Wyniki wyszukiwania

1

Worsening of long-term myocardial function after successful pharmacological pretreatment with cyclosporine

100%

Laudi S., Weimann J., Haschke M., Trump S., Schmitz V., Christians U., Kaisers U., Steudel W.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 1

Pretreatment with cyclosporine (CsA) decreases infarct size 24h after myocardial ischemia/reperfusion (I/R). The goal of this study was to determine effects of CsA pretreatment on long-term cardiac function after I/R-injury. Rats were randomly assigned to group1: vehicle-only, group2: CsA-5mg/kg/day, and group3: CsA-12.5mg/kg/day given orally for three days prior to I/R-injury (30 min of left anterior descending coronary artery occlusion). Post-I/R survival and cardiac function were evaluated 14 days after I/R-injury by echocardiography and invasive hemodynamic measurements. Rats with I/R-injury showed increased left ventricular pressure (LVEDP) compared to rats without I/R-injury (p<0.005). Although CsA initially decreased infarct size, no differences of LVEDP were seen 14 days after I/R-injury (vehicle: 21.2±8.9 mmHg, CsA-5mg/kg/day: 21.5±0.7 mmHg, CsA-12.5mg/kg/day: 20.5±9.4 mmHg). Ejection fraction and fractional shortening were decreased compared to baseline, but showed no differences between groups. On day 14, a dose-dependent increase in left ventricular end diastolic diameter was seen (p<0.001). CsA pretreatment was associated with a dose-dependent decrease in post-I/R-survival (vehicle: 56%, CsA-5mg/kg/day: 32%, CsA-12.5mg/kg/day: 16%; p=0.017). CsA pretreatment did not improve long-term cardiac function despite decreased infarct size 24h after I/R-injury, but increased post-I/R mortality significantly. Poor cardiac function after CsA pretreatment might be caused by left ventricular dilation.

2

Lung protection in cardio-pulmonary bypass

86%

Salameh A., Greimann W., Vollroth M., Dhein S., Bahramsoltani M., Dahnert I.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 1

3

Managing of ventricular reperfusion tachyarrhythmias - focus on a perfused myocardium

86%

Bernikova O. G., Sedova K. A., Durkina A. V., Azarov J. E.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 5

4

Accumulation of specific ceramides in ischemic-reperfused rat heart; effect of ischemic preconditioning

86%

Beresewicz A., Dobrzyn A., Gorski J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 3

Ceramide signalling has been implicated in the mechanism of myocardial ischemia/reperfusion injury (IR). This study tested the hypothesis that ceramides containing a specific amino-linked acyl residue mediate the injury, and that ischemic preconditioning (IPC) affords myocardial protection because it prevents increased ceramide accumulation in IR myocardium. Perfused rat hearts were subjected either to the sham perfusion or to 30 min global ischemia, 30 min ischemia/30 min reperfusion (IR) or were preconditioned prior to the standard IR. The ventricles were harvested for biochemical assay that involved transmethylation of ceramide amino-linked acyl residues, and gas liquid chromatography measurement of acyl methyl esters. Fourteen ceramides containing myrystic, palmitic, palmitoleic, stearic, oleic, linoleic, linolenic, arachidic, arachidonic, eicosapentaenoic, behenic, docosapentaenoic, docosahexaenoic or nervonic acid were identified in the myocardium of rats. The total basal ceramide concentration in the myocardium was 135 nmol/g tissue, and it was increased by 14.1% and 48.4% in the ischemia and IR group, respectively. However, in fact, IR increased the accumulation of only 7 out of 14 ceramides identified in the heart (i.e., those containing palmitic, stearic, oleic, linoleic, and arachidonic acid), and the relative magnitude of these increases varied between the particular ceramides and was independent from their basal tissue concentration. IPC improved postischemic hemodynamic recovery and partially prevented the reperfusion-induced increases in these 7 ceramides, while the other ceramides were unaffected by IPC. These results support the role of the specific ceramide signalling in the mechanism of myocardial IR injury. We speculate that by preventing tissue accumulation of certain ceramides, IPC attenuates this signalling, that adds to the mechanism of myocardial protection afforded by IPC.

5

Polyviewed expression of the altered contractility of the guinea-pig ileum after ischemia in situ and superfusion in vitro

86%

Santiago-Mejia J., Ventura-Martinez R., Gomez C., Parra-Gamez L., Gonzalez-Rios J., Rodriguez R.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 2

This study deals with the polyviewed expression of the altered contractility of the isolated ileum of the guinea-pig after ischemia/superfusion (I/S). Intestinal ischemia was produced by clamping the superior mesenteric artery for 40, 80 or 160 min. Ischemic and non-ischemic segments taken from the same guinea-pig were mounted for tension recording in organ baths and superfused (120 min) with an oxygenated Krebs-bicarbonate solution. Data were analyzed by means of the Polyview System software, which allows detecting simultaneously several events of one response. Histopathological changes in myenteric neurons were also examined. We found that ischemia in situ followed by superfusion in vitro (reoxygenation) severely reduces the spontaneous intestine contractile activity, and significantly decreases the maximal contractile response to ACh and to electrical field stimulation (EFS), the maximal rate of tension, and the sensitivity of the tissue to EFS. In addition, these ischemic intestines respond with a long-lasting contracture when electrical stimulation was started at supramaximal voltage. Functional alterations were time dependent. Neurons exhibited features of necrosis. These results provide clear evidence of detrimental effects of I/S on intestine contractile function. Digital analysis allows quantification of additional parameters important for evaluation of functional changes after I/S and of the degree of neuroprotection.

6

Antioxidant treatment prevents cardiac protein oxidation after ischemia-reperfusion and improves myocardial function and coronary perfusion in senescent hearts

86%

Besse S., Bulteau A. L., Boucher F., Riou B., Swynghedauw B., De Leiris J.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 4

Cardiovascular ageing is associated with an increase in cardiac susceptibility to ischaemia and reperfusion and production of reactive oxygen species has been suspected to be responsible for this age-associated particular vulnerability. To determine whether administration of antioxidant treatment could afford some protection against ischaemia and reperfusion during aging, isolated perfused hearts from adult and senescent rats were submitted to normoxia (180 min), prolonged low-flow ischaemia (15% of initial coronary flow;180 min) or low-flow ischaemia/reperfusion (45 min/30 min), without or with antioxidant enzymes (superoxide dismutase+catalase; 50IU/ml). Contractile function and coronary perfusion were measured and protein oxidation was quantitated in left ventricle after normoxia, ischaemia and ischaemia/reperfusion. Protein oxidation was higher in senescent than in adult hearts after ischaemia-reperfusion, in contrast to prolonged ischaemia. During prolonged ischaemia, antioxidant treatment prevented coronary vasoconstriction at both ages and delayed contractile dysfunction in senescent hearts but did not limit protein oxidation. During reperfusion, antioxidant treatment prevented coronary vasoconstriction and protein oxidation at both ages and considerably improved recovery of contractile function in senescent hearts. In conclusion, antioxidant treatment fully protects the senescent heart against ischaemia/reperfusion but not against prolonged ischaemia injury, indicating that oxidative stress plays a central role in the age-associated vulnerability to ischaemia-reperfusion.

7

Serum concentrations of MCP-1 and RANTES in patients during aortic surgery: the relationship with ischemia-reperfusion

86%

Jedynak M., Siemiatkowski A., Gacko M., Mroczko B., Borkowski J.

Archivum Immunologiae et Therapiae Experimentalis

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2004

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tom 52

|

nr 3

8

L-carnitine protects gastric mucosa by decreasing ischemia-reperfusion induced lipid peroxidation

86%

Derin N., Izgut-Uysal V. N., Agac A., Aliciguzel Y., Demir N.

Journal of Physiology and Pharmacology

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2004

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tom 55

|

nr 3

Studies have shown that reactive oxygen metabolites and lipid peroxidation play important roles in ischemia-reperfusion injury in many organs such as heart, brain and stomach. The aim of this study is to evaluate the antioxidant effect of L-carnitine on gastric mucosal barrier, lipid peroxidation and the activities of antioxidant enzymes in rat gastric mucosa subjected to ischemia-reperfusion injury. Rats were subjected to 30 min of ischemia followed by 60 min of reperfusion. L-carnitine (100 mg/kg), was given to rats intravenously five minutes before the ischemia. In our experiment, lesion index, thiobarbituric acid reactive substances, prostaglandin E2 and mucus content in gastric tissue were measured. The results indicated that the lesion index and the formation of thiobarbituric acid reactive substances increased significantly with the ischemia-reperfusion injury in the gastric mucosa. L-carnitine treatment reduced these parameters to the values of sham operated rats. The tissue catalase and superoxide dismutase activities and prostaglandin E2 production decreased significantly in the gastric mucosa of rats exposed to ischemia-reperfusion. L-carnitine pretreatment increased the tissue catalase activity and prostaglandin E2 to the levels of sham-operated rats but did not change superoxide dismutase activity. There were no significant difference in glutathione peroxidase activity and mucus content between the groups in the gastric mucosa. In summary, L-carnitine pretreatment protected gastric mucosa from ischemia-reperfusion injury by its decreasing effect on lipid peroxidation and by preventing the decrease in prostaglandin E2 content of gastric mucosa.

9

Neuroprotective effect of resveratrol against late cerebral ischemia reperfusion induced oxidative stress damage involves upregulation of osteopontin and inhibition of interleukin-1beta

72%

Al Dera H.

Journal of Physiology and Pharmacology

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2017

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tom 68

|

nr 1

10

Ageing influences the effect of pre-hypoxic administration of clonidine, an alpha2-adrenoceptor agonist, on post-hypoxic vasomotoricity

72%

Gourdin M. J., Ponchau O., Jamart J., De Kock M.

Journal of Physiology and Pharmacology

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2012

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tom 63

|

nr 2

11

Cardioprotective effect of 5-lipoxygenase gene [ALOX5] silencing in ischemia-reperfusion

72%

Lisovyy O. O., Dosenko V. E., Nagibin V. S., Tumanovska L. V., Korol M. O., Surova O. V., Moibenko O. O.

Acta Biochimica Polonica

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2009

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tom 56

|

nr 4

687-694

It is well known that 5-lipoxygenase derivates of arachidonic acid play an important pathogenic role during myocardial infarction. Therefore, the gene encoding arachidonate 5-lipoxygenase (ALOX5) appears to be an attractive target for RNA interference (RNAi) application. In experiments on cultivated cardiomyocytes with anoxia-reoxygenation (AR) and in vivo using rat model of heart ischemia-reperfusion (IR) we determined influence of ALOX5 silencing on myocardial cell death. ALOX5 silencing was quantified using real-time PCR, semi-quantitative PCR, and evaluation of LTC4 concentration in cardiac tissue. A 4.7-fold decrease of ALOX5 expression (P < 0.05) was observed in isolated cardiomyocytes together with a reduced number of necrotic cardiomyocytes (P < 0.05), increased number live (P < 0.05) and unchanged number of apoptotic cells during AR of cardiomyocytes. Downregulation of ALOX5 expression in myocardial tissue by 19% (P < 0.05) resulted in a 3.8-fold reduction of infarct size in an open chest rat model of heart IR (P < 0.05). Thus, RNAi targeting of ALOX5 protects heart cells against IR injury both in culture and in vivo.

12

Prophylactic effect of egualen sodium, a stable azulene derivative, on gastrointestinal damage induced by ischemia-reperfusion, double antiplatelet therapy and loxoprofen in rats

72%

Amagase K., Yoshida Y., Hara D., Murakami T., Takeuchi K.

Journal of Physiology and Pharmacology

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2013

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tom 64

|

nr 1

13

Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II

72%

Nakagiri A., Sunamoto M., Takeuchi K., Murakami M.

Journal of Physiology and Pharmacology

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2010

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tom 61

|

nr 2

Reactive oxygen species are known to be derived from NADPH oxidase in several tissues. Angiotensin II was suggested to be involved in the activation of NADPH oxidase; however, its role in the gastric mucosa is unclear. We examined the roles of angiotensin II receptor and NADPH oxidase in ischemia/reperfusion-induced gastric damage in rats. Under urethane anesthesia, male Sprague-Dawley rat stomachs were mounted in an ex-vivo chamber, had 100 mM HCl applied to them, and then a catheter was passed through the femoral vein. Ischemia/reperfusion was accompanied by blood collection and reperfusion through the catheter. Losartan, candesartan, valsartan, which are AT1 receptor blockers (ARB); PD123319, an AT2 receptor blocker; enalapril, an ACE inhibitor; or diphenylene iodonium, a NADPH oxidase inhibitor, was given i.v. 10 mins, and ß-NADPH, a NADPH oxidase substrate, was given i.v. 5 mins before reperfusion. The gastric damage by ischemia/reperfusion was attenuated by treatment with any of ARB or enalapril, but was not affected by PD123319. The increase in gastric H2O2 production and microvascular permeability by ischemia/reperfusion was also suppressed by treatment with any of ARB or enalapril. In rat gastric mucosa, the NADPH oxidase subunit p47phox was detected. Additionally, diphenylene iodonium had similar effects to ARB against ischemia/reperfusion-caused gastric damage, increased H2O2 production, and microvascular permeability. Ischemia/reperfusion activated NADPH oxidase in the gastric mucosa, and the activation was significantly attenuated by treatment with losartan or diphenylene iodonium. These results suggest that ischemia/reperfusion generated reactive oxygen species are derived from NADPH oxidase activation via AT1 receptor in rat stomachs.

14

Melatonin pretreatment does not modify extrasystolic burden in the rat ischemia-reperfusion model

72%

Durkina A. V., Bernikova O. G., Mikhaleva N. J., Paderin N. M., Sedova K. A., Gonotkov M. A., Kuzmin V. S., Azarov J. E.

Journal of Physiology and Pharmacology

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2021

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tom 72

|

nr 1

15

p-ERK involvement in the neuroprotection exerted by ischemic preconditioning in rat hippocampus subjected to four vessel occlusion

72%

Kovalska M., Kovalska L., Mikuskova K., Tatarkova Z., Lehotsky J.

Journal of Physiology and Pharmacology

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2014

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tom 65

|

nr 6

16

The presence of tau protein in blood as a potential prognostic factor in stroke patients

72%

Lasek-Bal A., Jedrzejowska-Szypulka H., Rozycka J., Bal W., Kowalczyk A., Holecki M., Dulawa J., Lewin-Kowalik J.

Journal of Physiology and Pharmacology

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2016

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tom 67

|

nr 5

17

Synergistic effects against post-ischemic cardiac dysfunction by sub-chronic nandrolone pretreatment and postconditioning: role of beta2-adrenoreceptors

72%

Penna C., Abbadessa G., Mancardi D., Tullio F., Piccione F., Spaccamiglio A., Racca S., Pagliaro P.

Journal of Physiology and Pharmacology

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2008

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tom 59

|

nr 4

645-659

ß2-adrenoreceptor overexpression is beneficial against ischemia/reperfusion (I/R) injury. Whether ß-adrenoreceptors are involved in postconditioning (PostC) is unknown. We investigated whether nandrolone-decanoate (ND)-pretreatment can modulate (1) ß-adrenoreceptor expression and (2) post-ischemic cardiac function in response to I/R and PostC. Finally, we tested whether cardioprotection can be prevented by the inhibition of ß2-adrenoreceptors. Isolated rat hearts from ND-pretreated (15 mg/kg/day i.m., for 14 days) and untreated-animals underwent 30-min ischemia and 120-min reperfusion. In subgroups, at the end of ischemia a PostC protocol (five cycles of 10-s reperfusion and 10-s ischemia) was applied and/or a ß2-adrenoreceptor blocker, ICI-118.551 (10 µM), was infused. Left ventricular pressure (LVP) was measured with an electromanometer, and infarct-size was evaluated using nitro-blue-tetrazolium staining. ND-pretreatment increased ß2-adrenoreceptor expression, but did not alter cardiac-weight, LVP and maximum rate of increase of LVP (dP/dtmax). After I/R, infarct-size was smaller in ND-pretreatment than in untreated-animals. Infarct-size was also reduced by PostC, both in untreated and ND-pretreated animals. Contracture was less marked in ND-pretreated animals. PostC reduced contracture in both ND-pretreated and untreated hearts. Moreover, PostC improved post-ischemic recovery of developed LVP and dP/dtmax much more in hearts of ND-pretreated than untreated-animals. ICI-118.551 abolished ND-protection and PostC-protection both in ND-pretreated and untreated hearts. Data show that two-weeks ND-pretreatment induces 1) an overexpression of ß2-ARs without cardiac hypertrophy and 2) improves the post-ischemic diastolic and systolic cardiac function. Intriguingly, ND-pretreatment potentiates the improvement of systolic function induced by postconditioning via ß2-adrenoreceptor activation.

18

Involvement of corticotropin-releasing factor and corticotropin-releasing factor 2 receptors in pathogenesis of ischemia/reperfusion-induced enteritis in rats

72%

Takeuchi K., Kumano A., Abe N., Kotani T.

Journal of Physiology and Pharmacology

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2016

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tom 67

|

nr 5

19

Heparin inhibits protective effect of ischemic preconditioning in ischemia/reperfusion-induced acute pancreatitis

72%

Warzecha Z., Dembinski A., Ceranowicz P., Dembinski M., Sendur R., Cieszkowski J., Sendur P., Tomaszewska R.

Journal of Physiology and Pharmacology

|

2012

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tom 63

|

nr 4

20

Low concentrations of an nitric oxide-donor combined with a liposoluble antioxidant compound enhance protection against reperfusion injury in isolated rat hearts

72%

Rastalo R., Cappello S., Folino A., Di Stilo A., Chegaev K., Tritto I., Pagliaro P., Losano G.

Journal of Physiology and Pharmacology

|

2010

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tom 61

|

nr 1

21-27

Nitric oxide (NO) and reactive oxygen species (ROS) are double-edged swords in reperfused hearts. The effects of a NO-donor and an antioxidant compound against ischemia/reperfusion were studied. The compounds were tested separately, as a mixture and as a new hybrid molecule containing both leads. Isolated rat hearts underwent 30 min global ischemia and 2 hrs reperfusion. Compounds were infused either at 1 or 10 µM concentrations during the first 20 min of reperfusion. Hybrid was also tested in the presence of mitochondrial K+ ATP-sensitive (mKATP) channel blockade by 5-HD (100 µM). Reduction of infarct size and recovery of left ventricular developed pressure during reperfusion were evaluated. When given at 1 µM concentration, hybrid significantly improved all indices of protection; its beneficial effects were abolished by mKATP channel blockade. At the same concentration, mixture and NO-donor alone improved recovery of left ventricular developed pressure but did not reduce infarct size; antioxidant was ineffective. When given at 10 µM concentration, antioxidant and mixture improved all parameters of protection; NO-donor and hybrid were ineffective. Our data suggest that different signaling cascades could be elicited by low and high concentrations of antioxidant compound and/or NO-donor. It is likely that a different NO-induced release of reactive oxygen species via mKATP channel activation may play a pivotal role in affecting infarct size and post-ischemic contractile recovery.

Ograniczanie wyników

Worsening of long-term myocardial function after successful pharmacological pretreatment with cyclosporine

Lung protection in cardio-pulmonary bypass

Managing of ventricular reperfusion tachyarrhythmias - focus on a perfused myocardium

Accumulation of specific ceramides in ischemic-reperfused rat heart; effect of ischemic preconditioning

Polyviewed expression of the altered contractility of the guinea-pig ileum after ischemia in situ and superfusion in vitro

Antioxidant treatment prevents cardiac protein oxidation after ischemia-reperfusion and improves myocardial function and coronary perfusion in senescent hearts

Serum concentrations of MCP-1 and RANTES in patients during aortic surgery: the relationship with ischemia-reperfusion

L-carnitine protects gastric mucosa by decreasing ischemia-reperfusion induced lipid peroxidation

Neuroprotective effect of resveratrol against late cerebral ischemia reperfusion induced oxidative stress damage involves upregulation of osteopontin and inhibition of interleukin-1beta

Ageing influences the effect of pre-hypoxic administration of clonidine, an alpha2-adrenoceptor agonist, on post-hypoxic vasomotoricity

Cardioprotective effect of 5-lipoxygenase gene [ALOX5] silencing in ischemia-reperfusion

Prophylactic effect of egualen sodium, a stable azulene derivative, on gastrointestinal damage induced by ischemia-reperfusion, double antiplatelet therapy and loxoprofen in rats

Evidence for the involvement of NADPH oxidase in ischemia/reperfusion-induced gastric damage via angiotensin II

Melatonin pretreatment does not modify extrasystolic burden in the rat ischemia-reperfusion model

p-ERK involvement in the neuroprotection exerted by ischemic preconditioning in rat hippocampus subjected to four vessel occlusion

The presence of tau protein in blood as a potential prognostic factor in stroke patients

Synergistic effects against post-ischemic cardiac dysfunction by sub-chronic nandrolone pretreatment and postconditioning: role of beta2-adrenoreceptors

Involvement of corticotropin-releasing factor and corticotropin-releasing factor 2 receptors in pathogenesis of ischemia/reperfusion-induced enteritis in rats

Heparin inhibits protective effect of ischemic preconditioning in ischemia/reperfusion-induced acute pancreatitis

Low concentrations of an nitric oxide-donor combined with a liposoluble antioxidant compound enhance protection against reperfusion injury in isolated rat hearts