scholarly journals Diltiazem Ameliorates Contractile Dysfunction Without Shortening of Action Potential Duration in Ischemic Heart of Anesthetized Dogs

2001 ◽  
Vol 86 (2) ◽  
pp. 251-253
Author(s):  
Kaori Hamada ◽  
Jun Yamazaki ◽  
Taku Nagao
CHEST Journal ◽  
2004 ◽  
Vol 125 (5) ◽  
pp. 1821-1829 ◽  
Author(s):  
Saeed Rasty ◽  
Neeta B. Amin ◽  
Hani N. Sabbah ◽  
Takayuki Mishima ◽  
Steven Borzak ◽  
...  

2011 ◽  
Vol 111 (3) ◽  
pp. 799-807 ◽  
Author(s):  
Justin T. Sambol ◽  
Marlon A. Lee ◽  
Mingshan Jiang ◽  
Garima Dosi ◽  
Wei Dong ◽  
...  

Myocardial contractile dysfunction develops following trauma-hemorrhagic shock (T/HS). We have previously shown that, in a rat fixed pressure model of T/HS (mean arterial pressure of 30–35 mmHg for 90 min), mesenteric lymph duct ligation before T/HS prevented T/HS-induced myocardial contractile depression. To determine whether T/HS lymph directly alters myocardial contractility, we examined the functional effects of physiologically relevant concentrations of mesenteric lymph collected from rats undergoing trauma-sham shock (T/SS) or T/HS on both isolated cardiac myocytes and Langendorff-perfused whole hearts. Acute application of T/HS lymph (0.1–2%), but not T/SS lymph, induced dual inotropic effects on myocytes with an immediate increase in the amplitude of cell shortening (1.4 ± 0.1-fold) followed by a complete block of contraction. Similarly, T/HS lymph caused dual, positive and negative effects on cellular Ca2+ transients. These effects were associated with changes in the electrophysiological properties of cardiac myocytes; T/HS lymph initially prolonged the action potential duration (action potential duration at 90% repolarization, 3.3 ± 0.4-fold), and this was followed by a decrease in the plateau potential and membrane depolarization. Furthermore, intravenous infusion of T/HS lymph, but not T/SS lymph, caused myocardial contractile dysfunction at 24 h after injection, which mimicked actual T/HS-induced changes; left ventricular developed pressure (LVDP) and the maximal rate of LVDP rise and fall (±dP/d tmax) were decreased and inotropic response to Ca2+ was blunted. However, the contractile responsiveness to β-adrenergic receptor stimulation in the T/HS lymph-infused hearts remained unchanged. These results suggest that T/HS lymph directly causes negative inotropic effects on the myocardium and that T/HS lymph-induced changes in myocyte function are likely to contribute to the development of T/HS-induced myocardial dysfunction.


2006 ◽  
Vol 290 (2) ◽  
pp. H778-H785 ◽  
Author(s):  
Atsuko Yatani ◽  
Da-Zhong Xu ◽  
Keiichi Irie ◽  
Kazunori Sano ◽  
Anoush Jidarian ◽  
...  

Gut-derived factors in intestinal lymph have been shown to trigger myocardial contractile dysfunction. However, the underlying cellular mechanisms remain unclear. We examined the effects of physiologically relevant concentrations of mesenteric lymph collected from rats with 40% burn injury (burn lymph) on excitation-contraction coupling in rat ventricular myocytes. Burn lymph (0.1–5%), but not control mesenteric lymph from sham-burn animals, induced dual positive and negative inotropic effects depending on the concentrations used. At lower concentrations (<0.5%), burn lymph increased the amplitude of myocyte contraction (1.6 ± 0.3-fold; n = 12). At higher concentrations (>0.5%), burn lymph initially enhanced myocyte contraction, which was followed by a block of contraction. These effects were partially reversible on washout. The initial positive inotropic effect was associated with a prolongation of action potential duration (measured at 90% repolarization, 2.5 ± 0.6-fold; n = 10), leading to significant increases in the net Ca2+ influx (1.7 ± 0.1-fold; n = 8). There were no significant changes in the resting membrane potential. The negative inotropic effect was accompanied by a decrease in the action potential plateau (overshoot decrease by 69 ± 10%; n = 4) and membrane depolarization. Voltage-clamp experiments revealed that the positive inotropic effects of burn lymph were due to an inhibition of the transient outward K+ currents that prolong action potential duration, and the inhibitory effects were due to a concentration-dependent inhibition of Ca2+ currents that lead to a reduction of action potential plateau. These burn lymph-induced changes in cardiac myocyte Ca2+ handling can contribute to burn-induced contractile dysfunction and ultimately to heart failure.


2000 ◽  
Vol 41 (4) ◽  
pp. 481-492
Author(s):  
Naohiko Takahashi ◽  
Morio Ito ◽  
Shuji Ishida ◽  
Takao Fujino ◽  
Mikiko Nakagawa ◽  
...  

2018 ◽  
Vol 114 (suppl_1) ◽  
pp. S120-S120
Author(s):  
L Sartiani ◽  
L Sartiani ◽  
M Cameli ◽  
L Dini ◽  
S Modillo ◽  
...  

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