Oral Sulfonylurea Hypoglycemic Agents Prevent Ischemic Preconditioning in Human Myocardium

Cleveland, Joseph C.; Meldrum, Daniel R.; Cain, Brian S.; Banerjee, Anirban; Harken, Alden H.

doi:10.1161/01.cir.96.1.29

Cited by 265 publications

(158 citation statements)

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“…The increase in PKG activity stimulates opening of mKATP, decreasing mitochondrial Ca 2+ overload, ROS production and prolonged opening of MPTP to maintain ATP production [29][30][31][32] . As well as its application in the myocardium, ischemic preconditioning can also be induced by brief interruptions of blood flow to other organs, particularly skeletal muscle.…”

Section: ■ Discussionmentioning

confidence: 99%

Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion

et al. 2018

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Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion 1 AbstractPurpose: To investigate the cardioprotective effects of ischemic preconditioning (preIC) and postconditioning (postIC) in animal model of cardiac ischemia/reperfusion. Methods: Adult rats were submitted to protocol of cardiac ischemia/reperfusion (I/R) and randomized into three experimental groups: cardiac I/R (n=33), preCI + cardiac I/R (n=7) and postCI + cardiac I/R (n=8). After this I/R protocol, the incidence of ventricular arrhythmia (VA), atrioventricular block (AVB) and lethality (LET) was evaluated using the electrocardiogram (ECG) analysis. Results: After reestablishment of coronary blood flow, we observed variations of the ECG trace with increased incidence of ventricular arrhythmia (VA) (85%), atrioventricular block (AVB) (79%), and increase of lethality (70%) in cardiac I/R group. The comparison between I/R + preIC group with I/R group demonstrated significant reduction in VA incidence to 28%, AVB to 0% and lethality to 14%. The comparison of I/R + postIC group with I/R group was observed significance reduction in AVB incidence to 25% and lethality to 25%. Conclusion:The preconditioning strategies produce cardioprotection more efficient that postconditioning against myocardial dysfunctions and lethality by cardiac ischemia and reperfusion.

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Section: ■ Discussionmentioning

confidence: 99%

Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion

et al. 2018

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“…End reperfusion tissue (90 min) CK activity was determined as described (18). Tissues were homogenized in 100 vol of ice-cold isotonic extraction buffer (5,18). The assay was performed with a CK kit (Sigma) by using an automated spectrophotometer.…”

Section: Methodsmentioning

confidence: 99%

“…However, human myocardial tissues obtained from patients undergoing elective cardiopulmonary bypass procedures have been studied under controlled ex vivo conditions (5,6). In this experimental model, human atrial trabeculae are suspended in a blood-free physiologically oxygenated buffer bath and then exposed to an episode of simulated ischemia.…”

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confidence: 99%

“…In this experimental model, human atrial trabeculae are suspended in a blood-free physiologically oxygenated buffer bath and then exposed to an episode of simulated ischemia. During this time, contractile force decreases dramatically; when the tissue is reexposed to oxygen, the contractile force returns but is diminished (60%-70% reduction) and evidence of myocardial damage is observed by release of creatine kinase (CK) (5,6). When TNF bioactivity is specifically neutralized during ischemia͞reperfusion (I͞R), a greater return of contractile force is observed, suggesting that endogenous myocardial TNF activity contributes to the contractile dysfunction induced by the ischemic event (7).…”

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confidence: 99%

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Inhibition of caspase 1 reduces human myocardial ischemic dysfunction via inhibition of IL-18 and IL-1β

Pomerantz

Reznikov

Harken

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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The proinflammatory cytokine IL-18 was investigated for its role in human myocardial function. An ischemia͞reperfusion (I͞R) model of suprafused human atrial myocardium was used to assess myocardial contractile force. Addition of IL-18 binding protein (IL-18BP), the constitutive inhibitor of IL-18 activity, to the perifusate during and after I͞R resulted in improved contractile function after I͞R from 35% of control to 76% with IL-18BP. IL-18BP treatment also preserved intracellular tissue creatine kinase levels (by 420%). Steady-state mRNA levels for IL-18 were elevated after I͞R, and the concentration of IL-18 in myocardial homogenates was increased (control, 5.8 pg͞mg vs. I͞R, 26 pg͞mg; P < 0.01). Active IL-18 requires cleavage of its precursor form by the IL-1␤-converting enzyme (caspase 1); inhibition of caspase 1 also attenuated the depression in contractile force after I͞R (from 35% of control to 75.8% in treated atrial muscle; P < 0.01). Because caspase 1 also cleaves the precursor IL-1␤, IL-1 receptor blockade was accomplished by using the IL-1 receptor antagonist. IL-1 receptor antagonist added to the perifusate also resulted in a reduction of ischemia-induced contractile dysfunction. These studies demonstrate that endogenous IL-18 and IL-1␤ play a significant role in I͞R-induced human myocardial injury and that inhibition of caspase 1 reduces the processing of endogenous precursors of IL-18 and IL-1␤ and thereby prevents ischemia-induced myocardial dysfunction.

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“…Ischemia/reperfusion process triggers macrophages and activated Küpffer cells release inflammatory cytokines 6 . Glibenclamide, an anti-diabetic agent, is a K ATP channel antagonist with half-life of 4±1 hour [7][8][9] . Some experimental studies have shown a possible relationship between glibenclamide action on the K ATP channel and effects in the inflammatory process 10,11 .…”

Section: Introductionmentioning

confidence: 99%

Serum concentrations and renal expressions of IL-1 and TNF-a early after hemorrhage in rats under the effect of glibenclamide

et al. 2016

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PURPOSE:To investigate changes in the serum concentration and renal expression of IL-1 and TNF-α cytokines in rats that received sevoflurane and glibenclamide prior to hemorrhage. METHODS:Two groups of sevoflurane-anesthetized Wistar rats (n=10): G1 (control) and G2 (glibenclamide, 1 µg/g i.v.); hemorrhage of 30% blood volume (10% every 10 min), with replacement using Ringer solution, 5 ml/kg/h. Serum concentrations of IL-1 and TNF-α were studied in the first hemorrhage (T1) and 50 min later (T2), renal expression, at T2. RESULTS:In serum, G1 TNF-α (pg/mL) was T1=178.6±33.5, T2=509.2±118.8 (p<0.05); IL-1 (pg/mL) was T1=148.8±31.3, T2=322.6±115.4 (p<0.05); in G2, TNF-α was T1=486.2±83.6, T2=261.8±79.5 (p<0.05); IL-1 was T1=347.0±72.0, T2= 327.3±90.9 (p>0.05). The expression of TNF-α and IL-1 in the glomerular and tubular cells was significantly higher in the G2 group. CONCLUSIONS:Hemorrhage and glibenclamide elevated TNF-α and IL-1 concentrations in serum and kidneys. High levels of TNF-α already present before the hemorrhage in the glibenclamide group may have attenuated the damages found in the kidneys after the ischemia event.Key words: Hemorrhage. Glyburide. Cytokines. Kidney. Rats. Serum concentrations and renal expressions of IL-1 and TNF-a early after hemorrhage in rats under the effect of glibenclamide

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Oral Sulfonylurea Hypoglycemic Agents Prevent Ischemic Preconditioning in Human Myocardium

Cited by 265 publications

References 14 publications

Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion

Cardioprotective effect of preconditioning is more efficient than postconditioning in rats submitted to cardiac ischemia and reperfusion

Inhibition of caspase 1 reduces human myocardial ischemic dysfunction via inhibition of IL-18 and IL-1β

Serum concentrations and renal expressions of IL-1 and TNF-a early after hemorrhage in rats under the effect of glibenclamide

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