2020
DOI: 10.3389/fphys.2020.00224
|View full text |Cite
|
Sign up to set email alerts
|

Effects of Hypoxia and Acidosis on Cardiac Electrophysiology and Hemodynamics. Is NHE-Inhibition by Cariporide Still Advantageous?

Abstract: Salameh et al. Hypoxic/Acidotic Injury of the Heart with additional acidosis. Acidosis without hypoxia only marginally disturbed LV function and electrophysiology, and was not affected by cariporide. Thus, our study demonstrated that several detrimental effects of hypoxia were mitigated or abrogated by acidosis and that NHE-inhibition improved only hypoxia-induced cardiac dysfunction.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
8
0

Year Published

2022
2022
2024
2024

Publication Types

Select...
6
1

Relationship

1
6

Authors

Journals

citations
Cited by 11 publications
(8 citation statements)
references
References 43 publications
0
8
0
Order By: Relevance
“…Moreover, impaired oxygenation of the myocardium leads to nitrosative stress and cell apoptosis or necrosis, conditions that may further reduce cardiac function. Typical reactions induced by hypoxia include formation of nitrotyrosine from nitrosylation of tyrosine residues by peroxynitrite radicals and activation of poly-ADP-ribose polymerase-1 (PARP-1) [11]. PARP-1 depletes cellular energy and mediates cell death via upregulation of poly-ADP-ribose (PAR) and translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus [12].…”
Section: Introductionmentioning
confidence: 99%
“…Moreover, impaired oxygenation of the myocardium leads to nitrosative stress and cell apoptosis or necrosis, conditions that may further reduce cardiac function. Typical reactions induced by hypoxia include formation of nitrotyrosine from nitrosylation of tyrosine residues by peroxynitrite radicals and activation of poly-ADP-ribose polymerase-1 (PARP-1) [11]. PARP-1 depletes cellular energy and mediates cell death via upregulation of poly-ADP-ribose (PAR) and translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus [12].…”
Section: Introductionmentioning
confidence: 99%
“…The myocardium has considerably lower demands as a result of the area's lack of contraction; therefore, the absence of blood and energy supply has less impact on the infarct's growth. 7 Glucose transporter (GLUT) 4 is the main GLUT in cardiomyocytes. 8 Myocardial ischemia inhibited GLUT4 translocation leading to reduced myocardial glucose uptake, indicating that utilization efficiency and glycogen content were significantly associated with cardiac ischemia-reperfusion injury (IRI).…”
Section: The Pathophysiological Mechanisms Of Ischemia-reperfusionmentioning
confidence: 99%
“…10 Anaerobic glycolysis not only leads to acidosis allowing Na + influx through the Na + /H + exchanger, but the lack of adenosine triphosphate (ATP) also inhibits Na + /K + -ATPase, both of which promote the accumulation of intracellular Na + . 7 Subsequently, the Na + / Ca 2+ exchanger works in reverse mode resulting in intracellular Ca 2+ overload. Once reperfusion occurs, increased cytoplasmic Ca 2+ accompanied by rapid normalization and reactivation of acidic pH induces the release-reuptake of Ca 2+ from the sarcoplasmic reticulum and uncontrolled sarcoplasmic fiber hypercontraction.…”
Section: The Pathophysiological Mechanisms Of Ischemia-reperfusionmentioning
confidence: 99%
See 1 more Smart Citation
“…NHE can increase damage to the pancreas due to its role in insulin release [31]. NHE affects Na+ and Ca2+ transport, which leads to hypoxia [32]. This, along with COVID-19 associated cell lysis, leads to increased lactate levels, insulin resistance and endothelial damage.…”
Section: Diabetes Mellitus and Diabetic Ketoacidosismentioning
confidence: 99%