Chronic heart failure induced by coronary artery ligation in Lewis inbred rats

1997 ◽  
Vol 272 (2) ◽  
pp. H722-H727 ◽  
Author(s):  
Y. H. Liu ◽  
X. P. Yang ◽  
O. Nass ◽  
H. N. Sabbah ◽  
E. Peterson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Artery ◽  
Cardiac Dysfunction ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Sprague Dawley ◽  
End Diastolic Volume ◽  
Lv Dysfunction ◽  
Sprague Dawley Rats ◽  
Inbred Rats

Rat models of heart failure (HF) secondary to myocardial infarction (MI) are useful in studying the progression of cardiac dysfunction and in testing therapeutic approaches. Sprague-Dawley rats are frequently used; however, this model is hampered by high mortality and a marked variability in infarct size and cardiac dysfunction, necessitating large numbers of rats and prolonged follow-up when studying the progression of dysfunction. In the present work, we developed a model of HF utilizing Lewis inbred rats. Ligation of the left anterior descending coronary artery in Lewis rats produced more uniform and larger infarcts (40 +/- 1.7 vs. 28 +/- 2.3%; P < 0.001) and lower mortality (16 vs. 36%; P < 0.001) than in Sprague-Dawley rats. Using this rat model, we further studied the course of left ventricular (LV) dysfunction and enlargement from 1 wk to 6 mo after MI with cineventriculography. LV end-systolic volume and end-diastolic volume were determined with the area-length method. LV ejection fraction ranged between 0.57 and 0.62 in control rats; after MI, it decreased significantly to 0.48 +/- 0.04 at 1 wk, 0.36 +/- 0.02 at 2 wk, 0.48 +/- 0.02 at 1 mo, 0.35 +/- 0.03 at 2 mo, 0.30 +/- 0.02 at 3 mo, 0.31 +/- 0.02 at 4 mo, and 0.24 +/- 0.02 at 6 mo (P < 0.001, MI vs. sham). LV end-diastolic volume in control rats ranged between 0.32 and 0.42 ml; it increased to 0.48 +/- 0.04 ml at 1 wk, 0.46 +/- 0.02 ml at 2 wk, and 0.46 +/- 0.03 ml at 1 mo. It markedly increased to 0.79 +/- 0.03, 0.79 +/- 0.06, 0.78 +/- 0.03, and 0.80 +/- 0.05 ml at 2, 3, 4, and 6 mo, respectively, after MI (P < 0.001 vs. sham). LV end-diastolic pressure was significantly elevated at all time points. Thus coronary ligation in Lewis inbred rats produces uniformly large infarcts with low mortality, progressive LV dysfunction, and increased LV chamber size. This model may be useful in studying chronic HF secondary to MI.

scholarly journals XPO1 Gene Therapy Attenuates Cardiac Dysfunction in Rats with Chronic Induced Myocardial Infarction

2019 ◽  
Vol 13 (4) ◽  
pp. 593-600
Author(s):  
María García-Manzanares ◽  
Estefanía Tarazón ◽  
Ana Ortega ◽  
Carolina Gil-Cayuela ◽  
Luis Martínez-Dolz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Dysfunction ◽  
Cardiac Tissue ◽  
Left Ventricular ◽  
Partial Recovery ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Coronary Ligation ◽  
Transcriptomic Signature ◽  
Echocardiographic Assessment

AbstractTranscriptomic signature of XPO1 was highly expressed and inversely related to left ventricular function in ischemic cardiomyopathy patients. We hypothesized that treatment with AAV9-shXPO1 attenuates left ventricular dysfunction and remodeling in a myocardial infarction rat model. We induced myocardial infarction by coronary ligation in Sprague-Dawley rats (n = 10), which received AAV9-shXPO1 (n = 5) or placebo AAV9-scramble (n = 5) treatment. Serial echocardiographic assessment was performed throughout the study. After myocardial infarction, AAV9-shXPO1-treated rats showed partial recovery of left ventricular fractional shortening (16.8 ± 2.8 vs 24.6 ± 4.1%, P < 0.05) and a maintained left ventricular dimension (6.17 ± 0.95 vs 4.70 ± 0.93 mm, P < 0.05), which was not observed in non-treated rats. Furthermore, lower levels of EXP-1 (P < 0.05) and lower collagen fibers and fibrosis in cardiac tissue were observed. However, no differences were found in the IL-6 or TNFR1 plasma levels of the myocardium of AAV9-shXPO1 rats. AAV9-shXPO1 administration attenuates cardiac dysfunction and remodeling in rats after myocardial infarction, producing the gene silencing of XPO1.

Abstract 16056: The Prevalence, Risk Factors and Outcome of Cardiac Dysfunction in Hospitalized Patients With Covid-19

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Mingxing XIE ◽  
Yuman Li ◽  
He Li ◽  
Yuji Xie ◽  
Meng Li ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Cardiac Dysfunction ◽  
Troponin I ◽  
High Sensitivity ◽  
Left Ventricular ◽  
Hospitalized Patients ◽  
Reduced Ejection Fraction ◽  
Lv Dysfunction

Objectives: We aimed to investigate the prevalence, risk factors and outcome of cardiac dysfunction, and explore the potential value of echocardiographic parameters in hospitalized patients with coronavirus disease 2019 (COVID-19). Background: Cardiac involvement is a prominent features in COVID-19. However, the prevalence and clinical significance of cardiac dysfunction in COVID-19 patients have not yet been well described. Methods: We studied 157 consecutive hospitalized COVID-19 patients, whose Left ventricular (LV) and right ventricular (RV) structure and function were evaluated by echocardiography. Results: RV dysfunction was found in 40 (25.5%) patients, and LV dysfunction in 28 (17.8%) patients consisting of 24 (15.3%) with heart failure with preserved ejection fraction and 4 (2.5%) with heart failure with reduced ejection fraction. Hypertension, acute respiratory distress syndrome (ARDS), high-sensitivity troponin I (hs-TNI) level and mechanical ventilation therapy was associated with cardiac dysfunction, which contributed to higher mortality (LV dysfunction: 28.6% vs 11.6%, P = 0.022; RV dysfunction: 37.5% vs 6.8%, P < 0.001, respectively). Moreover, LV and RV dysfunction were more frequent in patients with elevated hs-TNI than those without (37.5% vs 12.5 %, P = 0.001; 40.0 % vs 22.9%, P = 0.043, respectively). During hospitalization, 23 patients died. The mortality was 3.0% for patients without cardiac dysfunction and normal hs-TNI levels, 6.7% for those with cardiac dysfunction and normal hs-TNI levels, 13.3% for those without cardiac dysfunction but elevated hs-TNI levels, and 64.0% for those with cardiac dysfunction and elevated hs-TNI. In Cox analysis, RV dysfunction was independently predictor of higher mortality (hazard ratio=2.79; 95% CI: 1.10 to 7.06; P=0.031). HF, especially HFpEF, was not predictive of increased mortality. Conclusions: The prevalence of RV dysfunction was higher than that of HF. Moreover, HFpEF was more common than HFrEF. RV dysfunction is an independent predictor of higher mortality. Additionally, patients with cardiac dysfunction and elevated hs-TNI had the highest mortality, which may prompt physicians to pay attention not only to the hs-TNI level but also the cardiac dysfunction.

Abstract 4831: The A2B Adenosine Receptor Contributes to Post-Infarction Heart Failure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jason E Maas ◽  
Milka Koupenova ◽  
Katya Ravid ◽  
John A Auchampach
Keyword(s):  
Heart Failure ◽  
Coronary Artery ◽  
Infarct Size ◽  
Adenosine Receptor ◽  
Cardiac Remodeling ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Receptor Subtypes ◽  
Infarction Heart

Recent studies have been directed at understanding the role of the A 2B receptor in regulating cardioprotection, coronary blood flow, fibroblast function, and inflammation. Unlike the other adenosine receptor subtypes, the A 2B receptor is emerging as a promoter of inflammation in chronic diseases such as asthma and conditions associated with tissue fibrosis. In this study, we used A 2B receptor gene “knock-out” (A 2B −/− ) mice to test the role of the A 2B receptor in infarction-induced heart failure and cardiac remodeling. A 2B −/− mice or wild-type (WT) littermates were subjected to permanent ligation of the left coronary artery or sham surgery. Cardiac morphology and function were assessed at 4 and 8 weeks after surgery by echocardiography. At the end of the study, systemic arterial and left ventricular pressures were obtained, after which the hearts were removed and histologically assessed for infarct size and fibrosis. WT hearts experienced significant left ventricular dilation and reduced systolic (fractional area shortening, myocardial performance index, and +dP/dt max ) and diastolic (end-diastolic pressure [EDP] elevated from 3.2 ± 0.8 mmHg in sham mice to 8.8 ± 1.5 mmHg in infarcted mice and tau was prolonged from 11.6 ± 1.7 ms to 22.3 ± 2.0 ms) function at 8 weeks after coronary artery ligation. Compared to WT mice, there were no significant differences in measures of post-infarction systolic function in A 2B −/− mice. However, EDP and tau were significantly improved (2.5 ± 1.5 mmHg and 17 ± 1.4 ms, respectively) and were not worsened compared to sham-operated A 2B −/− mice (2.7 ± 2.1 mmHg and 14.5 ± 1.8 ms, respectively). Moreover, interstitial fibrosis was elevated in the non-infarcted myocardium of WT mice subjected to coronary ligation, but not in A 2B −/− mice. Importantly, infarct size (WT = 39 ± 2% of the left ventricle; A 2B −/− = 43 ± 3%) and systemic blood pressure were not significantly different between WT and A 2B −/− mice. The data suggest that absence of the A 2B receptor results in preservation of diastolic function and decreased development of reactive fibrosis following myocardial infarction. These findings support the concept that adenosine signaling via the A 2B receptor contributes to post-infarction heart failure and adverse cardiac remodeling. This research has received full or partial funding support from the American Heart Association, AHA National Center.

scholarly journals Mitigation of the progression of heart failure with sildenafil involves inhibition of RhoA/Rho-kinase pathway

2011 ◽  
Vol 300 (6) ◽  
pp. H2272-H2279 ◽  
Author(s):  
Vinh Q. Chau ◽  
Fadi N. Salloum ◽  
Nicholas N. Hoke ◽  
Antonio Abbate ◽  
Rakesh C. Kukreja
Keyword(s):  
Heart Failure ◽  
Coronary Artery ◽  
Rho Kinase ◽  
Inhibitory Effect ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Saline Treatment ◽  
Kinase Pathway ◽  
Fractional Shortening

Chronic inhibition of phosphodiesterase-5 with sildenafil immediately after permanent occlusion of the left anterior descending coronary artery was shown to limit ischemic heart failure (HF) in mice. To mimic a more clinical scenario, we postulated that treatment with sildenafil beginning at 3 days post-myocardial infarction (MI) would also reduce HF progression through the inhibition of the RhoA/Rho-kinase pathway. Adult male ICR mice with fractional shortening < 25% at day 3 following permanent left anterior descending coronary artery ligation were continuously treated with either saline (volume matched, ip, 2 times/day) or sildenafil (21 mg/kg, ip, 2 times/day) for 25 days. Echocardiography showed fractional shortening preservation and less left ventricular end-diastolic dilatation with sildenafil treatment compared with saline treatment at 7 and 28 days post-MI ( P < 0.05). Both fibrosis and apoptosis, determined by Masson's trichrome and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL), respectively, were attenuated in the sildenafil-treated mice ( P < 0.05 vs. saline). Western blot analysis showed enchanced Bcl-2-to-Bax ratio with sildenafil treatment ( P < 0.05 vs. saline). Activity assay showed sildenafil-mediated PKG activation 1 day after treatment ( P < 0.05 vs. sham and saline). PKG activation was associated with sildenafil-mediated inhibition of Rho kinase ( P < 0.05) compared with saline treatment, whereas PKG inhibition with KT-5823 abolished this inhibitory effect of sildenafil. In conclusion, for the first time, our findings show that chronic sildenafil treatment, initiated at 3 days post-MI, attenuates left ventricular dysfunction independent of its infarct-sparing effect, and this cardioprotection involves the inhibition of the RhoA/Rho-kinase pathway. Sildenafil may be a promising therapeutic tool for advanced HF in patients.

Heart failure progression is accelerated following myocardial infarction in type 2 diabetic rats

2007 ◽  
Vol 293 (3) ◽  
pp. H1609-H1616 ◽  
Author(s):  
Margaret P. Chandler ◽  
Eric E. Morgan ◽  
Tracy A. McElfresh ◽  
Theodore A. Kung ◽  
Julie H. Rennison ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Contractile Dysfunction ◽  
Lv Dysfunction ◽  
Lv Remodeling ◽  
Heart Failure Progression ◽  
Type 2 Diabetic

Clinical studies have shown a greater incidence of myocardial infarction in diabetic patients, and following an infarction, diabetes is associated with an increased risk for the development of left ventricular (LV) dysfunction and heart failure. The goal of this study was to determine if the progression of heart failure following myocardial infarction in type 2 diabetic (T2D) rats is accelerated compared with nondiabetic rats. Male nondiabetic Wistar-Kyoto (WKY) and T2D Goto-Kakizaki (GK) rats underwent coronary artery ligation or sham surgery to induce heart failure. Postligation (8 and 20 wk), two-dimensional echocardiography and LV pressure measurements were made. Heart failure progression, as assessed by enhanced LV remodeling and contractile dysfunction, was accelerated 8 wk postligation in the T2D animals. LV remodeling was evident from increased end-diastolic and end-systolic diameters and areas in the GK compared with the WKY infarcted group. Furthermore, enhanced LV contractile dysfunction was evident from a greater deterioration in fractional shortening and enhanced myocardial performance index (an index of global LV dysfunction) in the GK infarcted group. This accelerated progression was accompanied by greater increases in atrial natriuretic factor and skeletal α-actin (gene markers of heart failure and hypertrophy) mRNA levels in GK infarcted hearts. Despite similar decreases in metabolic gene expression (i.e., peroxisome proliferator-activated receptor-α-regulated genes associated with fatty acid oxidation) between infarcted WKY and GK rat hearts, myocardial triglyceride levels were elevated in the GK hearts only. These results, demonstrating enhanced remodeling and LV dysfunction 8 wk postligation provide evidence of an accelerated progression of heart failure in T2D rats.

Abstract 3659: High-Mobility Group Box 1 Restores Cardiac Dysfunction after Myocardial Infarction in Transgenic Mice

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Tatsuro Kitahara ◽  
Yasuchika Takeishi ◽  
Tetsuro Shishido ◽  
Satoshi Suzuki ◽  
Shigehiko Kato ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Cardiac Dysfunction ◽  
Nuclear Dna ◽  
Inflammatory Responses ◽  
High Mobility ◽  
Left Ventricular ◽  
High Mobility Group ◽  
Coronary Artery Ligation ◽  
Artery Ligation

High-mobility group box 1 (HMGB1) is a nuclear DNA-binding protein and is released from necrotic cells, inducing inflammatory responses and promoting tissue repair and angiogenesis. To test the hypothesis that HMGB1 enhances angiogenesis and restores cardiac dysfunction after myocardial infarction, we generated transgenic mouse with cardiac specific overexpression of HMGB1 (HMGB1-Tg) using α-myosin heavy chain (MHC) promoter. The left anterior descending coronary artery was ligated in HMGB1-Tg and wild-type littermate (Wt) mice. After coronary artery ligation, HMGB1 was released into circulation from the necrotic cardiomyocytes of HMGB1 overexpressing hearts. The size of myocardial infarction was smaller in HMGB1-Tg than in Wt mice (figure ). Echocardiography and cardiac catheterization demonstrated that cardiac remodeling and dysfunction after myocardial infarction were prevented in HMGB1-Tg mice compared to Wt mice. Furthermore, survival rate after myocardial infarction in HMGB1-Tg mice was higher than that in Wt mice (figure ). Immunohistochemical staining revealed that capillary and arteriole formations after myocardial infarction were enhanced in HMGB1-Tg mice. We demonstrated the first in vivo evidence that HMGB1 enhances angiogenesis, restores cardiac dysfunction, and improves survival after myocardial infarction. These results may provide a novel therapeutic approach for left ventricular dysfunction after myocardial infarction.

scholarly journals Variability in coronary artery anatomy affects consistency of cardiac damage after myocardial infarction in mice

2017 ◽  
Vol 313 (2) ◽  
pp. H275-H282 ◽  
Author(s):  
Jiqiu Chen ◽  
Delaine K. Ceholski ◽  
Lifan Liang ◽  
Kenneth Fish ◽  
Roger J. Hajjar
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Coronary Artery ◽  
Left Coronary Artery ◽  
Ex Vivo ◽  
Left Ventricular ◽  
Fluorescent Imaging ◽  
Lv Function ◽  
Coronary Artery Ligation ◽  
Functional Parameters

Low reliability and reproducibility in heart failure models are well established. The purpose of the present study is to explore factors that affect model consistency of myocardial infarction (MI) in mice. MI was induced by left coronary artery (LCA) ligation. The coronary artery was casted with resin and visualized with fluorescent imaging ex vivo. LCA characteristics and MI size were analyzed individually in each animal, and MI size was correlated with left ventricular (LV) function by echocardiography. Coronary anatomy varies widely in mice, posing challenges for surgical ligation and resulting in inconsistent MI size postligation. The length of coronary arterial trunk, level of bifurcation, number of branches, and territory supplied by these branches are unique in each animal. When the main LCA trunk is ligated, this results in a large MI, but when a single branch is ligated, MI size is variable due to differing levels of LCA ligation and area supplied by the branches. During the ligation procedure, nearly 40% of LCAs are not grossly visible to the surgeon. In these situations, the surgeon blindly sutures a wider and deeper area of tissue in an attempt to catch the LCA. Paradoxically, these situations have greater odds of resulting in smaller MIs. In conclusion, variation in MI size and LV function after LCA ligation in mice is difficult to avoid. Anatomic diversity of the LCA in mice leads to inconsistency in MI size and functional parameters, and this is independent of potential technical modifications made by the operator. NEW & NOTEWORTHY In the present study, we demonstrate that left coronary artery diversity in mice is one of the primary causes of variable myocardial infarction size and cardiac functional parameters in the left coronary artery ligation model. Recognition of anatomic diversity is essential to improve reliability and reproducibility in heart failure research.

Na+/H+ exchange inhibition reduces hypertrophy and heart failure after myocardial infarction in rats

2001 ◽  
Vol 280 (2) ◽  
pp. H738-H745 ◽  
Author(s):  
Keiji Kusumoto ◽  
James V. Haist ◽  
Morris Karmazyn
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Coronary Artery ◽  
Hydrogen Exchange ◽  
Diastolic Pressure ◽  
Control Diet ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Large Infarct

We investigated the effect of sodium/hydrogen exchange inhibition (NHE-1) on hypertrophy and heart failure after coronary artery ligation (CAL) in the rat. Animals were subjected to occlusion (or sham) of the left main coronary artery and immediately administered a control diet or one consisting of the NHE-1 inhibitor cariporide for 13–15 wk. Hearts were separated by small [≤30% of left ventricle (LV)] and large (>30% of LV) infarcts. CAL depressed change in left ventricular increase in pressure over time (LV +dP/d t) in small and large infarct groups by 18.8% ( P < 0.05) and 34% ( P < 0.01), respectively, whereas comparative values for the cariporide groups were 8.7% (not significant) and 23.1% ( P < 0.01), respectively. LV end-diastolic pressure was increased by 1,225% in the control large infarct group but was significantly reduced to 447% with cariporide. Cariporide also significantly reduced the degree of LV dilation in animals with large infarcts. Hypertrophy, defined by tissue weights and cell size, was reduced by cariporide, and shortening of surviving myocytes was preserved. Infarct sizes were unaffected by cariporide, and the drug had no influence on either blood pressure or the depressed inotropic response of infarcted hearts to dobutamine. These results suggest an important role for NHE-1 in the progression of heart failure after myocardial infarction.

Oxidative stress contributes to vascular endothelial dysfunction in heart failure

2001 ◽  
Vol 281 (4) ◽  
pp. H1767-H1770 ◽  
Author(s):  
Julia H. Indik ◽  
Steven Goldman ◽  
Mohamed A. Gaballa
Keyword(s):  
Heart Failure ◽  
Normal Control ◽  
Coronary Artery Ligation ◽  
No Production ◽  
Vascular Endothelial ◽  
Sprague Dawley ◽  
Artery Ligation ◽  
Sod Activity ◽  
Sprague Dawley Rats ◽  
Peripheral Arterial

Congestive heart failure (HF) is characterized by inadequate nitric oxide (NO) production in the vasculature. Because NO is degraded by oxygen radicals, we hypothesized that NO is degraded faster in HF from inadequate peripheral arterial antioxidant reserves. HF was induced in male Sprague-Dawley rats by left coronary artery ligation. Vascular endothelial function was evaluated by measuring the NO-mediated vasorelaxation response to acetylcholine (ACh; 10−9–10−4M) in excised aortas. This was repeated with the free radical generator pyrogallol (20 μM) and again with pyrogallol and superoxide dismutase (SOD; 60 U/ml). Aortic and myocardial SOD activity was also determined. ACh-induced vasorelaxation was reduced in HF ( n = 9) compared with normal control rats ( n = 11; P < 0.001). Pyrogallol further reduced vasorelaxation in HF: 74 ± 11% at 10−4M ACh versus 58 ± 10% in normal control rats ( P < 0.004). There was a trend ( P = 0.06) toward reduced SOD activity in HF aortas. In conclusion, altered NO-dependent vasorelaxation in HF is in part due to excessive degradation of NO and is likely related to reduced vascular SOD activity.

Normal contractions triggered by I Ca,L in ventricular myocytes from rats with postinfarction CHF

2002 ◽  
Vol 283 (3) ◽  
pp. H1225-H1236 ◽  
Author(s):  
Ivar Sjaastad ◽  
Janny Bøkenes ◽  
Fredrik Swift ◽  
J. Andrew Wasserstrom ◽  
Ole M. Sejersted
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Coronary Artery ◽  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Fractional Shortening

Attenuated L-type Ca2+ current ( I Ca,L), or current-contraction gain have been proposed to explain impaired cardiac contractility in congestive heart failure (CHF). Six weeks after coronary artery ligation, which induced CHF, left ventricular myocytes from isoflurane-anesthetized rats were current or voltage clamped from −70 mV. In both cases, contraction and contractility were attenuated in CHF cells compared with cells from sham-operated rats when cells were only minimally dialyzed using high-resistance microelectrodes. With patch pipettes, cell dialysis caused attenuation of contractions in sham cells, but not CHF cells. Stepping from −50 mV, the following variables were not different between sham and CHF, respectively: peak I Ca,L (4.5 ± 0.3 vs. 3.8 ± 0.3 pApF−1 at 23°C and 9.4 ± 0.5 vs. 8.4 ± 0.5 pApF−1 at 37°C), the bell-shaped voltage-contraction relationship in Cs+ solutions (fractional shortening, 15.2 ± 1.0% vs. 14.3 ± 0.7%, respectively, at 23°C and 7.5 ± 0.4% vs. 6.7 ± 0.5% at 37°C) and the sigmoidal voltage-contraction relationship in K+ solutions. Caffeine-induced Ca2+ release and sarcoplasmic reticulum Ca2+-ATPase-to-phospholamban ratio were not different. Thus CHF contractions triggered by I Ca,L were normal, and the contractile deficit was only seen in undialyzed cardiomyocytes stimulated from −70 mV.

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