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B C Yang

Publications and source records attributed to B C Yang.

At least 55 records · Page 3Linked to original sources

Inhibition of nitric oxide does not affect reperfusion-induced myocardial injury, but it prevents lipid peroxidation in the isolated rat heart.

To examine if inhibition of nitric oxide (NO) synthesis influences myocardial ischemia-reperfusion injury, male Sprague Dawley rats were administered the NO synthesis inhibitor N -nitro-L-arginine methyl ester (L-NAME, 10 mg/kg, i.p.) or saline 6 hours prior to excising the heart and aorta. Aortic ring contractile response to norepinephrine (NE) was more pronounced and relaxation in response to acetylcholine was abolished in L-NAME-treated group (P<0.05 vs. saline-treated group), indicating inhibition of NO synthesis in the vascular tissues. In the isolated perfused Langendorff hearts, force of cardiac contraction (FCC) and coronary perfusion pressure (CPP) were higher and coronary flow was lower in the L-NAME-treated group, again suggesting inhibition of NO synthesis. Global ischemia (40 min) followed by reperfusion (30 min) resulted in a decrease in FCC and coronary flow and an increase in CPP in all hearts. Myocardial CK also decreased similarly in all hearts. However, ischemia-reperfusion-induced decline in myocardial superoxide dismutase (SOD) activity and increase in malondialdehyde were prevented in the L-NAME-treated group (P<0.01 vs. saline-treated hearts). Thus treatment with L-NAME with resultant inhibition of NO synthesis does not affect ischemia-reperfusion-induced cardiac dysfunction and injury in the isolated rat hearts, although the reduction in SOD activity and the rise in lipid peroxidation following reperfusion are attenuated.

Acetylcholine↗

Reperfusion injury in the endotoxin-treated rat heart: reevaluation of the role of nitric oxide.

1. The role of nitric oxide (NO) in ischaemia-reperfusion injury to the heart continues to be debated. 2. The role of NO released during endotoxemia on myocardial reperfusion injury was examined in rats given saline or lipopolysaccharide (LPS, 10 mg. kg-1). 3. Aortic rings from LPS-treated rats showed a markedly decreased contractile response to both noradrenaline (NA) and U46619, and a diminished relaxation response to acetylcholine, thrombin and aggregating platelets. Treatment of rat aortic rings from LPS-treated rats with the NO synthesis inhibitor N omega-nitro-L-arginine (L-NOARG) reversed the diminished contractile response to NE and U46619. 4. Before ischaemia-reperfusion, baseline force of cardiac contraction (FCC) and coronary perfusion pressure (CPP) were lower and coronary flow was higher in hearts from LPS-treated rats (all P < 0.05 vs. saline-treated group). Treatment of hearts from LPS-treated rats with L-NOARG increased baseline FCC and CPP. 5. After ischaemia-reperfusion, hearts from saline-treated rats showed a 36 +/- 5% fall in FCC, a 38 +/- 6% rise in CPP and a 38 +/- 5% fall in coronary flow, whereas hearts from LPS-treated rats revealed only a 16 +/- 9% fall in FCC, a 10 +/- 3% rise in CPP and a 20 +/- 4% fall in coronary flow (all P < 0.05 vs. changes in saline-treated group). Fewer hearts from LPS-treated rats developed reperfusion arrhythmias (6% vs. 60% hearts from saline-treated rats, P < 0.02). Myocardial superoxide dismutase activity was higher in the LPS-treated group (P < 0.05). 6. NO synthesis, measured as formation of nitrite, was higher (P < 0.05) in cardiac and aortic tissues from LPS-treated rats. Prostacyclin (PGI2) release in coronary effluent was greater in LPS-treated rat hearts (P < 0.05 vs. saline-treated rats). 7. Thus LPS-treated hearts demonstrate a basal decrease in FCC and coronary vascular resistance. These hearts demonstrate a modest protection from reperfusion injury. Induction of NO synthesis, and possibly PGI2 release, may underlie cardioprotection from ischaemia-reperfusion.

Animals↗

Induction of apoptosis and cytokine gene expression in T-cell lines by sera of patients with systemic lupus erythematosus.

Accelerated apoptosis and improper expression of cytokine genes have been considered as important defects of lymphocytes for the development of systemic lupus erythematosus (SLE). This study was undertaken to test the possible contribution of serum factors obtained from SLE patients to these abnormalities. Molt-4 and Jurkat cells constantly exhibited a slower growth rate as well as more dead cells in culture with SLE sera tested than controls, although the cell cycle progression was apparently unaffected. Increased apoptosis was demonstrable among SLE sera-cultured cells by ELISA for apoptosis-specific DNA fragments and terminal deoxynucleotidyl transferase (TdT) in situ death analysis. Different levels of Fas, Fas-L, and Bcl-2 gene products were not detected between SLE sera-treated cells and the controls. The transcripts of interleukin-10 (IL-10) and interferon-gamma (IFN-gamma) genes of these two T cell lines were evidently increased in the presence of SLE sera, while IL-2 and IL-4 were unaffected. Elevated expression of IL-5 was also found in Molt-4 cells. By contrast, SLE sera reduced the transcripts of IL-6 gene in Jurkat cells. The effects of SLE sera were independent of corticosteroid medication. These results suggest that serum abnormalities may also play a role in T cell dysfunction.

Apoptosis↗

Dermatophagoides-farinae-induced pulmonary eosinophilic inflammation in mice.

Dermatophagoides farinae (Der f) is one of the most common species of dust mites that induce asthma and allergic rhinitis. We have reported that Der f challenge on sensitized mice elicited a distinct type of hypersensitivity, called early-type hypersensitivity (ETH), in subcutaneous tissues and in airways. The airway ETH was accompanied by a series of inflammatory and immunological events including cytokine production, adhesion molecule expression, inflammatory cell infiltration, eosinophilia, and airway hyperreactivity. In the present study, we further defined the course of the Der-f-induced eosinophilia and examined the local cytokine gene expression and the roles of cytokines, mast-cell-derived vasoactive amines, and corticosteroids in the development of pulmonary eosinophilia. BALB/c mice were sensitized with crude extract of Der f in complete Freund's adjuvant and were intranasally challenged with Der f on day 14 after sensitization. The number of blood eosinophils, total and differential leukocyte counts in bronchoalveolar lavage (BAL) fluids, and the expression of cytokine genes in BAL cells were assessed at various time points after challenge for up to 12 days. The total number of leukocytes in the BAL fluids was increased 6 h after challenge (AC) and peaked at 72 h. The early cellular response in the BAL fluids was dominated by neutrophils which were subsequently replaced by a marked infiltration of eosinophils. The number of eosinophils in BAL fluids increased at 24 h and peaked at 72 h, making up 43% of all cells recovered by BAL. BAL eosinophils declined gradually to normal background levels around day 12. Concurrently, there was a significant reduction in the number of eosinophils in blood 24 h AC. The number of blood eosinophils increased thereafter, reached a peak at 72 h, and remained above baseline level for up to 10 days. Saline challenge did not induce eosinophilia in BAL fluids and blood of sensitized mice. Histopathological examination revealed a mixed granulocytic, monocytic pulmonary inflammation with a large number of eosinophils accumulating within the submucosa of the airways and blood vessels of sensitized mice after challenge. Der f challenge induced a sequential expression pattern of eight cytokine genes in BAL cells. The mRNA of interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha strongly expressed throughout the course of the experiment. The IL-6 mRNA expression peaked at 0.5-72 h, IL-10 at 1-6 and 48-72 h, IL-4 at 6-72 h, IL-2 at 6-96 h, IL-5 at 24-72 h, and interferon-gamma at 24-96 h. Intraperitoneal injection of sensitized mice with monoclonal antibody (mAb) to murine IL-5 (TRFK5, 300 micrograms/mouse) 1 h before challenge caused 62% suppression of eosinophils in the BAL fluids. The concomitant accumulation of neutrophils and mononuclear cells, however, was not affected by this treatment. On the other hand, intranasal administration of mAb to murine TNF-alpha (MP6-XT3, 20 micrograms/ mouse), but not IL-5, 1 h before challenge and 24 h AC significantly reduced the numbers of eosinophils, neutrophils, and lymphocytes in the BAL fluids. The intraperitoneal injection of dexamethasone (50 mg/kg) for a total of four times resulted in total inhibition of the Der-f-induced cellular responses, whereas vasoactive amine antagonists (diphenhydramine, ketanserin and cyprohepatidine) did not show any effect.

Allergens↗

Transient induction of apoptosis in serum-starved glioma cells by insulin and IGF-1.

Insulin has a wide variety of biological effects. One of them is a mitogen-like activity whereby cell proliferation is stimulated. In this study we found a heretofore unreported insulin-elicited transient apoptosis of glioma cells. When serum-starved glioma cells were fed with a fresh regular medium, in the 6- to 12-h post-starvation period, the growth rate as determined by cell number was significantly suppressed by insulin, although cell cycle progression and DNA synthesis were actually accelerated. Increase in apoptosis in those growth-retarded cultures was demonstrable by Hoechst staining, detection of histone-associated DNA fragment, and in situ cell death detection. Apoptosis occurred among cells in all stages of cell cycle. After 24 h post-starvation, insulin increased the total cell number like a typical growth-promoting mitogen. In this regard, IGF-1, but not EGF nor TGF-beta 1, behaved like insulin.

Apoptosis↗

Adrenomedullin dilates rat pulmonary artery rings during hypoxia: role of nitric oxide and vasodilator prostaglandins.

Hypoxia decreases vasorelaxation and leads to pulmonary arterial hypertension. A newly identified 52 amino-acid peptide adrenomedullin (ADM) exerts vasodilator effect in intact animals under normoxic condition. We studied the effect of human ADM on rat pulmonary arterial and aortic rings under normoxic and hypoxic conditions. During normoxia, ADM caused a concentration-dependent relaxation of precontracted aortic and pulmonary arterial rings; the relaxation was much more pronounced in pulmonary arterial rings and was abolished by the nitric oxide (NO) synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) and by deendothelialization. A fragment of ADM, ADM13-52, caused a degree of relaxation similar to that induced by ADM in pulmonary arterial rings, but not in the aortic rings, and the relaxation of pulmonary artery caused by ADM13-52 was not affected by the cyclooxygenase inhibitor indomethacin but was abolished by L-NAME and by deendothelialization. During hypoxia, ADM13-52 failed to relax pulmonary arterial rings, whereas ADM caused modest relaxation of pulmonary arterial rings (one third of the relaxation during normoxia), which was abolished by pretreatment with indomethacin. Our results indicate that the vasorelaxant effect of ADM is more pronounced in pulmonary artery than in the aorta; ADM has more potent vasodilator effect than ADM13-52 during hypoxia; ADM relaxes hypoxic pulmonary artery through an indomethacin-sensitive pathway; amino acids 1-12 in ADM must be present for relaxation of chronic hypoxic pulmonary arterial rings; and last, the presence of endothelium is necessary for the expression of ADM-mediated relaxation.

Adrenomedullin↗

Increased IL-5 and IL-10 transcription in bronchial cells after Sauropus androgynus ingestion.

An outbreak of rapidly progressive obstructive lung disease in Taiwan was noted in some patients regularly ingesting the vegetable Sauropus androgynus because of its perceived weight reducing properties. Bronchoalveolar lavage (BAL) prior to administration of medication was performed in two women who had regularly ingested this vegetable and had developed obstructive ventilatory defects. Both patients showed a significant increase in neutrophils and, to a lesser extent, of eosinophils in the lavage fluid as compared to two unrelated controls. Interleukin (IL)-1 beta, IL-2, IL-5, IL-10, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha in cells recovered from BAL fluid were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). Augmented expression of the IL-10 gene was detected in only two patients who had regularly ingested S. androgynus. Our results suggest that altered cytokine expression and infiltration of eosinophils and neutrophils may be involved in the pathology of obstructive lung disease caused by regular ingestion of S. androgynus.

Adult↗

Rapid inhibition of protein histidine phosphorylation by UV-irradiation in Xanthomonas oryzae pv. oryzae.

Exposure of Xanthomonas oryzae pv. oryzae cells to 254 nm UV radiation resulted in an alteration of protein phosphorylation. Labelling of the phosphohistidine-containing proteins with molecular masses of 81 and 32 kDa, named p81 and p32, was rapidly reduced following UV irradiation in the early exponential cells, but the decrease was not detected in mid-exponential cells. Mitomycin C, a DNA replication inhibitor, and rifampicin, a drug generally used to inhibit RNA synthesis and DNA replication, were also found to reduce the histidyl phosphorylation. However, this alteration of protein phosphorylation was not hindered by chloramphenicol treatment. A possible role for these histidyl phosphoproteins in sensing UV light is proposed.

Bacterial Proteins↗

Effects of a gonadotropin releasing hormone agonist on oocyte maturation, fertilization, and embryonal development of mice.

PURPOSE: The effects of a GnRH agonist (GnRHa) on oocyte quality were investigated by assessing the influence of GnRHa on oocytes, and fertilized oocytes were examined in vivo and in vitro. Administration of gonadotropin in conjunction with GnRHa induced a significantly greater degree of germinal vesicle breakdown, significantly higher rates of in vitro fertilization, and significantly faster development of the oocytes than the pregnant mare serum gonadotropin alone RESULTS: The hatching-success rate in the GnRHa treated hypophysectomized mice was higher than in control mice. The rate of in vitro fertilization was also higher in oocytes cultured in the presence of low loses of GnRHa and these effects were reversed by a GnRH antagonist. CONCLUSION: Oocytes obtained following ovarian stimulation with GnRHa were of higher quality than control oocytes, and the efficacy of GnRHa may be due in part to its direct action on the ovary.

Animals↗

Critical role of endothelium in sustained arterial contraction during prolonged hypoxia.

Acute anoxia or severe hypoxia causes an initial transient contraction followed by marked relaxation of vascular tissues. We observed a spontaneous gradual sustained contraction of rat aortic rings following relaxation when hypoxia was prolonged. Deendothelialization as well as treatment of the endothelium-intact rings with nitric oxide synthase inhibitors or oxyhemoglobin abolished the late hypoxic contraction despite prolonged hypoxia. The prolonged hypoxia-induced sustained contraction was not affected by adenosine receptor blockade, cyclooxygenase inhibition, free radical scavengers, or the endothelin receptor antagonists. The ATP-sensitive K+ channel blocker glibenclamide abbreviated the duration of hypoxic relaxation and potentiated the magnitude of late hypoxic contraction. These data suggest that the late-sustained hypoxic contraction of arterial tissues is dependent on the presence of intact functional endothelium. Activation of ATP-sensitive K+ channels may participate in the genesis of hypoxic relaxation. However, cyclooxygenase products, free oxygen radicals, adenosine, and endothelin are not involved in the regulation of hypoxia-mediated events in rat aortic rings.

Adenosine Triphosphate↗

Alterations in pulmonary artery tone during repeated episodes of hypoxia.

To examine the basis of pulmonary constriction during chronic hypoxia, rat pulmonary artery rings were precontracted and exposed to multiple episodes of hypoxia. The first hypoxic episode resulted in a transient contraction, followed by potent relaxation, and then a slow sustained contraction. Repeated hypoxic exposure resulted in stronger initial contraction and attenuated relaxation. Prolongation of the normoxic interval between hypoxic episodes reversed the attenuation of hypoxic relaxation. Pulmonary artery rings that were deendothelialized or treated with the nitric oxide synthesis inhibitor N omega-nitro-L-arginine methyl ester or oxyhemoglobin displayed only hypoxic relaxation without initial or late contractions and no attenuation of relaxation during repeated hypoxia. Pretreatment of rings with indomethacin or adenosine or endothelin receptor antagonists had no effect on the hypoxia-mediated alterations. Thus repetitive exposure to hypoxia results in an increase in initial contraction and a decrease in relaxation of pulmonary artery rings. Frequency of hypoxic episodes and endothelial integrity determine pulmonary tone during repeated hypoxia. However, cyclooxygenase products, adenosine, or endothelin do not play a role in hypoxia-mediated changes in rat pulmonary artery tone.

Animals↗

Adenosine protects against attenuation of flow reserve and myocardial function after coronary occlusion and reperfusion.

Total coronary artery occlusion and reperfusion result in attenuation of coronary blood flow reserve, regional myocardial dysfunction, and myocardial leukocyte infiltration. To examine the effects of intracoronary adenosine on these occlusion and reperfusion-induced perturbations, we subjected 14 dogs to total left anterior descending (LAD) coronary artery occlusion (1 hour) and reperfusion (1 hour). Seven dogs received adenosine (3.75 mg/min into the LAD distal to the occlusion) over a 1-hour period starting 5 minutes before reperfusion, and the remaining seven dogs received saline solution. One dog in each group died of ventricular fibrillation during coronary artery occlusion. Coronary flow reserve, measured as peak reactive hyperemia (10 and 20 seconds of total coronary artery occlusion) and peak coronary blood flow response to acetylcholine (0.01 to 1.0 micrograms) and nitroglycerin (5 to 25 micrograms), was impaired in the LAD region after LAD occlusion and reperfusion in the saline-treated dogs (all p < 0.01 vs before occlusion and reperfusion); LAD regional myocardial shortening fraction measured by ultrasonic crystals was also diminished after occlusion and reperfusion in saline-treated dogs (-5% +/- 1% vs 12% +/- 2%; p < 0.02). The adenosine-treated dogs showed total protection against loss of coronary flow reserve (peak reactive hyperemia and blood flow increase in response to acetylcholine and nitroglycerin; all p values not significant vs before LAD occlusion and reperfusion). LAD regional myocardial shortening fraction was also preserved in adenosine-treated dogs (9% +/- 2% vs 14% +/- 2%; p not significant). Myocardial myeloperoxidase activity, measured as an index of myocardial leukocyte infiltration, was greater (p < 0.02) in the LAD ischemic-reperfused regions than in nonischemic circumflex regions in the saline-treated dogs. A similar difference in myeloperoxidase activities in the reperfused and control regions was not observed in the adenosine-treated dogs. Thus adenosine protects against loss of coronary flow reserve and regional myocardial function in dogs subjected to coronary artery occlusion and reperfusion.

Acetylcholine↗

Failure of brief ischemic episodes to protect against myocardial dysfunction caused by ischemia and reperfusion in isolated rat hearts.

Brief periods of ischemia have been suggested to protect against myocardial injury caused by a subsequent episode of prolonged ischemia and reperfusion. However, the protective effects of brief ischemic periods against myocardial dysfunction after prolonged myocardial ischemia are controversial. To examine whether the protective effects of brief ischemic episodes relate to the extent of prior ischemic events, isolated rat hearts were subjected to either no preischemia (group A); one 5-minute episode of preischemia and 10 minutes of reperfusion (group B); or two 1-minute episodes of ischemia, each followed by 5 minutes of reperfusion (group C). All hearts were then subjected to 15 minutes of total ischemia and 10 minutes of reperfusion. In group A, after 10 min of reperfusion coronary perfusion pressure (CPP) was 31% +/- 10% (mean +/- SEM) higher than the control value, peak force of cardiac contraction (FCC) was 64% +/- 5% lower, and heart rate was 18% +/- 3% lower. In group B, CPP increased 26% +/- 6%, FCC fell 58% +/- 7%, and heart rate decreased 22% +/- 8% (group B vs group A, P value not significant) after ischemia and reperfusion. In group C, CPP increased 23% +/- 7%, FCC decreased 57% +/- 8%, and heart rate fell 8% +/- 4% on reperfusion (group C vs groups A and B, P value not significant). Creatine kinase (CK) was measured in the hearts from different groups and was found to be similar. Release of the adenosine triphosphate (ATP) metabolites hypoxanthine, inosine, and adenosine was also not different in the coronary effluents of the three groups of hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

Cardioprotective effects of platelets against ischaemia-reperfusion injury are related in part to platelet glutathione redox cycle.

OBJECTIVE: Washed platelets have been shown to protect isolated buffer perfused rat hearts from injury and dysfunction following ischaemia-reperfusion. This study was designed to investigate whether platelet glutathione redox cycle contributes to the protective effect of platelets. METHODS: Isolated rat hearts were perfused with Krebs-Henseleit buffer alone, buffer containing platelets, or buffer containing platelets pretreated with inhibitors of glutathione redox cycle. All hearts were subjected to 40 min of global ischaemia followed by 30 min of reperfusion. RESULTS: Following ischaemia and reperfusion, hearts perfused with buffer alone showed a marked reduction in force of cardiac contraction and heart rate, an increase in coronary perfusion pressure and diastolic tone, and a release of creatine kinase in the coronary effluent. Myocardial creatine kinase, superoxide dismutase activity, and glutathione content all fell. Perfusion of hearts with washed platelets provided significant protection from ischaemia-reperfusion related myocardial injury and dysfunction. The cardioprotective effects of platelets were attenuated when they were preincubated with the glutathione redox cycle inhibitors dehydroepiandrosterone, 1,3-bis (2-chloroethyl)-1-nitrosurea, or 1-chloro-2,4-dinitrobenzene. Pretreatment of platelets with glutathione redox cycle inhibitors did not affect the platelet mediated preservation of myocardial superoxide dismutase activity. CONCLUSIONS: Platelet glutathione redox cycle contributes in part to the cardioprotective effects of platelets against ischaemia-reperfusion injury and dysfunction in the isolated rat heart.

Animals↗

Monoclonal antibody to P-selectin (PB1.3) protects against myocardial reperfusion injury in the dog.

OBJECTIVE: The aim was to determine whether a monoclonal antibody directed at P-selectin (PB1.3) would diminish neutrophil accumulation and protect against decrease in coronary flow reserve and myocardial function after coronary occlusion-reperfusion. METHODS: Sixteen open chest anaesthetised dogs were randomly given PB1.3 (2 mg.kg-1) or buffer intravenously after 50 min of total left anterior descending coronary artery occlusion. Ten minutes later, the artery was reperfused for 1 h. Coronary flow reserve was measured as peak reactive hyperaemic flow and as increase in coronary flow in response to acetylcholine and glyceryl trinitrate. Myocardial contractile fraction was measured by ultrasonic crystals. Neutrophil infiltration and oxidative burst in the reperfused area were also measured. RESULTS: Coronary flow reserve and myocardial contractile function were markedly impaired in the supply region following left anterior descending coronary artery occlusion-reperfusion in the buffer treated dogs. In contrast, both coronary flow reserve and contractile fraction were preserved in PB1.3 treated dogs despite coronary occlusion-reperfusion. Myeloperoxidase, an index of neutrophil infiltration, was increased in the reperfused region in buffer treated dogs, but not in the PB1.3 treated dogs. Myocardial histology confirmed the reduction in neutrophil accumulation in the reperfused regions in PB1.3 treated dogs. Flow cytometry of the regions supplied by the left anterior descending coronary artery showed a marked decrease in neutrophil oxidative burst in the reperfused region in these dogs. CONCLUSIONS: Antibody to P-selectin (PB1.3) protects against attenuation of coronary flow reserve and myocardial contractile function after coronary occlusion-reperfusion, and decreases neutrophil deposition and activation in the reperfused region.

Animals↗

Platelet-derived adenosine contributes to the cardioprotective effects of platelets against ischemia-reperfusion injury in isolated rat heart.

Platelets have been shown to protect isolated perfused rat hearts from injury and dysfunction after ischemia and reperfusion. We examined the role of platelet-derived adenosine in the cardioprotective effects of platelets against reperfusion injury. Isolated perfused rat hearts were subjected to 40-min global ischemia followed by 30-min reperfusion. The buffer-perfused hearts developed dysfunction, as indicated by 40 +/- 4% decrease in force of cardiac contraction (FCC) and 24 +/- 3% increase in coronary perfusion pressure (CPP). Creatine kinase (CK) was released in coronary effluent during reperfusion, indicating myocardial injury. At the end of reperfusion, myocardial CK content and superoxide dismutase (SOD) activity were lower than in sham ischemia-reperfused hearts. Perfusion of hearts with washed platelets resulted in protection against myocardial dysfunction and injury after ischemia and reperfusion, indicated by preservation of FCC (-2 +/- 5%) and CPP (-3 +/- 2%) (both p < 0.01 vs. buffer-perfused hearts). Myocardial CK and SOD activity were also preserved, and release of CK in the coronary effluent was minimal (all p < 0.05 vs. buffer-perfused hearts). The cardioprotective effects of platelets were attenuated by preincubation of platelets with adenosine deaminase. Perfusion with adenosine or the adenosine2 receptor agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2- methylphenyl)-ethyl]adenosine (DPMA) also protected heart from myocardial dysfunction and injury after ischemia and reperfusion. Both adenosine and DPMA had salutary effects on indexes of cardiac injury. Platelet-derived adenosine contributes at least in part to the cardioprotective effects of platelets against ischemia and reperfusion in isolated rat heart.

Adenosine↗

Prior episode of anoxia attenuates vasorelaxation in response to subsequent episode of anoxia.

To examine the effect of a prior episode of anoxia on subsequent anoxia-mediated vasorelaxation, norepinephrine-precontracted endothelium-intact rat aortic rings were first exposed to anoxia (95% N2-5% CO2 for 5, 15, or 30 min) then to normoxia (95% O2-5% CO2 for 15 min). These rings were exposed again to anoxia for 30 min. First exposure of rings to anoxia for 30 min resulted in 77 +/- 4% decrease in tone (vasorelaxation), whereas second exposure resulted in only 10 +/- 4% relaxation (n = 11, P < 0.001 vs. relaxation during first exposure). First exposure of rings to anoxia for 5 or 15 min also diminished relaxation to 59 +/- 3 and 19 +/- 8%, respectively, on second exposure to anoxia (both P < 0.01 vs. relaxation during 1st anoxia). Attenuation of vasorelaxation by prior episode of anoxia was not affected by treatment of rings with indomethacin (10(-5) M), the Ca2+ channel blocker felodipine (10(-6) M), the superoxide anion scavenger superoxide dismutase (100 micrograms/ml), or adenosine A1 and A2 blockers (each 10(-6) M). To examine the role of intact functional endothelium in attenuation of vasorelaxation during second anoxic exposure, rings were deendothelialized and treated with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA; 10(-4) M) or the guanylate cyclase inhibitor methylene blue (MB; 2 x 10(-5) M). In all deendothelialized rings, vasorelaxation during second anoxic exposure was similar to that during first anoxic exposure (100 +/- 0 vs. 98 +/- 3%, P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗

Blockade of platelet-mediated relaxation in rat aortic rings exposed to xanthine-xanthine oxidase.

Platelet-induced relaxation of endothelium-intact vascular tissues, mediated via release of endothelium-derived relaxing factor (EDRF), is diminished or lost after ischemia and reperfusion. Release of oxygen free radicals during ischemia-reperfusion may degrade EDRF and influence response of vascular tissues to platelets. To determine platelet modulation of tone of blood vessels treated with oxygen free radicals, rat aortic rings with intact endothelium were exposed to xanthine (X) plus xanthine oxidase (XO) 5 min before contraction with norepinephrine followed by exposure of rings to platelets. Treatment of aortic rings with X+XO caused a modest contraction, potentiated norepinephrine-mediated contraction, and inhibited platelet-mediated vasorelaxation. Exposure of aortic rings to X+XO also decreased ADP- as well as acetylcholine-mediated relaxation. Pretreatment of rings with superoxide dismutase or catalase did not change X+XO-induced inhibition of platelet-mediated relaxation, but it abolished the X+XO-induced contraction of rings as well as subsequent potentiation of norepinephrine-mediated contraction. Pretreatment of rings with hydroxyl radical scavengers dimethyl-2-thiourea, dimethyl sulfoxide, mannitol, or histidine attenuated the X+XO-induced inhibition of platelet-mediated relaxation, although these agents did not affect X+XO-induced contraction of rings. This study indicates that the vasoconstriction on exposure of aortic rings to X+XO is due to generation of superoxide anions, whereas inhibition of platelet-mediated relaxation after exposure of vessels to X+XO is due, at least in part, to release of hydroxyl radicals. Release of superoxide anions and hydroxyl radicals after temporary arterial occlusion may be the basis of subsequent modulation of vascular tone.

Animals↗