scholarly journals Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes

1998 ◽  
Vol 84 (2) ◽  
pp. 544-552 ◽  
Author(s):  
Xue-Qian Zhang ◽  
Yuk-Chow Ng ◽  
Timothy I. Musch ◽  
Russell L. Moore ◽  
R. Zelis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Citrate Synthase ◽  
Contractile Function ◽  
Sprint Training ◽  
Cardiac Contractile Function ◽  
Myocyte Hypertrophy ◽  
Cellular Hypertrophy ◽  
Cardiac Contractile ◽  
Rat Hearts ◽  
Exercise Activity

Zhang, Xue-Qian, Yuk-Chow Ng, Timothy I. Musch, Russell L. Moore, R. Zelis, and Joseph Y. Cheung. Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes. J. Appl. Physiol. 84(2): 544–552, 1998.—Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had decreased Na+/Ca2+exchange currents ( I Na/Ca; 3 Na+ out:1 Ca2+ in) and sarcoplasmic reticulum (SR)-releasable Ca2+contents. These defects in Ca2+regulation may contribute to abnormal contractility in MI myocytes. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca2+ regulation, the present study examined whether 6–8 wk of high-intensity sprint training (HIST) would ameliorate some of the cellular maladaptations observed in post-MI rats with limited exercise activity (Sed). In MI rats, HIST did not affect citrate synthase activities of plantaris muscles but significantly increased the percentage of cardiac α-myosin heavy chain (MHC) isoforms (57.2 ± 1.9 vs. 49.3 ± 3.5 in MI-HIST vs. MI-Sed, respectively; P ≤ 0.05). At the single myocyte level, HIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 ± 4 vs. 130 ± 5 μm in MI-HIST vs. MI-Sed, respectively; P ≤ 0.005) and cell capacitances (212 ± 8 vs. 242 ± 9 pF in MI-HIST vs. MI-Sed, respectively; P ≤ 0.015). Reverse I Na/Ca was significantly lower ( P ≤ 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. HIST significantly increased reverse I Na/Ca( P ≤ 0.05) without affecting the amount of Na+/Ca2+exchangers (detected by immunoblotting) in MI myocytes. SR-releasable Ca2+ content, as estimated by integrating forward I Na/Ca during caffeine-induced SR Ca2+ release, was also significantly increased ( P ≤ 0.02) by HIST in MI myocytes. We conclude that the enhanced cardiac output and stroke volume in post-MI rats subjected to HIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.

Sprint training normalizes Ca2+ transients and SR function in postinfarction rat myocytes

2000 ◽  
Vol 89 (1) ◽  
pp. 38-46 ◽  
Author(s):  
Lian-Qin Zhang ◽  
Xue-Qian Zhang ◽  
Yuk-Chow Ng ◽  
Lawrence I. Rothblum ◽  
Timothy I. Musch ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sarcoplasmic Reticulum ◽  
Contractile Function ◽  
Half Time ◽  
Sprint Training ◽  
Cardiac Contractile Function ◽  
Cardiac Contractile ◽  
Rat Hearts ◽  
Intracellular Ca ◽  
Rat Myocytes

Previous studies have shown that myocytes isolated from sedentary (Sed) rat hearts 3 wk after myocardial infarction (MI) undergo hypertrophy, exhibit altered intracellular Ca2+ concentration ([Ca2+]i) dynamics and abnormal contraction, and impaired sarcoplasmic reticulum (SR) function manifested as prolonged half-time of [Ca2+]idecline. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca2+ regulation, the present study examined whether 6–8 wk of high-intensity sprint training (HIST) would restore [Ca2+]i dynamics and SR function in MI myocytes toward normal. In MI rats, HIST ameliorated myocyte hypertrophy as indicated by significant ( P ≤ 0.05) decreases in whole cell capacitances [Sham-Sed 179 ±12 ( n = 20); MI-Sed 226 ± 7 ( n = 20); MI-HIST 183 ± 11 pF ( n = 19)]. HIST significantly ( P < 0.0001) restored both systolic [Ca2+]i [Sham-Sed 421 ± 9 ( n = 79); MI-Sed 350 ± 6 ( n = 70); MI-HIST 399 ± 9 nM ( n = 70)] and half-time of [Ca2+]i decline (Sham-Sed 0.197 ± 0.005; MI-Sed 0.247 ± 0.006; MI-HIST 0.195 ± 0.006 s) toward normal. Compared with Sham-Sed myocytes, SR Ca2+-ATPase expression significantly ( P < 0.001) decreased by 44% in MI-Sed myocytes. Surprisingly, expression of SR Ca2+-ATPase was further reduced in MI-HIST myocytes to 26% of that measured in Sham-Sed myocytes. There were no differences in calsequestrin expression among the three groups. Expression of phospholamban was not different between Sham-Sed and MI-Sed myocytes but was significantly ( P < 0.01) reduced in MI-HIST myocytes by 25%. Our results indicate that HIST instituted shortly after MI improves [Ca2+]idynamics in surviving myocytes. Improvement in SR function by HIST is mediated not by increased SR Ca2+-ATPase expression, but by modulating phospholamban regulation of SR Ca2+-ATPase activity.

scholarly journals ALTERED CONTRACTILE FUNCTION IN DOGS AFTER CLINICAL DEATH FOLLOWING ACUTE MIOCARDIAL INFARCTION AND INTACT HEART

2018 ◽  
Vol 7 (2) ◽  
pp. 121-128 ◽  
Author(s):  
G. V. Lisachenko ◽  
A. V. Budaev ◽  
S. V. Bannih
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Contractile Function ◽  
Clinical Death ◽  
Postresuscitation Period ◽  
Systemic Hemodynamics ◽  
Cardiac Contractile Function ◽  
Cardiac Contractile ◽  
Circulatory Insufficiency ◽  
Myocardial Contractile

Aim. To assess myocardial contractile function in dogs after clinical death following acute myocardial infarction and to determine its role in the development of hemodynamic derangements after cardiopulmonary resuscitation. Methods. 180 dogs included in the experiment received pentobarbital anesthesia to assess contractile function and systemic hemodynamics after a 5-min clinical death caused by myocardial infarction. Results Dogs had phase changes in the myocardial contractile function with its initial increase, subsequent depression and normalization in the early postresuscitation period after myocardial infarction. Depressed cardiac contractile function was accompanied by a decrease in the myocardial functional reserve. A similar tendency was found in the restoration of systemic hemocirculation. Conclusion. Similar phase alterations in the myocardial contractile function and systemic hemodynamics developed in the postresuscitation period of acute myocardial infarction. Immediately after recovery, the parameters of systemic hemoperfusion increased due to the activation of the cardiac contractile function. The subsequent initial (3 – 60 min) decrease in the volumetric perfusion parameters was mainly caused by the depressed cardiac contractile function. Rhythm disturbances affected on-going circulatory insufficiency 4 - 5 hours after the recovery. The subsequent progressive decrease in the volumetric perfusion was caused by the extracardiac factors.

Isolated ventricular myocytes from copper-deficient rat hearts exhibit enhanced contractile function

2001 ◽  
Vol 281 (2) ◽  
pp. H476-H481 ◽  
Author(s):  
Loren E. Wold ◽  
Jack T. Saari ◽  
Jun Ren
Keyword(s):  
Cardiac Fibrosis ◽  
Copper Deficiency ◽  
Ventricular Myocytes ◽  
Contractile Function ◽  
Detection System ◽  
Cardiac Contractile Function ◽  
Acetoxymethyl Ester ◽  
Cardiac Contractile ◽  
Rat Hearts ◽  
Intracellular Ca

Dietary copper deficiency leads to cardiac hypertrophy, cardiac fibrosis, derangement of myofibrils, and impaired cardiac contractile and electrophysiological function. The purpose of this study was to determine whether impaired cardiac function from copper deficiency is due to depressed contractile function at the single myocyte level. Male Sprague-Dawley rats were fed diets that were either copper adequate (5.59–6.05 μg copper/g body wt; n = 11) or copper deficient (0.29–0.34 μg copper/g body wt; n = 11) for 5 wk. Ventricular myocytes were dispersed and mechanical properties were evaluated using the SoftEdge video-based edge-detection system. Intracellular Ca2+ transients were examined using fura 2-acetoxymethyl ester. Myocytes were electrically stimulated to contract at 0.5 Hz. Properties evaluated included peak shortening (PS), time to peak shortening (TPS), time to 90% relengthening (TR90), and maximal velocities of shortening and relengthening (±d L/d t). Myocytes from the copper-deficient rat hearts exhibited significantly enhanced PS values associated with shortened TR90 measurements compared with those from copper-adequate rat hearts. The ±d L/d t values were enhanced and the intracellular Ca2+ transient decay rate was depressed in myocytes from copper-deficient rats. These data indicate that impaired cardiac contractile function that is seen in copper-deficient whole hearts might not be due to depressed cardiac contractile function at the single cell level but rather to other mechanisms such as cardiac fibrosis.

scholarly journals The German–Austrian S3 Guideline “Cardiogenic Shock Due to Myocardial Infarction: Diagnosis, Monitoring, and Treatment”

2020 ◽  
Author(s):  
Kevin Pilarczyk ◽  
Karl Werdan ◽  
Martin Russ ◽  
Holger Thiele ◽  
Guido Michels ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiogenic Shock ◽  
Contractile Function ◽  
German Society ◽  
Evidence Based ◽  
Cardiac Contractile Function ◽  
Intensive Care Unit Treatment ◽  
S3 Guideline ◽  
Cardiac Contractile

AbstractDespite advances in the treatment of acute myocardial infarction with subsequent mortality reduction, which are mainly caused by the early timing of revascularization, cardiogenic shock still remains the leading cause of death with mortality rates still approaching 40 to 50%. Cardiogenic shock is characterized by a multiorgan dysfunction syndrome, often complicated by a systemic inflammatory response syndrome that affects the outcome more than the reduction of the cardiac contractile function. However, both European and American guidelines on myocardial infarction focus on interventional or surgical aspects only. Therefore, experts from eight German and Austrian specialty societies including the German Society for Thoracic and Cardiovascular Surgery published the German–Austrian S3 guideline “cardiogenic shock due to myocardial infarction: diagnosis, monitoring, and treatment” to provide evidence-based recommendations for the diagnosis and treatment of infarction-related cardiogenic shock in 2010 covering the topics of early revascularization, revascularization techniques, intensive care unit treatment including ventilation, transfusion regimens, adjunctive medical therapy, and mechanical support devices. Within the last 3 years, this guideline was updated as some major recommendations were outdated, or new evidence had been found. This review will therefore outline the management of patients with cardiogenic shock complicating acute myocardial infarction according to the updated guideline with a major focus on evidence-based recommendations which have been found relevant for cardiac surgery.

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