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PubMed2004

Nitric oxide control of cardiac function: is neuronal nitric oxide synthase a key component?

Nitric oxide (NO) has been shown to regulate cardiac function, both in physiological conditions and in disease states. However, several aspects of NO signalling in the myocardium remain poorly understood. It is becoming increasingly apparent that the disparate functions ascribed to NO result from its generation by different isoforms of the NO synthase (NOS) enzyme, the varying subcellular localization and regulation of NOS isoforms and their effector proteins. Some apparently contrasting findings may have arisen from the use of non-isoform-specific inhibitors of NOS, and from the assumption that NO donors may be able to mimic the actions of endogenously produced NO. In recent years an at least partial explanation for some of the disagreements, although by no means all, may be found from studies that have focused on the role of the neuronal NOS (nNOS) isoform. These data have shown a key role for nNOS in the control of basal and adrenergically stimulated cardiac contractility and in the autonomic control of heart rate. Whether or not the role of nNOS carries implications for cardiovascular disease remains an intriguing possibility requiring future study.

Autonomic Nervous System↗
PubMed2003

Model of functional cardiac aging: young adult mice with mild overexpression of serum response factor.

Serum response factor (SRF) is an important transcription factor that may have a role in the maintenance of cardiac structure and function. The level of SRF mRNA expression increases approximately 16% in the hearts of mice during adult aging. To model the effect of mild SRF elevation in the aging heart, transgenic mice with low levels of SRF overexpression were generated. By 6 mo of age, the transgenic mice had a 19% increase of heart-to-body weight ratio compared with nontransgenic mice. In addition, they had a 12% increase in myocyte size, a 6.7% increase in collagen deposition, and altered gene expression of a number of muscle-specific and cardiac genes. Doppler echocardiography revealed that these transgenic mice had increased left ventricular wall thickness and decreased left ventricular (LV) volumes, increased LV stiffness with 20% reduction in early diastolic LV filling (peak E), and 35% decline in peak E-to-peak A (late diastolic filling) ratio. The observed changes, especially those in the E/A ratio, are similar to those seen clinically in late life as a part of human adult myocardial aging.

Aging↗
PubMedDate not supplied

Protective effect of glutamic acid on cardiac function and metabolism during cardioplegia and reperfusion.

The effect of glutamic acid added to cardioplegic solution containing 20 mM K+ on the cardiac function and metabolism was studied in isolated working rat hearts. 30-min cardiac arrest resulted in profound fall in creatine phosphate and ATP content, by four- and two-fold, respectively, as well as in four-fold rise in AMP content. Simultaneously, during cardioplegia a decline in tissue glutamate and aspartate content and an increase in tissue ammonia and alanine content were found. After reperfusion, an incomplete restoration of ATP, AMP, and creatine phosphate content were observed; the cardiac output recovered only to 39 percent of the initial value. An addition of glutamic acid to cardioplegic solution was associated with significantly less decline in the content of high-energy phosphates and less prominent rise in AMP content during cardioplegia. It also prevented the decline in tissue aspartate content and caused a lesser ammonia accumulation in myocardial tissue due to the activation of glutamine synthesis. In spite of this the tissue ammonia level remained elevated. Reperfusion with Krebs-Henseleit buffer resulted in the recovery of cardiac output to 75% of the initial value as well as better restoration of high-energy phosphate content. The addition of glutamic acid in the perfusate during reperfusion led to further improvement of ATP and creatine phosphate content. It is suggested that an addition of glutamic acid may have beneficial effect in open heart surgery.

Adenine Nucleotides↗
PubMed1987

Influence of diltiazem on cardiac function at organ and molecular level during hypothermic cardiac arrest.

The present study was undertaken to assess the effects of cold crystalloid cardioplegia with and without diltiazem on the functional recovery of the heart, calcium binding and uptake by the sarcoplasmic reticulum, Ca++ATPase of sarcoplasmic reticulum and coronary sinus serum MBCK (MB fraction of creatine kinase) of dogs, after 1.5 h of reperfusion following 1 h of ischemic cardiac arrest. The dogs were divided into three groups: group I, sham bypass (no ischemic cardiac arrest); group II, cold crystalloid cardioplegia; group III, cold crystalloid cardioplegia with diltiazem. The results showed that the decrease in the index of cardiac contractility and cardiac index which accompanies cold crystalloid cardioplegia is associated with a decrease in the calcium uptake by sarcoplasmic reticulum. The index of myocardial contractility was better preserved with cold crystalloid plus diltiazem than with cold crystalloid alone. This improvement, although partial, in cardiac contractility with cold crystalloid plus diltiazem, was associated with a tendency for an increase towards control values in the calcium uptake by sarcoplasmic reticulum. There were no changes in Ca++ATPase of, and calcium binding by, the sarcoplasmic reticulum of groups II and III when compared to group I. There was a progressive increase in the MBCK of coronary sinus blood in groups II and III. The MBCK of group I was unchanged throughout the experimental protocol. The increases in the MBCK of coronary sinus blood were less in group III than in group II indicating the protective effect of diltiazem on ischemic and reperfusion myocardial injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Selective cerebral overexpression of growth hormone alters cardiac function, morphology, energy metabolism and catecholamines in transgenic mice.

BACKGROUND: Growth hormone (GH) has important regulatory effects on cardiac morphology and function both during normal development as well as in pathophysiological settings such as myocardial infarction (MI) and congestive heart failure (CHF). In order to investigate in more detail the interaction between GH and sympathetic nervous system (SNS) system we studied the effects of selective cerebral GH overexpression on myocardial content of catecholamines, myocardial and brain energy metabolism as well as on cardiac function during resting and stress conditions in a transgenic mouse model. METHODS: Transgenic mice with selective bovine GH overexpression under control of glial fibrillary acidic protein promoter in the brain (GFAP-bGH, n=15) were created and compared to genetically matched non-transgenic mates (Control, n=15). Cardiac morphology and function were evaluated in vivo using transthoracic echocardiography during resting and stress conditions induced pharmacologically by dopamine (D) and isoprotenolol (ISO). Myocardial and brain energy metabolism were evaluated non-invasively using in vivo volume-selective phosphorus magnetic resonance spectroscopy ((31)P MRS). Myocardial content of catecholamines was analyzed by means of HPLC. RESULTS: Compared to the C animals, the GFAP-bGH mice have showed several differences in the cardiac phenotype. Systolic (fractional shortening) and diastolic function (E/A wave ratio of mitral flow) was disturbed in the GFAP-bGH mice (both p<0.05). During the dopamine stress, there was chronotropic insufficiency in the GFAP-bGH group (p<0.01) while no difference was observed in response to isoprotenolol. Left ventricular dimensions were increased in GFAP-bGH mice (p<0.05). There was a tendency for higher body weight in GFAP-bGH compared to the control group (p=0.06) while no difference was observed in heart weight and brain weight when normalized for body weight. Myocardial content of noradrenaline was lower in the GFAP-bGH group (p<0.05). PCr/ATP ratio was higher (p<0.05) in the brain and lower in the heart (p<0.05) in the GFAP-bGH mice. CONCLUSIONS: Selective cerebral overexpression of GH results in alterations of cardiac function, morphology and metabolism in transgenic mice. Decreased myocardial content of catecholamines in the GFAP-bGH mice suggests central interaction between GH and sympathetic nervous system.

Animals↗
PubMed1994

Cardiac function in patients with human immunodeficiency virus infection and with no other active infections.

OBJECTIVE: to investigate cardiac function and prognostic significance of echocardiographic findings in patients with uncomplicated human immunodeficiency virus (HIV)-infection. PATIENTS AND METHODS: Doppler echocardiography was performed in 60 male patients with HIV-infection and no signs of other active infections, and in 36 age and sex matched normal control subjects. The survival time of the patients was assessed 36 months after the echocardiographic examination. RESULTS: None of the patients had significant pericardial effusions, intracardiac tumors, signs of valvular endocarditis or dilated cardiomyopathy. In none of the patients were the fractional shortening or the early and atrial mitral flow ration (E/A ratio) below the 95% confidence limit of the control group. The E/A ratio was slightly, but significantly, decreased in AIDS patients both as compared to asymptomatic HIV-infected patients and as compared to normal control subjects because of increased heart rated in the AIDS patients. Within the three-year observation period, 28 of the patients died from HIV-related disease. In the group of deceased patients, there was no significant correlation between blood pressure, heart rate, left ventricular diameters, fractional shortening, E/A ratio and the survival time. CONCLUSION: In a population of HIV-infected patients with no other active infections, cardiac abnormalities seen to be uncommon, and the echocardiographic fractional shortening and E/A ratio were not related to the survival time of such patients. Thus, our data does not evidence that HIV is a direct cardiac pathogen.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Losartan reduces left ventricular hypertrophy proportionally to blood pressure reduction in hypertensives, but does not affect diastolic cardiac function.

In contrast to the well-recognized salutary effects of angiotensin-converting enzyme inhibition, the value of angiotensin II type I (ATl)-receptor blockade on left ventricular hypertrophy (LVH) is controversial. In addition, the data on the influence of this therapy on cardiac diastolic function are scarce. Thirty-nine patients with moderate primary hypertension, LVH, and normal systolic function received losartan, 50 to 100 mg daily. Transthoracic echocardiography was performed at baseline and after 6 months of treatment. Thirty-one patients completed and were included in the study (16 males, 61.1 +/- 1.0 years). The patients were divided into responders if mean blood pressure (BP) decreased > 5 mm Hg at the end of the study (20 patients) and non-responders (mean BP decrease < or = 5 mm Hg, 11 patients). The BP and the LVH were significantly reduced (systolic BP by 10.0%, diastolic BP 6.5%, mean BP 8.2%, left ventricular mass index [LVMI] 6.2%, interventricular septum 5.8%, posterior wall 3.0%) (p< or =0.02), attributed to the reduction of BP and LVH in responders; the LVH in non-responders did not alter with treatment. A significant correlation was noted between changes in BP and LVMI (r=0.60, p<0.001). The systolic cardiac function remained normal. The Doppler parameters usually used to assess the diastolic function of the LV (early diastolic filling velocity [E wave], late diastolic filling velocity [A wave], ratio of E/A waves, isovolumic relaxation time), which were abnormal at baseline, did not change with treatment. The size of the left atrium increased (p<0.05) at the end of the study. In conclusion, a 6-month course with losartan decreased BP and LVH. However, the LVH regression was rather associated with the reduction of the hemodynamic stimulus per se, than any trophic effect of the drug in the myocardium. The diastolic cardiac function remained abnormal with treatment.

Antihypertensive Agents↗
PubMed2001

Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy is a genetic disease characterized by cardiac hypertrophy, myocyte disarray, interstitial fibrosis, and left ventricular (LV) dysfunction. We have proposed that hypertrophy and fibrosis, the major determinants of mortality and morbidity, are potentially reversible. We tested this hypothesis in beta-myosin heavy chain-Q(403) transgenic rabbits. METHODS AND RESULTS: We randomized 24 beta-myosin heavy chain-Q(403) rabbits to treatment with either a placebo or simvastatin (5 mg. kg(-1). d(-1)) for 12 weeks and included 12 nontransgenic controls. We performed 2D and Doppler echocardiography and tissue Doppler imaging before and after treatment. Demographic data were similar among the groups. Baseline mean LV mass and interventricular septal thickness in nontransgenic, placebo, and simvastatin groups were 3.9+/-0.7, 6.2+/-2.0, and 7.5+/-2.1 g (P<0.001) and 2.2+/-0.2, 3.1+/-0.5, and 3.3+/-0.5 mm (P=0.002), respectively. Simvastatin reduced LV mass by 37%, interventricular septal thickness by 21%, and posterior wall thickness by 13%. Doppler indices of LV filling pressure were improved. Collagen volume fraction was reduced by 44% (P<0.001). Disarray was unchanged. Levels of activated extracellular signal-regulated kinase (ERK) 1/2 were increased in the placebo group and were less than normal in the simvastatin group. Levels of activated and total p38, Jun N-terminal kinase, p70S6 kinase, Ras, Rac, and RhoA and the membrane association of Ras, RhoA, and Rac1 were unchanged. CONCLUSIONS: Simvastatin induced the regression of hypertrophy and fibrosis, improved cardiac function, and reduced ERK1/2 activity in the beta-myosin heavy chain-Q(403) rabbits. These findings highlight the need for clinical trials to determine the effects of simvastatin on cardiac hypertrophy, fibrosis, and dysfunction in humans with hypertrophic cardiomyopathy and heart failure.

Animals↗
PubMed1997

Global cardiac function using fast breath-hold MRI: validation of new acquisition and analysis techniques.

Calculation of global cardiac function parameters has been validated using fast, segmented k-space, breath-hold, gradient-echo, magnetic resonance images. Images of phantoms, experimental animals, normal volunteers, and patients were acquired with a 1.5 T clinical scanner. Humans were imaged using two phased-array surface coils in multicoil mode. Myocardial contours were extracted using a new interactive, semi-automated method based on the active contour model method. Images were acquired in the short-axis orientation, and, using a new imaging and analysis strategy, in rotating plane long-axis orientations, to provide better definition of the valve planes and the apex, and also to reduce the number of slices (compared with the short-axis method) required to sample the whole heart. Validation was accomplished through calculation of the volumes of phantoms and left and right ventricular masses of animal hearts. Functional parameters from MRI were compared with those from echocardiograms and radionuclide angiograms in normal volunteers and patients, respectively.

Adult↗
PubMed1989

Effects of terbutaline sulfate on fetal cardiac function.

An isolated heart preparation was used to study the effects of terbutaline sulfate (Brethine) on fetal cardiac function. Pregnant guinea pigs received daily subcutaneous injections of terbutaline for 10 day, whereas a control group received placebo injections. Fetal guinea pig hearts were evaluated for cariodynamic and pathologic differences. Fetuses exposed to terbutaline demonstrated a higher mean heart rate (p less than 0.01), a higher mean heart weight (p less than 0.05), a higher mean heart weight/body weight ratio (p less than 0.01), and a trend toward higher left ventricular systolic pressure levels (p less than 0.1). These hemodynamic responses in fetuses exposed to terbutaline may result in increased functional demands that may predispose myocardial tissue to damage.

Animals↗
PubMed2000

Modulation of mouse cardiac function in vivo by eNOS and ANP.

To study the role of endothelial nitric oxide synthase (eNOS) in cardiac function, we compared eNOS expression, contractility, and relaxation in the left ventricles of wild-type and eNOS-deficient mice. eNOS immunostaining is localized to the macro- and microvascular endothelium throughout the myocardium in wild-type mice and is absent in eNOS-/- mice. Whereas blood pressure is elevated in eNOS-/- mice, baseline cardiac contractility (dP/dt(max)) is similar in wild-type and eNOS-/- mice (9,673 +/- 2, 447 and 9,928 +/- 1,566 mmHg/s, respectively). The beta-adrenergic agonist isoproterenol (Iso) at doses of >/=1 ng causes enhanced increases in dP/dt(max) in eNOS-/- mice compared with wild-type controls in vivo (P < 0.01) as well as in Langendorff isolated heart preparations (P < 0.02). beta-Adrenergic receptor binding (B(max)) is not significantly different in the two groups of animals (B(max) = 41.4 +/- 9.4 and 36.1 +/- 5.1 fmol/mg for wild-type and eNOS-/-). Iso-stimulated ventricular relaxation is also enhanced in the eNOS-/- mice, as measured by dP/dt(min) in the isolated heart. However, baseline ventricular relaxation is normal in eNOS-/- mice (tau = 5.2 +/- 1.0 and 5.6 +/- 1.5 ms for wild-type and eNOS-/-, respectively), whereas it is impaired in wild-type mice after NOS inhibition (tau = 8.3 +/- 2.4 ms). cGMP levels in the left ventricle are unaffected by eNOS gene deletion (wild-type: 3.1 +/- 0.8 pmol/mg, eNOS-/-: 3.1 +/- 0.6 pmol/mg), leading us to examine the level of another physiological regulator of cGMP. Atrial natriuretic peptide (ANP) expression is markedly upregulated in the eNOS-/- mice, and exogenous ANP restores ventricular relaxation in wild-type mice treated with NOS inhibitors. These results suggest that eNOS attenuates both inotropic and lusitropic responses to beta-adrenergic stimulation, and it also appears to regulate baseline ventricular relaxation in conjunction with ANP.

Adrenergic beta-Agonists↗
PubMed1993

[Effect of percutaneous cardiopulmonary support (PCPS) on cardiac function with special reference to the significance of left ventricular venting].

Direct effects of percutaneous cardiopulmonary support (PCPS) on cardiac function were evaluated. Also, the efficacy of left ventricular venting to unload the heart was assessed. Eleven open-chested dogs were placed on PCPS with the flow equal to the baseline cardiac output for 30 minutes. Six out of eleven had left ventricle vented (VENT) by means of venting tube which was indwelt in the left ventricular cavity, while other five did not (NONVENT). Hemodynamic indices were obtained before and on PCPS. Measured, derived or calculated variables included heart rate (HR), mean aortic pressure (mean AOP), left ventricular end-diastolic pressure (LVEDP), peak left ventricular pressure (peak LVP), peak LVdp/dt, rate-pressure product (RPP, HR x peak LVP) and aortic-coronary sinus oxygen content difference (ACsO2D). There was no difference in any variables between the groups at baseline. On PCPS, in the VENT group, HR increased 27% from baseline (p < 0.05), while mean AOP did not change. All other variables showed significant (p < 0.05) reduction in VENT. Percent change from baseline value in VENT was: -24% for LVEDP, -47% for peak LVP, -41% for peak LVdp/dt, -32% for RPP and -42% for ACsO2D. No variable differed significantly from baseline in the NONVENT group on PCPS. The author concluded that left ventricular venting favorably alters the loading and contractile profile of the heart on PCPS without affecting systemic circulation.

Animals↗
PubMed2002

Decreased susceptibility of cardiac function to hypoxia-reoxygenation in renin-angiotensinogen transgenic rats.

We tested the hypothesis that the renin-angiotensin system (RAS) protects the contractile function of the myocardium against the damaging effect of hypoxia-reoxygenation. For this purpose, the contractility of isolated papillary muscles from wild-type (WT) rats and from rats expressing human renin and angiotensinogen as transgenes (TGR) was compared. After 15 min of hypoxia, peak force (PF) was decreased to 24 +/- 5% of the normoxic values in TGR (n = 10) and to 18 +/- 1% in WT rats (n = 12). PF and relaxation rates recovered completely in TGR but not in WT rats during 45 min of reoxygenation. Improved contractility of the papillary muscles from TGR during hypoxia-reoxygenation correlated with increased glutathione peroxidase activities and creatine kinase (CK)-MB and CK-BB isoenzyme levels. On the other hand, inhibition of the RAS with ramipril (1 mg/kg body wt for 3 wk) in WT animals resulted in deterioration of the contractile function of the papillary muscles during reoxygenation compared with untreated rats. These findings suggest that activation of the RAS protects contractile function of the cardiac muscle against hypoxia-reoxygenation, possibly through changes in CK isoenzymes and enhanced antioxidant capacity.

Animals↗
PubMed1986

Augmentation of cardiac function in end-stage heart failure by combined use of dobutamine and amrinone.

A patient with end-stage congestive cardiomyopathy had progressive hemodynamic deterioration while awaiting orthotopic heart transplantation. Attempts to support cardiovascular function by high-dose dobutamine infusions were complicated by life-threatening cardiac arrhythmias. The addition of the noncatecholamine inotropic agent, amrinone, improved ventricular performance, enabling reduction of the dose of dobutamine and resolution of the cardiac arrhythmias. Beta receptor stimulation by dobutamine combined with phosphodiesterase inhibition by amrinone may additively or synergistically augment cardiac function despite severe congestive heart failure and also have an adrenergic "sparing effect."

Aminopyridines↗
PubMed2001

The estimation of cardiac function from the rotary blood pump.

The rotary blood pump is implanted as a bridge to cardiac transplantation. Mechanical, histological, and biochemical improvements have been described in patients after implantation of left ventricular assist devices (LVADs). Thus, the rotary blood pump might be used as a bridge to recovery of myocardial function. However, unlike a pulsatile pump, the rotary blood pump cannot be stopped to estimate cardiac function: if the rotary blood pump stops, backflow will occur. In this study, a new method that can estimate cardiac function without pump stop was examined. Six pigs were the subjects of this acute study. The pump was implanted as an LVAD: the inlet cannula was inserted into the left ventricle, and the outlet cannula was inserted into the ascending aorta. The motor speed was regulated at a pump flow rate of 0 L/min at diastolic phase. Then, the relationship between the dp/dt of left ventricular pressure and external stroke work of actuator was examined. This method was studied at normal, hyperdynamic, and heart-failure conditions. There was a high positive correlation between the dp/dt of left ventricular pressure and external stroke work of actuator. This method is useful and simple to estimate cardiac function without pump stop.

Animals↗
PubMed1991

Beneficial effects of yohimbine on posthypoxic recovery of cardiac function and myocardial metabolism in isolated perfused rabbit hearts.

The present study was undertaken to elucidate the possible actions of yohimbine on cardiac function and metabolism in the hypoxic and subsequently reoxygenated myocardium. For this purpose, rabbit hearts were perfused for 20 min under hypoxic conditions, followed by 45 min reoxygenated perfusion, and their functional and metabolic alterations with and without yohimbine treatment were examined. Hypoxia induced cessation of cardiac contractile force, rise in resting tension and depletion of tissue high-energy phosphates, which were poorly recovered by subsequent reoxygenation. Hypoxia also induced release of creatine kinase and ATP metabolites from perfused hearts and increases in tissue calcium and sodium contents, which were further enhanced upon subsequent reoxygenation. When hypoxic hearts were treated with 3 to 30 microM yohimbine, several beneficial effects were observed in a concentration-dependent manner. This included enhancement of posthypoxic recovery of contractile function and suppression of the hypoxia- and reoxygenation-induced rise in resting tension. Hypoxia/reoxygenation-induced release of ATP metabolites was inhibited and restoration of myocardial high-energy phosphates enhanced. Inhibition of reoxygenation-induced rise in tissue calcium and sodium and creatine kinase release were also noted. The findings suggest that suppression of transmembrane flux of ions, substrates and enzymes during hypoxia/reoxygenation plays a role in the posthypoxic functional and metabolic recovery. Yohimbine (3-30 microM) significantly depressed the maximal stimulus frequency the left atria could follow. These results suggest a close relationship between depression in the maximal driving frequency of atria and enhancement of the posthypoxic contractile and metabolic recovery of perfused hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1995

Exacerbated tamponade: deterioration of cardiac function by lowering excessive arterial pressure in hypertensive cardiac tamponade.

Patients with cardiac tamponade usually have significant hypotension; hypertension is rare. Before administering any medication during tamponade one must consider the complex physiology and compensatory mechanisms of cardiac compression [1]. We observed both an accentuation of pulsus paradoxus and retrospectively recognized fluctuations of left-ventricular function after progressively rising arterial blood pressure had been lowered.

Antihypertensive Agents↗
PubMed1992

Exercise training improves cardiac function after ischemia in the isolated, working rat heart.

The aim of this study was to determine whether exercise training produces a myocardium intrinsically more tolerant to ischemic-reperfusion injury. Male Fischer 344 rats were treadmill trained for 11-16 wk at one of the following intensities: LOW (20 m/min, 0% grade, 60 min/day), moderate (MOD; 30 m/min, 5% grade, 60 min/day) or intensive (INT; 10 bouts of alternating 2-min runs at 16 and 60 m/min, 5% grade). Cardiac function was evaluated both before and after 25 min of global, zero-flow ischemia in the isolated, working heart model. Compared to hearts from sedentary (SED) rats, postischemic cardiac output (CO) and work were significantly higher in all trained groups. Percent recovery of CO (relative to preischemia) was 36.0 +/- 7.1 in SED and 61.2 +/- 6.5, 68.1 +/- 9.3, and 73.2 +/- 5.0 in LOW, MOD, and INT, respectively. Postischemic increases in stroke volume with increased preload and cardiac work at high work load were significantly higher in INT compared with SED. Coronary flow during initial retrograde reperfusion was significantly enhanced with training and correlated with subsequent recovery of CO (R2 = 0.613). Furthermore, trained hearts had higher phosphocreatine (P less than 0.05) and ATP (P less than 0.01) contents after 45 min reperfusion. It is concluded that exercise training results in an intrinsic myocardial adaptation, allowing greater recovery of cardiac pump function after global ischemia in the isolated rat heart.

Adenosine Triphosphate↗