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1
Content available remote

Hypercholesterolemia antagonized heart adaptation and functional remodeling of the mitochondria observed in acute diabetes mellitus subjected to ischemia/reperfusion injury

100%
Ferko M., Farkasova V., Jasova M., Kancirova I., Ravingerova T., Duris Adameova A., Andelova N., Waczulikova I.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 5
2

Role of the mitochondrial ATP-sensitive Kplus channels in cardioprotection

100%
Ardehali H.
Acta Biochimica Polonica
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2004
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tom 51
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nr 2
The mitochondrial ATP-sensitive K+ (mitoKATP) channel was discovered more than a decade ago. Since then, several pharmacological studies have identified agents that target this channel some of which selectively target mitoKATP. These and other studies have also suggested that mitoKATP plays a key role in the process of ischemic preconditioning (IPC) and prevention of apoptosis. The mechanism by which mitoKATP exerts its protective effects is unclear, however, changes in mitochondrial Ca2+ uptake and levels of reactive oxygen species, and mitochondrial matrix swelling are believed to be involved. Despite major advances, several important issues re­garding mitoKATP remain unanswered. These questions include, but are not limited to: the molecular structure of mitoKATP, the downstream and upstream mechanisms that leads to IPC and cell death, and the pharmacological profile of the channel. This review attempts to provide an up-to-date overview of the role of mitoKATP in cardioprotection.
3

In vivo cardioprotective effects and pharmacokinetic profile of N-propyl caffeamide against ischemia reperfusion injury

84%
Cheng Y.-Y., Luo D., Xia Z., Tse H.-F., Li X., Rong J.
Archivum Immunologiae et Therapiae Experimentalis
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2017
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tom 65
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nr 2
4
Content available remote

Exposure to sixty minutes of hyperoxia upregulates myocardial humanins in patients with coronary artery disease - a pilot study

84%
Karu I., Tahepold P., Ruusalepp A., Reimann E., Koks S., Starkopf J.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 6
5
Content available remote

The role of urocortins in the cardiovascular system

84%
Walczewska J., Dzieza-Grudnik A., Siga O., Grodzicki T.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 6
6

Potassium channels in brain mitochondria

84%
Bednarczyk P.
Acta Biochimica Polonica
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2009
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tom 56
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nr 3
385-392
 Potassium channels are the most widely distributed class of ion channels. These channels are transmembrane proteins known to play important roles in both normal and pathophysiological functions in all cell types. Various potassium channels are recognised as potential therapeutic targets in the treatment of Parkinson's disease, Alzheimer's disease, brain/spinal cord ischaemia and sepsis. In addition to their importance as therapeutic targets, certain potassium channels are known for their beneficial roles in anaesthesia, cardioprotection and neuroprotection. Some types of potassium channels present in the plasma membrane of various cells have been found in the inner mitochondrial membrane as well. Potassium channels have been proposed to regulate mitochondrial membrane potential, respiration, matrix volume and Ca2+ ion homeostasis. It has been proposed that mitochondrial potassium channels mediate ischaemic preconditioning in various tissues. However, the specificity of a pharmacological agents and the mechanisms underlying their effects on ischaemic preconditioning remain controversial. The following potassium channels from various tissues have been identified in the inner mitochondrial membrane: ATP-regulated (mitoKATP) channel, large conductance Ca2+-regulated (mitoBKCa) channel, intermediate conductance Ca2+-regulated (mitoIKCa) channel, voltage-gated (mitoKv1.3 type) channel, and twin-pore domain (mitoTASK-3) channel. It has been shown that increased potassium flux into brain mitochondria induced by either the mitoKATP channel or mitoBKCa channel affects the beneficial effects on neuronal cell survival under pathological conditions. Recently, differential distribution of mitoBKCa channels has been observed in neuronal mitochondria. These findings may suggest a neuroprotective role for the mitoBKCa channel in specific brain structures. This minireview summarises current data on brain mitochondrial potassium channels and the efforts to identify their molecular correlates.
7
Content available remote

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

84%
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
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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.
8
Content available remote

A new face of endocannabinoids in pharmacotherapy. Part I: Protective role of endocannabinoids in hypertension and myocardial infarction

84%
Zubrzycki M., Liebold A., Janecka A., Zubrzycka M.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 2
9

A new physiological role of copper amine oxidases: cardioprotection against reactive oxygen intermediates

84%
Mateescu M. A., Dumoulin M. J., Wang X. T., Nadeau R., Mondovi B.
Journal of Physiology and Pharmacology. Supplement
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1997
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tom 48
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nr 2
10
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Content available

Permissive effect of molsidomine towards cardioprotective action of iloprost in myocardial ischaemia in cats

84%
Gryglewski R. J., Swies J., Chlopicki S., Niezabitowski P.
Journal of Physiology and Pharmacology
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1993
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tom 44
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nr 3
11
Content available remote

Cardioprotective role of sphingosine-1-phosphate

67%
Knapp M.
Journal of Physiology and Pharmacology
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2011
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tom 62
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nr 6
12
Content available remote

Cardioprotection of exogenous erythropoietin in mice with ligature-induced aortic stenosis: effects on maladaptive cardiac hypertrophy

67%
Zheng L., Xu J., Qiu W., Liu X., Zhao C.-M., Chen D., Chen Y.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 1
13-20
Pre-operative treatment with recombinant human erythropoietin may improve aortic stenosis patients' condition, including anemia and/or cardiac dysfunction, for subjecting to aortic valve replacement. In this study, we tested this hypothesis in a mouse model of aortic stenosis. Adult male mice were subjected to either aortic stenosis created by aortic ligature or sham operation. Aortic stenosis for 4 weeks caused cardiac hypertrophy, pulmonary congestion and left ventricular dysfunction. It was associated with increased levels of tumor necrosis factor-a in serum and myocardium, and reduced levels of interleukin-10 in myocardium but not in serum. Mytocyte apoptosis rate, level of cleaved caspase 3, activity of nuclear factor-B and expression of p38-MAPK pathway were also elevated. Erythropoietin treatment increased hematocrit but did not prevent the development of cardiac hypertrophy. It, however, reduced the apoptosis, prevented the increases in tumor necrosis factor-, nuclear factor-B activation and phosphorylation of p38, and attenuated the increases in lung weight, the decreases in LVEF and LVFS, and the increases in LVDd and LVDs. In conclusion recombinant human erythropoietin has cardioprotective effects in maladaptive cardiac hypertrophy by inhibiting nuclear factor-B activation, phosphorylation of p38-MAPK pathway, and production of tumor necrosis factor-, together leading to a reduced apoptosis.
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