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At least 1,261 records · Page 70Linked to original sources
PubMed2001

STAT3 exerts two-way regulation in the biological effects of IL-6 in M1 leukemia cells.

The signal transducer and activator of transcription (STAT) proteins have been implicated in cytokine-regulated proliferation, differentiation and cell survival. Interleukin-6 (IL-6), a pleiotropic cytokine, induces a robust and sustained activation of STAT3 in M1 acute myeloid leukemia cells, which in turn undergo growth arrest, terminal differentiation and apoptosis in response to IL-6. The roles of STAT3 activation in IL-6-mediated responses in M1 cells are not fully understood. We introduced STAT3 antisense cDNA into M1 cells. STAT3 antisense cDNA blocked the expression and IL-6-induced tyrosine phosphorylation and DNA binding of STAT3, and resulted in reduction of both IL-6-induced growth arrest at G(0)/G(1) phase and macrophage differentiation in the M1 transformants. This observation is in accordance with previous reports and confirms that STAT3 plays an essential role in IL-6-induced growth arrest and terminal differentiation in M1 leukemia cells. On the other hand, STAT3 antisense cDNA augmented IL-6-induced apoptosis of M1 cells, which was supported by the cell cycle assay, DNA fragmentation assay and detection of the p17 active fragment of Caspase 3. As proliferation inhibition and differentiation induction stands for a negative signal, while survival maintenance stands for a positive signal, we conclude that STAT3 exerts two-way regulation on the biological effects of IL-6 in M1 leukemia cells.

Animals↗
PubMed2001

Does trimetazidine exert cytoprotective activity on astrocytes subjected to hypoxia in vitro?

The aim of the present study was to establish whether trimetazidine (TMZ) is capable of protecting astrocytes against hypoxic injury. Using the model of astrocyte cell culture we tried to observe the cells treated with TMZ before, during and after hypoxia simulated in vitro. Cell viability was determined by Live/Dead (viability/cytotoxicity) Assay Kit and MTT conversion test. Apoptotic cell death was distinguished by a method using fluorescence microscopy with Hoechst 33342. The effect of the drug on the DNA synthesis was evaluated by measuring the incorporation of [3H]thymidine into DNA of astrocytes. TMZ stimulates the proliferation of astrocytes most significant one when the astrocytes are exposed to the drug in normoxia, hypoxia and/or re-oxygenation. Adding TMZ into cultures during re-oxygenation and hypoxial re-oxygenation significantly decreases the number of dead and apoptotic cells. Our experiment has proved that TMZ exerts the most significantly cytoprotective effect on astrocytes in vitro when added during hypoxia and/or re-oxygenation. We may conclude that the protective effect of TMZ depends on the sequence of drug adding and hypoxia/ re-oxygenation onset.

Animals↗
PubMed2001

Ethanol exerts different effects on myelin basic protein and 2',3'-cyclic nucleotide 3'-phosphodiesterase expression in differentiating CG-4 oligodendrocytes.

Evidence suggests that abnormal myelination is one factor contributing to the neuoropathology associated with fetal alcohol syndrome. We investigated the potential teratogenic effects of ethanol (EtOH) on myelin formation by determining its effects on the developmentally regulated increased expression of myelin basic protein (MBP) and 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP) in differentiating CG-4 oligodendrocytes (OLGs). By using CG-4 OLGs in vitro we identified processes altered by ethanol actions exerted directly on OLGs. During the first 8 days of development, EtOH decreased the expression of the major structural 18.5 and 14 kDa MBP isoforms by at least 40% at 4 days of development. EtOH concentrations between 25 and 75 mM inhibited MBP expression in a dose-dependent manner. Adding or withdrawing EtOH on specific days of differentiation reversibly modulated the expression of MBP, and the degree of inhibition was directly related to the length of ethanol exposure. As little as two consecutive days of EtOH exposure either early or late during development caused at least a 20% inhibition, however, no short critical time window of EtOH vulnerability for the inhibition was observed. The ethanol effect was selective for MBP expression, as EtOH did not alter the developmentally-regulated increased expression of CNP isozymes or enzyme activity. The results indicate that one factor contributing to the development of fetal alcohol syndrome may be defective myelination resulting from delayed and decreased MBP expression.

2',3'-Cyclic Nucleotide 3'-Phosphodiesterase↗
PubMed2003

Interleukin-1 receptor antagonist exerts agonist activity in the hippocampus independent of the interleukin-1 type I receptor.

Interleukin-1 receptor antagonist (IL-1ra) selectively and competitively inhibits the actions of IL-1 at its receptors and has not been reported to have agonist activity. This study demonstrates that stimulation of synaptosomes with IL-1ra in vitro, mimicked the effects of IL-1 beta by decreasing glutamate release and increasing JNK phosphorylation. These effects of IL-1ra, but not IL-1 beta, were maintained in IL-1 type I receptor (IL-1RI) defective mice. IL-1 beta blocked these IL-1ra-induced effects suggesting that it may also act independently of IL-1RI in some circumstances. Furthermore, IL-1ra mimicked the inhibitory effect of IL-1 beta on long-term potentiation (LTP) in the hippocampus. These data, taken together with our findings that IL-1ra binds to hippocampal synaptosomes in the absence of IL-1RI, provide evidence that IL-1ra exerts agonist activity in the hippocampus independent of IL-1RI.

Animals↗
PubMed2003

Peptides from the N-terminal domain of chromogranin A (vasostatins) exert negative inotropic effects in the isolated frog heart.

The negative inotropic effects of synthetic peptides derived from the N-terminus of chromogranin A (CgA) were studied in an avascular model of the vertebrate myocardium, the isolated working frog heart (Rana esculenta). The peptides were frog and bovine CgA(4-16) and CgA(47-66), and bovine CgA(1-40) with (CgA(1-40SS)) and without an intact disulfide bridge (CgA(1-40SH)). Under basal cardiac conditions, four of the peptides caused a concentration-dependent negative inotropism that was comparable to the negative inotropy reported for human recombinant vasostatin I (CgA(1-78)) and bovine CgA(7-57). By comparison of the structural characteristics of the bovine and frog sequences with their minimally effective concentrations ranging from 68 to 125 nM of peptide, the results were consistent with the natural structure (CgA(17-38SS)) being essential for the negative inotropism. In addition, the partial sequences of the frog and bovine vasostatin I were effective in counteracting the characteristic positive inotropism exerted by isoproterenol (1 nM) at minimally effective concentrations ranging from 45 to 272 nM. Taken together, these results extend the first evidence for a cardiosuppressive role of the N-terminal domain of chromogranin A known for its co-storage with catecholamines in the sympathoadrenal system of vertebrates.

Adrenergic beta-Agonists↗
PubMed2001

[Recurrent rhabdomyolysis revealing chronic exertional compartment syndrome of the biceps].

UNLABELLED: OBJECTIVE AND PATIENT: To report, an uncommon case of recurrent effort-related biceps compartment syndrome induced by strengthening exercises (body building) in a thirty-years-old white man. DISCUSSION-CONCLUSION: compartment syndrome is typically observed in the lower leg or in the forearm with pain, muscle tightness, cramp-like feeling during exertion. The involvement of the biceps was only described after traumatisms. Patient was initially thought to have metabolic myopathy because acute episodes of exercise induced myalgia and elevated serum CK. Tissue pressure monitoring prior and after a standard exercise test is helpful for diagnosing the recurrent form. The only alternative to fasciotomy is to stop sports activities.

Adult↗
PubMed1998

Tamoxifen exerts testosterone-dependent and independent effects on thymic involution.

Circulating testosterone concentrations and seminal vesicles weights, as well as thymus and spleen weights and histology were assessed in male Wistar rats from the infantile to post-pubertal period. The widely used anti-estrogenic agent tamoxifen was then administered in adult intact and castrated male rats and its long-term effects on thymic involution and splenic growth were examined. The results showed that: (1) age-related involution of the male thymus from the juvenile period through puberty to post-puberty depends on the rising testosterone levels and represents mainly a decrease of thymic lymphoid-cell elements; (2) tamoxifen administration reverses thymic involution in intact adult male rats and this effect is related to a dose-dependent, tamoxifen-induced castration and decrease of testosterone levels; (3) the changes of circulating testosterone levels, either resulting from maturity, or induced by tamoxifen or by castration, have a minimal effect on splenic growth and weight; and (4) in contrast to intact animals, administration of tamoxifen at pharmacological doses to adult castrated rats results in thymic regression. Underscoring the critical role of testosterone on thymic involution, these findings show that tamoxifen is able to reverse ageing changes in the thymus by suppressing testosterone production, while conversely, exerts thymolytic effects in the absence of androgens.

Animals↗
PubMed2001

The environmental estrogenic compound bisphenol A exerts estrogenic effects on mouse hippocampal (HT-22) cells: neuroprotection against glutamate and amyloid beta protein toxicity.

We have examined using immortalized clonal mouse hippocampal cell line (HT-22) whether the environmental estrogenic compound bisphenol A (BPA), like estrogen, has any neuroprotective effect against glutamate and amyloid beta protein-induced neurotoxicity. BPA protects HT-cells against both 5 mM glutamate and 2 microM amyloid beta protein-induced cell death in a dose dependent manner. Optimum protection was attained at 1 microM and 500 nM BPA against 5 mM glutamate and 2 microM amyloid beta protein-induced HT-22 cell death, respectively. Using confocal immunoflourescence microscopy technique, we observed that 20 h of treatment with 5 mM glutamate resulted in intense nuclear localization of the glucocorticoid receptors (GR) in HT-22 cells as compared to control untreated cells. Interestingly, 1 microM BPA treatment for 24 h, followed by 20-h treatment with 5 mM glutamate, resulted in dramatic reduction in GR nuclear localization. We conclude that: (i) BPA mimics estrogen and exerts neuroprotective effects against both neurotoxins used; (ii) BPA inhibits enhanced nuclear localization of GR induced by glutamate; and (iii) HT-22 cells provide a good in vitro model system for screening the potencies of various environmental compounds for their estrogenic activity.

Amyloid beta-Peptides↗
PubMed2002

Evaluation of acute hepatotoxic effects exerted by environmental estrogens nonylphenol and 4-octylphenol in immature male rats.

Nonylphenol (NP) and 4-Octylphenol (4OP) have shown estrogenic properties both in vivo and in vitro. Researchers have known for years that estrogens induce a wide number of hepatotoxic actions in rodents. In order to study the acute hepatic effects exerted by NP and 4OP on rat liver the following endpoints were evaluated: relative liver weight (RLW), morphology, cell cycle and ploidy status, monooxygenase enzymes content and levels of both, cytosolic estrogen receptor (cER) and microsomal binding sites for estrogens (mEBS). Immature male Sprague-Dawley rats were injected intraperitoneally (i.p.) with 60 mg/kg of NP or 4OP for 1, 5 or 10 days. Despite the fact that RLW of the animals was not modified but any treatment, the histopathological study revealed the presence of an increase in the percentage of both, mitotic activity and Ki-67-labeling index (LI) in the livers from animals treated with alkylphenols in absence of any degenerative lesion. Furthermore, all the livers from alkylphenols-treated groups showed the presence of abnormal mitosis and c-mitosis. Although the levels of both, cER and cytochrome P450 (Cyt. P450) were not affected by any treatment, concentration of the mEBS was decreased after 10 days of treatment with alkylphenols. These findings taken together suggest that the exposition to alkylphenols induce cell proliferation and spindle disturbances and that these compounds are capable of modulating the expression of putative membrane receptors for estrogens.

Animals↗
PubMed2001

Quercetin modifies reactive oxygen levels but exerts only partial protection against oxidative stress within HL-60 cells.

Quercetin may contribute to the protection afforded by fruit- and vegetable-rich diets against diseases for which excess production of reactive oxygen species (ROS) has been implicated as a causal or contributory factor. We examine the effect of short term (90 min) quercetin (1-100 microM) exposure on the progress of menadione induced oxidative stress within HL-60 cells. 2',7'-dichlorofluorescein and rhodamine-123 fluorescence, resulting from oxidation of the ROS-sensitive dyes dichlorodihydrofluorescein and dihydrorhodamine-123 respectively, were utilised as indicators of general ROS levels. Ethidium fluorescence, resulting from oxidation of dihydroethidium, was used as a potentially more specific indicator of O(2)(-). Exposure to quercetin alone induced a decrease in DCF and rhodamine fluorescence. Conversely, ethidium fluorescence was enhanced by treatment with >or=40 microM quercetin. Incubation with 1-100 microM quercetin reduced the extent of menadione-induced increase in DCF and rhodamine fluorescence but the menadione-induced increase in ethidium fluorescence was further elevated for cells treated with >or=25 microM quercetin. Exposure to >or=10 microM quercetin abrogated menadione-induced DNA single-strand breaks but, paradoxically, quercetin exacerbated membrane damage and failed to enhance the viability of menadione-challenged cells. In conclusion, quercetin exerts only site-specific protection against oxidative stress.

Cell Membrane Permeability↗
PubMed2002

Chondroitin sulfate B exerts its inhibitory effect on secondary lymphoid tissue chemokine (SLC) by binding to the C-terminus of SLC.

We previously reported that certain glycosaminoglycans (GAGs) bind secondary lymphoid tissue chemokine (SLC, CCL21) and that the SLC-binding GAGs, including chondroitin sulfate B (CS B), negatively modulate the function of SLC, although the mechanism remains unknown [J. Biol. Chem. 276 (2001) 5228]. To gain insight into the mechanism of inhibition, we used a C-terminally truncated SLC (SLC-T) that lacked clusters of basic amino acid residues that have been implicated in GAG binding. While SLC-T failed to bind any GAGs, it induced prominent intracellular Ca(2+) mobilization in CC chemokine receptor (CCR) 7-expressing cells, as did wild-type SLC. However, the SLC-T-induced Ca(2+) influx was not inhibited by CS B, unlike the SLC-induced Ca(2+) influx. These results demonstrate the requirement of the C-terminus of SLC for the inhibition of chemokine responses by CS B; that is, CS B exerts its inhibitory effect by binding to the C-terminus of SLC, thus defining the mode of action of CS B on certain chemokines.

Amino Acid Sequence↗
PubMed1999

Glucose and non-glucidic nutrients exert permissive effects on 2-keto acid regulation of pancreatic beta-cell function.

Insulin-releasing effects of straight and branched chain 2-keto acids were assessed using clonal glucose-responsive beta-cells. Pyruvic acid (PA), 2-ketovaleric acid (KV), 2-ketoisovaleric acid (KIV) or 2-keto-3-methylvaleric acid (KMV) dose-dependently promoted the stimulatory effects of D-glucose, whereas 2-ketobutyric acid (KB) did not affect insulin release. The stimulatory 2-keto acids also promoted the stimulatory activity of D-glyceraldehyde, L-leucine or L-arginine. Responses to PA, KV, KIV or KMV were significantly reduced by transport inhibition with 2-cyano-3 hydroxycinnamate, glucokinase inhibition with mannoheptulose or metabolic inhibition with sodium azide or sodium cyanide. Membrane hyperpolarisation with K+ depletion or diazoxide reduced insulin output, but failed to abolish secretory responses to KV, KIV and KMV. Secretory effects of these 2-keto acids also persisted in beta-cells depolarised with high KCl and glucose. Voltage-dependent Ca2+ channel blockade, with verapamil, or depletion of extracellular Ca2+ abolished the secretory activity of 2-keto acids. Collectively, these results indicate that glucose and metabolisable nutrients exert permissive effects on 2-keto acid-induced insulin release. In addition, KV, KIV and KMV can regulate beta-cell function at least partially independently of K+-ATP channel activity, both through their mitochondrial metabolism and regulation of Ca2+ influx.

Animals↗
PubMed1998

Nerve-induced release of nitric oxide exerts dual effects on nicotinic transmission within the coeliac ganglion in the rabbit.

The involvement of nitric oxide in the modulation of nicotinic activation was investigated in vitro in isolated rabbit coeliac ganglion. The electrical activity of the ganglionic neurons was recorded using intracellular recording techniques. When a train of pulses of supramaximum intensity was applied to the splanchnic nerves, gradual depression of fast nicotinic activation occurred: the pulses do not systematically elicit action potentials, but very often elicit excitatory postsynaptic potentials only. This phenomenon appeared between 15 and 20 Hz and increased with the frequency of stimulation. It was not related to any change in the membrane potential of the ganglionic neurons. For a given frequency, the depression appeared progressively and it was particularly strong at the end of the train. The use of pharmacological agents that interfere with the nitric oxide pathway, such as L-arginine (precursor of nitric oxide), D-arginine (non-precursor of nitric oxide) N(omega_-nitro-L-arginine and N(omega)-nitro-L-arginine methyl ester (inhibitors of nitric oxide synthase), and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (nitric oxide scavenger), demonstrated that nitric oxide modulated this depression phenomenon by exerting a dual effect on the nicotinic activation, i.e. facilitation or inhibition. Agents interfering with the guanosine 3',5'-cyclic monophosphate pathway, such as oxadiazolo[4,3-a] quinoxalin-1-one (selective inhibitor of the nitric oxide-activated soluble guanylate cyclase) and zaprinast (selective inhibitor of the phosphodiesterases involved in the guanosine 3',5'-cyclic monophosphate pathway) demonstrated that only the facilitatory effect of nitric oxide on the nicotinic activation was mediated through the guanosine 3',5'-cyclic monophosphate pathway. The mechanism sustaining the inhibitory effect remains to be determined. By modulating the nicotinic activation, nitric oxide plays a role in the integrative properties of the prevertebral ganglia. This opens new perspectives with regard to the control of visceral functions by the prevertebral level of regulation.

Animals↗
PubMed2001

Sex steroid hormones exert biphasic effects on cytosolic magnesium ions in cerebral vascular smooth muscle cells: possible relationships to migraine frequency in premenstrual syndromes and stroke incidence.

Clinically, it is known that: (1) magnesium (Mg) supplementation relieves premenstrual problems (e.g., migraine, bloating and edema) occurring in the late luteal phase of the menstrual cycle; and (2) migraine syndromes, particularly in women, are associated with deficits in brain and serum ionized Mg levels. We investigated whether concentrations of sex steroid hormones, found in the serum during the menstrual cycle of women, are associated with changes in the levels of cytosolic free magnesium ions ([Mg2+]i in single cultured canine cerebral vascular smooth muscle cells. The resting level of [Mg2+]i in these cells was 645 +/- 89 microM before exposure to sex steroid hormones. Exposure of these vascular cells to a low concentration of estrogen (10 pg/ml) failed to interfere with the levels of [Mg2+]i. However, exposure to estrogen, at concentrations ranging from 40 to 200 pg/ml, induced significant loss of [Mg2+]i in a concentration-dependent manner. At a concentration of 200 pg/ml estrogen, the level of [Mg2+]i decreased approximately 30% in comparison with controls. Progesterone produced biphasic effects on the levels of [Mg2+]i, depending on its concentration. Exposure of the cultured cells to a low concentration of progesterone (0.5 ng/ml) resulted in an increased level of [Mg2+]i (from 690 +/- 50 microM to 753 +/- 56 microM, p < 0.05). However, when these cells were exposed to higher concentrations of progesterone (i.e., from 5.0 to 20 ng/ml), the cellular levels of [Mg2+]i were decreased significantly. The higher the estrogen or progesterone concentration, the lower the levels of [Mg2+]i. In contrast, testosterone, a male hormone, didn't produce any significant alteration in [Mg2+]i levels in these cerebral vascular smooth muscle cells. These data indicate that low, physiological concentrations of female sex hormones, estrogen and progesterone, help cerebral vascular smooth cells sustain normal concentrations of [Mg2+]i, which are beneficial to vascular function, whereas high levels of estrogen and progesterone deplete, significantly, [Mg2+]i in cerebral vascular smooth muscle cells, possibly resulting in cerebrovasospasms and reduced cerebral blood flows related to premenstrual syndromes, migraine and stroke risk. Our findings could provide new insight into the mechanism whereby migraine occurs frequently in the late luteal phase in the premenstrual syndrome. In addition, our results demonstrate that female sex steroids but not testosterone (in physiologic concentrations) can exert direct effects on [Mg2+]i in cerebral vascular cells.

Animals↗
PubMed2000

Subcutaneous treatment of p-tert-octylphenol exerts estrogenic activity on the female reproductive tract in normal cycling rats of two different strains.

Effects of p-tert-octylphenol (OP), an endocrine disrupting chemical (EDC), on the female reproductive tract of normal cycling Fischer 344 (F344) and Donryu rats were investigated. OP was subcutaneously injected at concentrations of 12.5, 25, 50 or 100 mg/kg for 28 days. The most notable changes were the disappearance of normal cyclicity in the 50 mg/kg or more OP-treated groups of both the strains, and the appearance of persistent estrus (PE) evident on examination of vaginal smears in the 100 mg/kg groups of both the strains, the effects being time- and dose-dependent. In PE rats of both the strains, the uterine morphology deviated from the normal for each estrous stage of the cycling rats, and proliferation in the endometrium was slightly increased. The data for uterine weights, luminal epithelial cell-heights and/or numbers of epithelial cells in the endometrium demonstrated equivocal alteration. In both the strains, the serum 17beta-estradiol (E2) levels were decreased with 50 mg/kg of OP or more. Serum concentrations of the administrated chemical were dose and duration-dependently increased in all the treated groups of both the strains. The results demonstrate that subcutaneous administration of OP at doses of 50 mg/kg or more exerts time- and dose-dependent estrogenic activity on the reproductive tract of normal cycling female Donryu and F344 rats, indicating similar qualitative sensitivity to the effects in both the strains. Vaginal cytology may be the most sensitive endpoint for the detection of estrogenic activity of potential EDCs using adult cycling rats.

Animals↗
PubMed2000

The class III antiarrhythmic effect of sotalol exerts a reverse use-dependent positive inotropic effect in the intact canine heart.

OBJECTIVES: We sought to study the rate related effects of sotalol on myocardial contractility and to test the hypothesis that the class III antiarrhythmic effect of sotalol has a reverse use-dependent positive inotropic effect in the intact heart. BACKGROUND: Antiarrhythmic drugs exert significant negative inotropic effects. Sotalol, a beta-adrenergic blocking agent with class III antiarrhythmic properties, may augment contractility by virtue of its ability to prolong the action potential duration (APD). METHODS: In 10 anesthetized dogs, measurements of left ventricle (LV) peak (+)dP/dt and simultaneous endocardial action potentials were made during baseline conditions and after sequential administration of esmolol and sotalol. In addition, electrical and mechanical restitution curves were constructed at a basic pacing cycle length of 600 ms by introducing a test pulse of altered cycle length ranging from 200 ms to 2,000 ms. RESULTS: In the steady state pacing experiments, sotalol prolonged the APD in a reverse use-dependent manner; such an effect was not seen with esmolol. At cycle lengths exceeding 400 ms, LV (+)dP/dt was significantly higher with sotalol than it was with esmolol. There was a direct relation between APD and LV (+)dP/dt with sotalol (r = 0.46, p < 0.001), but there was no significant relation between APD and LV (+)dP/dt with esmolol (r = 0.27, p = NS). Results in the single beat (restitution) studies were qualitatively similar to the steady state results; APD (at cycle length >400 ms) and LV (+)dP/dt (at cycle length >600 ms) were significantly higher with sotalol than they were with esmolol. CONCLUSIONS: The reverse use-dependent prolongation of APD by sotalol is associated with a positive inotropic effect.

Action Potentials↗
PubMed1996

Initial experience with venous stents in exertional axillary-subclavian vein thrombosis.

PURPOSE: Exertional thrombosis of the axillary and subclavian veins, also known as Paget-Schrötter syndrome, has been increasingly recognized in recent years as a cause of long-term morbidity. Recent aggressive approaches to treating Paget-Schrötter syndrome have suggested the association of early failure with residual subclavian vein stenosis. As a result, the use of endoluminal stents has been proposed as an aid to venous percutaneous transluminal angioplasty for this disorder. METHODS: This report outlines the therapy of 11 consecutive patients with Paget-Schrötter syndrome who were treated at our institution between October, 1992, and December, 1995. Stents were placed when percutaneous transluminal angioplasty was unsuccessful at achieving an adequate residual lumen. RESULTS: Stents were placed after initial thrombolysis in six patients and in late follow-up in two patients. Of the six patients who had stents placed at initial thrombolysis, first-rib resection was eventually performed in four. In two patients first-rib resection was not performed, and stent fracture occurred in both. Late patency was achieved in the stents of six of the eight patients. CONCLUSIONS: Trials to evaluate stents as an adjunct to conventional therapy seem warranted. The use of stents alone without first-rib resection, however, appears to be associated with stent fracture.

Adult↗
PubMed1999

[Role of nitric oxide synthase III and guanosine 3':5'- cyclic monophosphate in the protection exerted by nitric oxide on hepatic ischemia-reperfusion injury].

Nitric oxide (NO) exerts cytoprotective effects against hepatic ischemia-reperfusion damage. This study was designed to evaluate which isoform of NO synthase (NOS) is implicated in the generation of cytoprotective NO and to investigate whether NO effects are mediated by cyclic GMP (cGMP). After partial ischemia for 45 min, liver damage was estimated by the release into plasma of cytolytic enzymes. Ischemia-reperfusion induced marked increases in plasma creatine kinase and lactate dehydrogenase after 1 h of reperfusion and of aminotransferases after 6 h of reperfusion. The pretreatment of ischemic rats with 8-bromo-cGMP (16 mg/kg i.v. 30 min before ischemia) or with L-arginine (the endogenous precursor of NO, 100 mg/kg i.v.) significantly diminished the ischemia-reperfusion-induced release of all these enzymes. This demonstrates that cGMP possesses hepatoprotective properties. By immunohistochemistry, we observed, after 6 h of reperfusion, an increase in endothelial NOS-III immunoreactivity, particularly in the small arteries and sinusoids. This NOS-III accumulation in endothelial cells could protect the liver against ischemia-reperfusion by the local generation of NO probably via cGMP.

Animals↗