scholarly journals The relationship between regional myocardial flow and myocardial dysfunction in isolated underperfused diabetic and nondiabetic rat hearts; effect of KATP channel agents

1997 ◽  
Vol 73 ◽  
pp. 240
Author(s):  
Makie Higuchi ◽  
Kanako Miyagi ◽  
Junko Nakasone ◽  
Matao Sakanashi
Keyword(s):  
Katp Channel ◽  
Myocardial Dysfunction ◽  
Rat Hearts ◽  
The Relationship ◽  
Myocardial Flow ◽  
Regional Myocardial Flow

Ischemia-induced and reperfusion-induced arrhythmias: importance of heart rate

1989 ◽  
Vol 256 (1) ◽  
pp. H21-H31 ◽  
Author(s):  
M. Bernier ◽  
M. J. Curtis ◽  
D. J. Hearse
Keyword(s):  
Heart Rate ◽  
Coronary Occlusion ◽  
Ischemia And Reperfusion ◽  
Rate Of Development ◽  
Rate Dependent ◽  
Rat Hearts ◽  
Wide Range ◽  
The Right ◽  
The Relationship ◽  
Isolated Rat

The relationship between heart rate and ischemia-induced and reperfusion-induced arrhythmias was studied using 573 isolated rat hearts. Hearts (12/group), subjected to 7 min of coronary occlusion and 10 min reperfusion, were paced at 300, 330, 360, 390, 420, 480, or 540 beats/min. Pacing either throughout the experiment or during ischemia alone led to a rate-dependent increase in the incidence of reperfusion-induced ventricular fibrillation (VF) from 25% in the unpaced hearts to greater than 90% when the rate was 420 beats/min or higher. However, pacing during reperfusion alone did not increase the incidence of reperfusion-induced VF. In separate hearts, the right atrium was removed to permit examination of both low and high rates (167 +/- 2, 240, 336 +/- 3, or 480 beats/min throughout the experiment) over a wide range of durations of occlusion (3, 5, 7, 10, 15, 20, or 40 min). Ischemia-induced VF incidence was critically dependent on heart rate, low rates being protective. During reperfusion, the incidence of VF was also highly rate dependent if reperfusion was initiated within 10 min of the onset of ischemia (ranging from 8% when rate was 167 +/- 2 beats/min to 100% when rate was 480 beats/min) but was unrelated to heart rate when reperfusion occurred at later times (ranging from 33 to 50% when ischemia duration was 40 min). Heart rate can therefore influence susceptibility to ischemia- and reperfusion-induced arrhythmias, probably as a result of an effect on the rate of development of ischemic injury.

scholarly journals Hydrogen sulfide-mediated cardioprotection against ischemia reperfusion is linked to KATP channel for mitochondrial preservation but not for its distinct preference on interfibrillar mitochondria

2019 ◽  
Vol 14 (2) ◽  
pp. 107-115 ◽  
Author(s):  
Priyadharshini Chandrasekaran ◽  
Sriram Ravindran ◽  
Sri Rahavi Boovarahan ◽  
Gino A. Kurian
Keyword(s):  
Hydrogen Sulfide ◽  
Reperfusion Injury ◽  
Katp Channel ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
Significant Difference ◽  
Interfibrillar Mitochondria ◽  
Subsarcolemmal Mitochondria

Hydrogen sulfide has been shown to protect  myocardium against ischemia-reperfusion injury by preserving interfibrillar mitochondria functional activi-ties than subsarcolemmal mitochondria. In this study, the role of the KATP channel in modulating the mitochondrial subpopulations during the cardioprotection mediated by NaSH (H2S donor) was investigated. Isolated rat hearts were treated with mitochondrial KATP channel closer glibenclamide (10 μM)/opener diazoxide (0.8 mM) via Langendorff perfusion apparatus before ischemia-reperfusion. The results showed that NaSH pre-conditioning in presence of glibenclamide significantly improved cardiac recovery without any significant difference between interfibrillar mitochondria and subsarcolemmal mitochondria.  In conclusion, targeting KATP channel may not be good option to target interfibrillar mitochondria/subsarcolemmal mitochondria against ischemia-reperfusion injury.

Nitric oxide-cGMP pathway is involved in endotoxin-induced contractile dysfunction in rat hearts

2004 ◽  
Vol 96 (3) ◽  
pp. 853-860 ◽  
Author(s):  
Tetsuya Tatsumi ◽  
Natsuya Keira ◽  
Kazuko Akashi ◽  
Miyuki Kobara ◽  
Satoaki Matoba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Soluble Guanylate Cyclase ◽  
Myocardial Dysfunction ◽  
Significant Negative Correlation ◽  
Left Ventricular ◽  
No Production ◽  
Contractile Dysfunction ◽  
Cardiac Depression ◽  
Rat Hearts ◽  
Developed Pressure

The mechanisms by which endotoxemia causes cardiac depression have not been fully elucidated. The present study examined the involvement of nitric oxide (NO) in this pathology. Rats were infused with lipopolysaccharide (LPS) or saline, and the plasma and myocardial [Formula: see text] and [Formula: see text] (NOx) concentrations were measured before or 3, 6, and 24 h after treatment. The hearts were then immediately isolated and mounted in a Langendorff apparatus, and left ventricular developed pressure (LVDP) was determined before biochemical analysis of the myocardium. LPS injection effected the expression of inducible NO synthase (iNOS) in the myocardium, a marked increase in plasma and myocardial NOx levels, and a significant decline in LVDP compared with saline controls. The LPS-induced NO production and concomitant cardiac depression were most pronounced 6 h after LPS injection and were accompanied by a significant increase in myocardial cGMP content. Myocardial ATP levels were not significantly altered after LPS injection. Significant negative correlation was observed between LVDP and myocardial cGMP content, as well as between LVDP and plasma NOx levels. Aminoguanidine, an inhibitor of iNOS, significantly attenuated the LPS-induced NOx production and contractile dysfunction. Furthermore, 1 H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one, an inhibitor of soluble guanylate cyclase, significantly decreased myocardial cGMP content and attenuated the contractile depression, although aminoguanidine or 1 H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one was not able to completely reverse myocardial dysfunction. Our data suggest that endotoxin-induced contractile dysfunction in rat hearts is associated with NO production by myocardial iNOS and a concomitant increase in myocardial cGMP.

Nature of [Ca2+]i transients during ventricular fibrillation and quinidine treatment in perfused rat hearts

1994 ◽  
Vol 266 (4) ◽  
pp. H1473-H1484
Author(s):  
S. Kojima ◽  
J. Wikman-Coffelt ◽  
S. T. Wu ◽  
W. W. Parmley
Keyword(s):  
Ventricular Fibrillation ◽  
Control Level ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Acetoxymethyl Ester ◽  
Ecg Signals ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Electrocardiogram Ecg ◽  
The Relationship

We studied intracellular Ca2+ concentration ([Ca2+]i) and the electrocardiographic signals during pacing-induced ventricular fibrillation (VF) and quinidine treatment (0.4 mg/min) using surface fluorometry in indo 1-acetoxymethyl ester (AM)-loaded perfused rat hearts. [Ca2+]i was evaluated as the indo 1 fluorescence ratio (F400/F510) and expressed as a percentage of the control amplitude of F400/F510 transients. F400/F510 increased to approximately 250% during 2- (n = 14) or 20-min (n = 9) VF. Quinidine significantly decreased F400/F510 by 60% after 2-min VF; however, this effect was blunted after 20-min VF. After 2-min VF, F400/F510 and left ventricular pressure recovered almost to the control level. However, recovery of F400/F510 and ventricular function was poor after 20-min VF. The relationship between [Ca2+]i and the electrocardiogram (ECG) during VF was evaluated by power spectrum analysis of F400/F510 and ECG signals. During VF (25 +/- 3 Hz) with high irregularity, there were no clear [Ca2+]i transients (n = 110). When the cardiac rhythm (22 +/- 3 Hz) was regular, including ventricular tachycardia, there were recognizable [Ca2+]i signals with dominant frequencies that were the same (n = 2), one-half (n = 12), or one-third (n = 1) of the ECG frequencies. The highest frequency of the [Ca2+]i transients was 19 Hz. During quinidine treatment, the VF rate decreased significantly, and clear [Ca2+]i transients were noted in all records responding to every one or two ECG signals. The conclusions were the following: 1) [Ca2+]i responds to electrical signals rapidly (up to 19 Hz) during VF. This fast [Ca2+]i response is a probable cause of high [Ca2+]i during VF. 2) Quinidine decreased [Ca2+]i after 2-min VF possibly in part by slowing the VF and [Ca2+]i transients rates. 3) 20-min VF caused [Ca2+]i overload and poor functional recovery after defibrillation.

scholarly journals Staircase, rest contractions, and potentiation in the isolated rat heart

1962 ◽  
Vol 202 (4) ◽  
pp. 636-640 ◽  
Author(s):  
F. L. Meijler
Keyword(s):  
Cycle Length ◽  
Rest Period ◽  
Isolated Rat Heart ◽  
Stimulation Rate ◽  
Rat Hearts ◽  
Constant Rate ◽  
Theoretical Evidence ◽  
The Relationship ◽  
Isotonic Contractions ◽  
Isolated Rat

Variation in amplitude of isotonic contractions of intact isolated rat hearts, following changes in cycle length, were studied. It was found that a staircase-like phenomenon resembling the original Bowditch effect cannot be evoked in a intact mammalian heart without special measures, such as adding acetylcholine to the perfusion fluid. A steady state relation of rate to amplitude of isotonic contractions was demonstrated. Potentiation of contractility can be originated by sudden changes in stimulation rate. A rest period preceding the changes in stimulation rate does not change the potentiation found originally. At a constant rate the amplitude of a contraction is determined by the preceding cycle length. This relation has been called restitution. Theoretical evidence is presented in an attempt to demonstrate that restitution and potentiation are due to the same process. It can be concluded that Bowditch's staircase does not play a role in the relationship between cycle length and contractility in intact hearts and the statement that restitution and potentiation are due to the same process offers an opportunity to describe all effects of changes in cycle length on isotonic contractions as one phenomenon.

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