Protective Effects of Antiarrhythmic Agents on Oxygen-Deficiency-Induced Contractile Dysfunction of Isolated Perfused Hearts

Takeo, Satoshi; Tanonaka, Kouichi; Liu, Jianxun; Ohtsuka, Y.

doi:10.1007/978-4-431-68219-6_3

Cited by 7 publications

(3 citation statements)

References 8 publications

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“…The effects of IV administration of lidocaine on cardiac and cerebral ischemia and reperfusion in other mammalian species have been evaluated experimentally. [12][13][14][15][16] In dogs with experimentally induced cardiac ischemia, IV administration of lidocaine improved cardiac contractility, 12 reduced the size of myocardial infarcts, 15 and reduced the formation of a lipid peroxidation product, 15 compared with findings in dogs that received a control treatment. Similar benefits have been detected in rats with experimentally induced cerebral ischemia.…”

mentioning

confidence: 96%

Anti-inflammatory effects of intravenously administered lidocaine hydrochloride on ischemia-injured jejunum in horses

Cook¹,

Shults²,

McDowell³

et al. 2009

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mentioning

confidence: 96%

Anti-inflammatory effects of intravenously administered lidocaine hydrochloride on ischemia-injured jejunum in horses

Cook¹,

Shults²,

McDowell³

et al. 2009

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“…Originally, analogous studies in hypoxic and reperfused isolated rabbit hearts appeared to confirm this hypothesis. Investigators in 1 study 21 found that lidocaine was able to decrease the release of adenosine, other ATP metabolites, and CK from heart muscle when administered during the hypoxic period, thereby increasing the contractile performance of cardiac muscle. Higher membrane stability of blood vessel endothelial cells was also assessed in a study 22 of morphological changes in IRinjured intestinal wall influenced by lidocaine.…”

Section: Discussionmentioning

confidence: 99%

Effects of in vivo lidocaine administration at the time of ischemia and reperfusion on in vitro contractility of equine jejunal smooth muscle

Guschlbauer

Feige²,

Geburek³

et al. 2011

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“…Evidence is accumulated that sodium overload is caused by increased sodium flux into the intracellular space from the extracellular space under conditions of ischemia and hypoxia and may play an important role in the genesis of IRI [ 8 ]. It has been shown that inhibition of sodium entry pathways into cardiomyocytes by pharmacological agents reduces sodium overload during ischemia and thus leads to better functional recovery after reperfusion [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Peptide Sodium Channels Modulator Mu-Agatoxin-Aa1a Prevents Ischemia-Reperfusion Injury of Cells

et al. 2023

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Ischemia-reperfusion injury (IRI) is an irreversible functional and structural injury. Restoration of normal oxygen concentration exacerbates the emergence and development of deadly cells. One of the possible moments of reperfusion damage to cells is an increase in the intracellular concentration of sodium ions. In this article, we study the mu-agatoxin-Aa1a, a modulator of sodium channels, on the processes of IRI cells damage. The toxin was synthesized using an automatic peptide synthesizer. Hypoxia was induced by reducing the content of serum and oxygen in the CHO-K1 culture. The influence of the toxin on the level of apoptosis; intracellular concentration of sodium, calcium, and potassium ions; intracellular pH; totality of reactive oxygen species (ROS), nitric oxide (NO), and ATP; and changes in the mitochondrial potential were studied. The experiments performed show that mu-agatoxin-Aa1a effectively prevents IRI of cells. Toxin reduces the level of apoptosis and prevents a decrease in the intracellular concentration of sodium and calcium ions during IRI. Mu-agatoxin-Aa1a contributes to the maintenance of elevated intracellular pH, reduces the intracellular concentration of ROS, and prevents the decrease in intracellular NO concentration and mitochondrial potential under conditions of reoxygenation/reperfusion. An analysis of experimental data shows that the mu-agatoxin-Aa1a peptide has adaptogenic properties. In the future, this peptide can be used to prevent ischemia/reperfusion tissue damage different genesis.

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Protective Effects of Antiarrhythmic Agents on Oxygen-Deficiency-Induced Contractile Dysfunction of Isolated Perfused Hearts

Cited by 7 publications

References 8 publications

Anti-inflammatory effects of intravenously administered lidocaine hydrochloride on ischemia-injured jejunum in horses

Anti-inflammatory effects of intravenously administered lidocaine hydrochloride on ischemia-injured jejunum in horses

Effects of in vivo lidocaine administration at the time of ischemia and reperfusion on in vitro contractility of equine jejunal smooth muscle

Peptide Sodium Channels Modulator Mu-Agatoxin-Aa1a Prevents Ischemia-Reperfusion Injury of Cells

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