Metabolism of the isolated perfused rabbit heart. III. Energy stores and creatine kinase release during prolonged reoxygenation and atrial pacing

1979 ◽  
Vol 57 (10) ◽  
pp. 1058-1066 ◽  
Author(s):  
Miguel A. Chiong ◽  
Timothy L. Winton
Keyword(s):  
Creatine Kinase ◽  
Mechanical Performance ◽  
Recovery Period ◽  
Systolic Pressure ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Myocardial Uptake ◽  
Ventricular Systolic Pressure ◽  
Perfused Rabbit Heart

When the perfused rabbit heart is reoxygenated for 75 min after 25 min of anoxic perfusion, left ventricle performance stabilizes at 50% of control levels, but the rate of creatine kinase (CK) release is high (1.9 U/min) and ATP stores are low (5 μmol/g dry weight). These results suggest that the preparation is on the verge of severe failure. This possibility was investigated by following the recovery for an extra 60 min of reoxygenation and by stressing the hearts with atrial pacing.The data show that no deterioration occurred during the extra recovery period; on the contrary, mechanical performance remained stable, while the rate of CK release fell to 1.1 U/min, and ATP stores increased by 204%. In aerobic hearts, pacing increased the product of left ventricular systolic pressure (LVSP) and heart rate, myocardial uptake of oxygen [Formula: see text], coronary sinus flow, and O2 extraction, but LVSP and [Formula: see text] per beat fell. Similar responses were seen in postanoxic hearts, but LVSP improved during pacing while the rate of CK loss declined and ATP stores increased. These metabolic changes were inversely related to the rate of contraction. It is concluded that the preparation was not deteriorating at 75 min of reoxygenation, and that its metabolism was improved by cardiac pacing.

Low extracellular Ca2+ and enzyme release in the perfused rabbit heart

1984 ◽  
Vol 62 (9) ◽  
pp. 1158-1165 ◽  
Author(s):  
Pierre A. Fortier ◽  
Gary K. Bedford ◽  
Miguel A. Chiong
Keyword(s):  
Creatine Kinase ◽  
Systolic Pressure ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Control Group ◽  
Enzyme Release ◽  
Ventricular Systolic Pressure ◽  
Coronary Sinus Flow ◽  
Perfused Rabbit Heart ◽  
Cardiac Functions

Previous studies have shown that the well-oxygenated perfused rabbit heart releases creatine kinase when treated with the calcium antagonist drug verapamil (VER) in a dose-related manner. It is possible that this effect is related to Ca2+ ion deprivation of the sarcolemma. This possibility was explored by perfusing hearts with low Ca2+ (0.5, 0.23, 0.15, and 0 mM) versus a control group (1.27 mM Ca2+) for 60 min. Low Ca2+ perfusion was associated with (i) reduction in the heart rate – left ventricular systolic pressure product and O2 consumption, (ii) tendency for the coronary sinus flow to increase, (iii) electromechanical dissociation, prolongation of atrioventricular conduction and QT interval, and (iv) decrease in myocardial glycogen. Lower total adenosine nucleotides were found only in the 0 mM Ca2+ group. As the Ca2+ concentration was reduced, the hearts lost increasing amounts of creatine kinase, aspartate aminotransferase, and lactate dehydrogenase. These results confirm the importance of Ca2+ ions in contractile and electrical cardiac functions and show that decreased availability of this cation leads to increasing enzyme leakage resembling that seen in VER-treated hearts.

Metabolism of the perfused rabbit heart. V. Verapamil-induced release of creatine kinase

1982 ◽  
Vol 60 (7) ◽  
pp. 952-959 ◽  
Author(s):  
Miguel A. Chiong
Keyword(s):  
Creatine Kinase ◽  
Adenine Nucleotides ◽  
Systolic Pressure ◽  
Creatine Phosphate ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Calcium Stores ◽  
Ventricular Performance ◽  
Permeability Characteristics ◽  
Energy Stores

The effects of verapamil (VER), at concentrations of 0, 10−9, 10−8, 10−7, and 5 × 10−7 M (or 0, 0.5, 5, 50, and 250 ng/mL) were studied in the isolated rabbit heart during 70 min of aerobic perfusion with a standard Krebs–bicarbonate medium at 37 °C. The studied variables were left ventricular performance (RPP, heart rate times left ventricular (LV) systolic pressure), coronary sinus flow (CSF), oxygen uptake [Formula: see text], rate of creatine kinase (CK) release, and energy stores (glycogen, creatine phosphate (CP), ATP, and total adenine nucleotides (TAN)).The results show that (i) VER depressed RPP in a dose-related manner; (ii) [Formula: see text] declined as VER concentration increased except in the 5 × 10−7 M group which showed a paradoxical increase in O2 uptake; (iii) CSF was only slightly decreased by VER with the exception of the 5 × 10−7 M group, which showed an increase in flow; (iv) VER was associated with increments in the rates of CK release in a dose-related fashion (2, 4, 15, and 29 times the rate observed in the untreated group), and (v) VER was associated with slight decrease in glycogen levels, but no changes in CP or adenine nucleotides.It is concluded that, in our preparation, VER caused marked increases in the rate of CK loss in the absence of depletion of total energy stores. The data suggest that the drug affects the permeability characteristics of the sarcolemma, perhaps via localized depletion of calcium stores.

Metabolism of the perfused rabbit heart. IV. Effects of β-adrenergic blockade on enzyme release and late energy stores during postanoxic reoxygenation

1980 ◽  
Vol 58 (5) ◽  
pp. 469-476 ◽  
Author(s):  
Miguel A. Chiong ◽  
Henry Stefaniszyn
Keyword(s):  
Heart Rate ◽  
Energy Charge ◽  
Systolic Pressure ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Enzyme Release ◽  
Ventricular Systolic Pressure ◽  
Energy Stores ◽  
Left Ventricular Systolic Pressure

The effects of 80 μM dl-propranolol on left ventricular (LV) performance, energy stores, and creatine kinase (CK) release were studied in a modified Langendorff rabbit heart preparation during 75 min of aerobic perfusion and postanoxic reoxygenation.The data showed that this concentration of propranolol, which blocked the effects of β-adrenergic stimulation without affecting LV performance, coronary sinus flow (CSF), or oxygen consumption [Formula: see text], was associated with greater stores of glycogen and adenine nucleotides at the end of aerobic perfusion. Similar effects were observed during postanoxic reoxygenation, when recoveries of left ventricular systolic pressure, heart rate, heart rate - left ventricular systolic pressure product, CSF, and [Formula: see text] remained unchanged during propranolol administration, but myocardial concentrations of glycogen, creatine phosphate, and ATP were greater and the ATP:AMP ratio and the energy charge were higher than in untreated hearts. In addition, the rate of CK loss was lower in the blocked postanoxic hearts than in the unblocked group. These results indicate that propranolol had a beneficial effect on cardiac metabolism during postanoxic recovery tending to normalize energy stores and to reduce enzyme loss during reoxygenation of perfused rabbit hearts without affecting mechanical performance, coronary flow, or O2 metabolism.

Cardiac responses to moderate training in rats

1977 ◽  
Vol 42 (2) ◽  
pp. 262-266 ◽  
Author(s):  
M. A. Codini ◽  
T. Yipintsoi ◽  
J. Scheuer
Keyword(s):  
Sinus Rhythm ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Base Line ◽  
Atrial Pacing ◽  
Ventricular Systolic Pressure ◽  
Cardiac Responses ◽  
Left Ventricular Systolic Pressure ◽  
Aortic Obstruction

Left ventricular (LV) performance was studied in 30 rats conditioned by swimming and in 27 sedentary controls. Hearts were studied in the open chest both during sinus rhythm and during atrial pacing. Afterload was increased by occlusion of the aorta. Sinus rates were 328 beats/min in sedentary and 300 in conditioned animals (P less than 0.01). During ejection (E), peak left ventricular systolic pressure (PLVSP) and maximum LV dP/dt were significantly higher in conditioned than in sedentary animals. When data from hearts matched for similar heart rates were compared, increased LV performance was still seen during aortic obstruction in conditioned animals. Performance at pacing rates up to 400 beats/min was similar in hearts from conditioned and sedentary animals. At pacing rates above 400 beats/min cardiac performance was less in sedentary than in the conditioned animals. These data illustrate that although base-line cardiac performance may be the same in rats conditioned by a moderate swimming program and in sedentary animals, cardiac reserve is improved by the swimming program.

Abstract 16574: Heart Failure Biomarkers (NT-proBNP, Gal-3, sST2) Correlate With Right Ventricular Systolic Pressure and Provide Insight to Poor CRT Response: A BIOCRT Substudy

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Roderick C Deaño ◽  
Jackie Szymonifka ◽  
Qing Zhou ◽  
Jigar H Contractor ◽  
Zachary Lavender ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Fold Increase ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Cardiac Transplant ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Crt Response

Objective: Patients with heart failure (HF) and pulmonary hypertension (PH) have worse outcomes after cardiac resynchronization therapy (CRT). The relationship of circulating HF biomarkers and right ventricular systolic pressure (RVSP) may provide insight to the mechanism between PH and poor CRT response. Methods: In 90 patients (age 65 ± 13, 78% male, EF 26 ± 8%, RVSP 44 ± 12 mmHg) undergoing CRT, we measured baseline RVSP by echocardiography and obtained peripheral blood samples drawn at the time of device implantation. We measured levels of established and emerging HF biomarkers (Table 1). CRT non-response was defined as no improvement of adjudicated HF Clinical Composite Score at 6 months. Major adverse cardiac event (MACE) was defined as composite endpoint of death, cardiac transplant, left ventricular assist device, and HF hospitalization within 2 years. Results: There were 34% CRT non-responders and 27% had MACE. Per 1 unit increase in log-transformed RVSP, there was an 11-fold increase risk of having CRT non-response (odd ratio [OR] 11.0, p=0.01) and over 5-fold increase of developing 2-year MACE (hazard ratio [HR] 5.8, p=0.02). When comparing patients with severe PH (RVSP>60 mmHg) to those without PH (RVSP < 35 mmHg), there was an 8-fold increase in CRT nonresponse (OR 8.4, p=0.03) but no difference in MACE (p=NS). RVSP was correlated with increased biomarker levels of myocardial stretch and fibrosis, but not myocardial necrosis (Table 1). Conclusions: Higher RVSP is associated with greater rates of CRT non-response and adverse clinical outcomes. The mechanistic association between severe PH and CRT nonresponse may be explained by the biomarker profile reflective of myocardial wall stretch and fibrosis.

The Effect of Gypenosides on Cardiac Function and Expression of Cytoskeletal Genes of Myocardium in Diabetic Cardiomyopathy Rats

2009 ◽  
Vol 37 (06) ◽  
pp. 1059-1068 ◽  
Author(s):  
Min Ge ◽  
Shanfeng Ma ◽  
Liang Tao ◽  
Sudong Guan
Keyword(s):  
Cardiac Function ◽  
Diabetic Cardiomyopathy ◽  
Diastolic Pressure ◽  
Pure Water ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Sprague Dawley ◽  
Gene Expressions ◽  
Ventricular Systolic Pressure

The relationship between changes of cardiac function and the gene expressions of two major myocardial skeleton proteins, titin and nebulin, and the effect of gypenosides on these gene expressions in diabetic cardiomyopathy rat were explored in the present study. Forty Sprague-Dawley rats were randomly divided into three groups: control group, diabetic cardiomyopathy group and gypenosides-treated diabetic cardiomyopathy group. The diabetic cardiomyopathy was induced in rats by injecting streptozotocin (STZ, 55 mg/kg) intraperitoneally. Seven weeks after the rats suffered from diabetes, the rats were treated with gypenosides 100 mg/kg per day orally for six weeks in gypenosides-treated group. In the meanwhile, the pure water was given to diabetic cardiomyopathy and the control groups. Subsequently, the cardiac functions, including left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), ± dP/dtmax and t–dP/dmaxt, as well as the mRNA content and proteins of titin and nebulin in myocardium were determined. The results indicated that (1) the diabetic cardiomyopathy rats had decreased LVSP and ± dP/dtmax, increased LVEDP, and prolonged t–dP/dtmax than normal rats; (2) LVSP and ± dP/dtmax in diabetic cardiomyopathy rats treated with gypenosides were significantly higher and LVEDP and t–dP/dtmax were significantly lower than those without giving gypenosides; (3) the mRNA contents and proteins of titin and nebulin in diabetic cardiomyopathy rats were remarkably lower than those in the control rats and gypenosides had no effect on mRNA and protein expression levels of titin and nebulin in diabetic cardiomyopathy rats. We conclude that (1) the cardiac function as well as the mRNA expressions of titin and nebulin decreased in diabetic cardiomyopathy rats; (2) gypenosides secure cardiac muscles and their function from diabetic impairment and these beneficial effects of gypenosides are not by changing the expressions of titin and nebulin.

Effect of human urotensin-II infusion on hemodynamics and cardiac function

2003 ◽  
Vol 81 (2) ◽  
pp. 125-128 ◽  
Author(s):  
Ghada S Hassan ◽  
Fazila Chouiali ◽  
Takayuki Saito ◽  
Fu Hu ◽  
Stephen A Douglas ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Urotensin Ii ◽  
Ventricular Systolic Pressure ◽  
Wide Range ◽  
Dose Dependent Decrease

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by ±dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.Key words: urotensin-II, rat, infusion, heart.

Abstract P144: Effects of Alamandine in Post-ischemic Function

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Jonathas F Almeida ◽  
Robson A Santos
Keyword(s):  
Ischemia Reperfusion ◽  
Systolic Pressure ◽  
Baseline Period ◽  
Left Ventricular ◽  
Biologically Active ◽  
Ventricular Systolic Pressure ◽  
Infarcted Area ◽  
Rat Hearts ◽  
Ischemic Period ◽  
Isolated Rat

Alamandine, a biologically active peptide of the renin-angiotensin system (RAS), was recently described and characterized. Further it has been shown to present effects similar to those elicited by Ang-(1-7). It has been described that Ang-(1-7) decreases the incidence and duration of ischemia-reperfusion arrhythmias and improved the post-ischemic function in isolated perfused rat hearts. In this study we aimed to evaluate the effects of Alamandine in isolated rat hearts subjected to myocardial infarction (MI). Wistar rats weighing between 250-300g were euthanized and their hearts were placed on Langendorff apparatus to evaluate the cardiac parameters. Hearts were submitted to 30min of stabilization, 30min of partial ischemia by occlusion of the left descending coronary artery and 30min of reperfusion. Drugs (alamandine 22pM, d-pro7-ang-(1-7) 220pM) were added to the perfusion setting from the beginning of the experiment until the end. 2,3,5-trypheniltetrazolium chloride were used to evaluate the extension of infarcted area. In control hearts (CON), there was a decrease on the left ventricular systolic pressure (LVSP) on ischemic period (54,6 ± 6,9mmHg) compared to the baseline period (84,6 ± 11,6mmHg). Alamandine (ALA) attenuated that decrease in the ischemic period (66,9 ± 7,9mmHg) vs (82,3 ± 8,9mmHg). Further, ischemia led to a decrease in the left ventricular developed pressure (dLVP), dP/dt maximum and minimum when compared to baseline values. ALA, once more, kept the ischemic parameters of dLVP and dP/dt max and min (58,9 ± 8mmHg; 1629 ± 202,2mmHg/s; 1101 ± 130mmHg/s, respectively) similar to those of baseline period (68,9 ± 8,92; 1682 ± 248,8; 1179 ± 118,6 mmHg, respectively). Ischemia/reperfusion induced an arrhythmia severity index (ASI) in control hearts (4,9 ± 1,26) higher than in hearts treated with ALA (1,10 ± 0,58). ALA also reduced infarcted area (19,64 ± 2,61%) compared with CON (33,85 ± 4,55%). All those effects were blocked by D-PRO7-Ang-(1-7). In conclusion, our data shown that Alamandine exert cardioprotective effects in post-ischemic function in isolated rat hearts by preventing LVSP, dLVP , dP/dt max and min decrease. Furthermore it reduced the infarcted area and I/R arrhythmias, apparently involving MrgD receptor participation.

Severe diastolic dysfunction with preserved energy conversion efficiency after countershock

1997 ◽  
Vol 273 (2) ◽  
pp. H583-H592 ◽  
Author(s):  
S. Yasuda ◽  
T. Shishido ◽  
Y. Goto
Keyword(s):  
Diastolic Dysfunction ◽  
Mechanical Performance ◽  
Diastolic Pressure ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Myocardial Edema ◽  
Energy Conversion Efficiency ◽  
Left Ventricular ◽  
Stunned Myocardium ◽  
Before And After

The left ventricular (LV) mechanical performance and the LV myocardial oxygen consumption (VO2)-to-pressure-volume area (PVA; LV total mechanical energy index) relationship were measured in isovolumic contraction of isolated blood-perfused dog hearts before and after direct current (DC) countershocks. At a constant LV volume, DC shocks increased LV end-diastolic pressure progressively and strikingly with the progression of myocardial edema and a marked prolongation of the time constant of LV pressure decay. In contrast, DC shocks changed neither the slope of the LV end-systolic pressure-volume relationship nor the contractile efficiency (the slope of the Vo2-PVA relationship). The oxygen cost of contractility (the slope of the relationship between PVA-independent VO2 and LV contractility) increased 27% after DC shocks. However, the magnitude of this change was considerably smaller than that previously reported in postischemic stunned myocardium (123%), suggesting that the adverse effect of DC shocks on the energy cost of excitation-contraction coupling is relatively minor. Thus, despite the severe diastolic dysfunction, DC shocks do not substantially impair either the efficiency of cross-bridge cycling or calcium cycling. Myocardial interstitial edema is more likely a potential mechanism of diastolic dysfunction after DC shocks.

Role of reflexes following myocardial necrobiosis

1965 ◽  
Vol 209 (6) ◽  
pp. 1081-1088 ◽  
Author(s):  
G. Ascanio ◽  
F. Barrera ◽  
E. V. Lautsch ◽  
M. J. Oppenheimer
Keyword(s):  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Hemodynamic Changes ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood ◽  
Bilateral Vagotomy ◽  
Left Ventricular Systolic Pressure

Intracoronary administration of hexachlorotetrafluorobutane (Hexa) into non-thoracotomized dogs produced a statistically significant decrease in left ventricular systolic pressure (LVSP), mean femoral arterial blood pressure (MFAP), first derivative of left ventricular pressure pulse (dP/d t), total peripheral resistance (TPR), and cardiac output (C.O.) lasting up to 1 hr after injection. Femoral vascular resistance decreased during the first 3 min after production of necrobiosis. Fifty percent of the dogs died of ventricular fibrillation (VF) after Hexa infarction. Prereserpinized dogs did not show significant changes in the parameters which were significantly changed in normal dogs after Hexa necrobiosis except in the case of VF which was almost absent in this group. Bilateral vagotomy prior to Hexa administration prevented most hemodynamic changes after necrobiosis whereas atropine did not. Bilateral vagotomy and atropine 1 hr after necrobiosis increased MFAP, dP/d t, LVSP, C.O., and TPR. Apparently excitatory efferent sympathetic activity on heart and femoral arterial vessels is reflexly inhibited by the effects of intracoronary injection of Hexa. The afferent pathway is via the vagus nerve.

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