenced by a 13.7-fold increase in plasma alanine aminotransferase activity. Induction of liver injury was associated with an increase in neutrophil accumulation in ischemic lobes of livers [215 +/- 27 polymorphonuclear neutrophil leukocytes/50 high-power field (HPF), P < .05 compared with sham control] and 8-fold augmentation of inducible NO synthase (NOS) activity. However, NO levels in the liver decreased; this decrease may be caused by peroxynitrite formation by the reaction of NO with superoxide. Sections of ischemic lobes of the liver tissue of I/R animals exhibited marked immunoreactivity with anti-nitrotyrosine antibody, which indicates the presence of nitrotyrosine. Administration of Nw-nitro-L-arginine methyl ester (10 mg/kg i.v. before reperfusion) attenuated total and inducible NOS activity in both ischemic and nonischemic lobes of liver, and reduced NO levels in plasma and liver. However, NOS inhibition aggravated liver injury as alanine aminotransferase increased by 61% compared with rats subjected to reperfusion injury. Neutrophil accumulation was enhanced in ischemic (436 +/- 48/50 HPF, P < .05 compared with I/R animal) and nonischemic lobes of livers (34 +/- 3.2/50 HPF, P < .05 compared with sham control). NOS inhibition also attenuated immunohistochemically detected nitrotyrosine formation, but increased superoxide production in the liver. The NO-dependent regulation of neutrophil accumulation in the liver may be linked closely to P-selectin and intracellular adhesion molecule-1 expression because inhibition of NOS resulted in significant increases in gene expression of these two adhesion molecules (determined by reverse transcription-polymerase chain reaction analysis). These results suggest that NO is important in attenuating neutrophil accumulation and liver damage in ischemia-reperfusion injury. Inhibition of NOS activity reduces peroxynitrite formation but aggravates liver injury and increases neutrophil accumulation, which suggests that the anti-inflammatory function of NO is more important than the cytotoxic potential of peroxynitrite in acute inflammation.

Alanine Transaminase↗