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PubMed1988

No significant increase in O2 consumption of KCl-arrested dog heart with filling and dobutamine.

In the cross-circulated dog hearts arrested with KCl, we examined the effects of left ventricular volume and dobutamine on the resting oxygen consumption (MVO2). The perfusion pressure of the excised heart was stable under the cross-circulation for 1-1.5 h with a dialyzer to normalize coronary venous KCl despite continuous coronary arterial injection of KCl. The resting MVO2 declined gradually during the first 10 min of cardiac arrest but changed little thereafter. The resting MVO2 at 5 min and 30 min of arrest were 30.5 +/- 9.3 (SD) and 23.8 +/- 12.9%, respectively, of unloaded MVO2 before arrest. The resting MVO2 after its stabilization was 1.02 +/- 0.42 ml O2.min-1.100 g ventricle-1 in the control. It was 1.12 +/- 0.48 ml O2.min-1.100 g ventricle-1 under a continuous infusion of dobutamine at rate of 10-25 micrograms/min. This change with dobutamine was statistically insignificant. The resting MVO2 was not affected by changes in left ventricular volume both before and under dobutamine. The present result implies that MVO2 for basal metabolism in a working dog heart is virtually constant regardless of ventricular volume and contractility.

Animals↗
PubMed1993

Improvement of long-term preservation of isolated arrested rat heart: beneficial effect of the antiischemic agent trimetazidine.

Rat hearts, arrested in situ after intracaval injection of a simple mineral cardioplegic solution (St. Thomas), were preserved for 15 h at 4 degrees C either by simple immersion in the cardioplegic solution or low-flow perfusion by the same liquid (0.3 ml/min). Trimetazidine (TMZ) was added to the cardioplegic solution at a concentration of 10(-6) M in two additional groups corresponding to both preservation conditions. The biochemically determined ventricular ATP content was increased in immersed hearts by TMZ (+ 78%). The [ATP]/[Pi] ratio, as calculated from 31P nuclear magnetic resonance (NMR) spectroscopy, was significantly increased in both preservation conditions by TMZ: 0.08 +/- 0.03 versus 0.04 +/- 0.01 in immersed hearts and 0.53 +/- 0.13 versus 0.26 +/- 0.16 in perfused hearts (mean +/- SD). Intracellular pH was increased when TMZ was administered in perfused hearts (7.02 +/- 0.14 vs. 6.67 +/- 0.14, mean +/- SD). Functional recovery, estimated by the pressure developed by the left ventricle (intraventricular isovolumic balloon) when hearts were reperfused with a physiologic solution, was improved by TMZ in both preservation conditions: +137% in immersed hearts and +54% in perfused hearts. These results demonstrate that both the bioenergetic status of the myocardial cell and the functional capabilities of isolated, arrested, stored rat heart can be significantly improved by addition of the antiischemic drug TMZ to the preservation solution.

Adenosine Triphosphate↗
PubMed1995

Improvement of long-term preservation of the isolated arrested rat heart by trimetazidine: effects on the energy state and mitochondrial function.

Rat hearts, arrested in situ after intracaval injection of a cardioplegic solution, were preserved for 15 hours at 4 degrees C either by simple immersion or by low-flow (0.3 mL/min) perfusion. After preservation under both conditions, the left ventricular pressure developed by the reperfused hearts reached 8% and 43% of the control value (80 mm Hg), respectively. The addition of trimetazidine (TMZ; 10(-6) M) to the cardioplegic solution induced an improvement in functional recovery (by 2.4 and 1.5, respectively). This effect of TMZ was accompanied by a better energy profile illustrated by a 2-fold increase in the adenosine triphosphate to inorganic phosphate ratio and a reduction of intracellular acidosis as determined by 31P nuclear magnetic resonance spectroscopy. The function of the mitochondria (state 3, reduced nicotinamide-adenine dinucleotide [NADH] formation) isolated from the preserved hearts was significantly depressed in the stored hearts. The addition of TMZ to the cardioplegic solution partially protected oxoglutarate (and succinate) mitochondrial respiration and induced an increase in Ca2+ triggered NADH formation. These results show that the bioenergy status of the myocardial cell in isolated arrested stored rat heart is improved by the presence of TMZ in the preservation solution. Moreover, the experiments demonstrate that this effect includes protection of mitochondrial function and suggest that the drug could exert some control in the Ca2+ regulation of mitochondria.

Analysis of Variance↗
PubMed2006

Time to give the first medication during resuscitation in out-of-hospital cardiac arrest.

OBJECTIVE: There is no evidence showing an impact from any advanced cardiac life support (ACLS) medications on patient survival following cardiac arrest. One potential reason for a lack of such benefit may be medication timing. We formed the hypothesis that medications are given late after rescuer arrival, limiting any benefit. We performed a meta-analysis to determine the time from emergency medical services (EMS) dispatch to first medication administration, regardless of route, during out-of-hospital cardiac arrest (OOHCA). Then, the mean time and ranges of reported study medication delivery in clinical trials where medication was the experimental intervention was determined. METHODS: We conducted a comprehensive literature review between January 1990 and August 2005 in MEDLINE using the following MeSH headings: cardiopulmonary resuscitation, cardiac arrest, heart arrest, EMS, EMT, ambulance, and the names of all ACLS medications. We reviewed the abstracts of 632 studies and full manuscripts of 248 published papers. We eliminated the following articles from further analysis: non-peer reviewed; all without human primary data (includes review articles, guidelines or consensus manuscripts, editorials, or simulation studies); animal data; case reports. We used no language restriction. From this search, our independent reviewers found 17 papers that contained information on time to medication administration. RESULTS: We analyzed reporting of drug delivery time to 7617 patients in 32 different emergency medical services systems. Time to first medication delivery by any route was a mean of 17.7 min (range 10.0-25.0; 95% CI around mean 10.6, 24.8). Time to intravenous experimental medication administration was a mean of 19.4 min (range 13.3-25.0; 95% CI around mean 12.8, 25.9). CONCLUSIONS: Medications are given late during out-of-hospital cardiac arrest, even in cohorts where drug delivery is a key study intervention.

Algorithms↗
PubMed2001

Swelling of capillary endothelial cells and cardiomyocytes in the ischaemic myocardium of artificially arrested canine hearts.

To establish whether coronary perfusion with cardioplegic solutions results in better intraischaemic structural preservation of endothelial cells than of cardiomyocytes, we determined intraischaemic swelling of these two cell types in hearts differently arrested during global ischaemia at 5 degrees C. Cardiac arrest was induced in situ by aortic cross clamping or by additional coronary perfusion with various cardioplegic solutions. Parameters for cellular swelling were determined, i.e. barrier thickness of capillary endothelial cells and sum of the volume fractions (V(V)) of free sarcoplasm and mitochondria (V(VSp) + V(VMi)) in cardiomyocytes. In order to test the intraischaemic relative increase of cellular volume in both cell types, regression analyses were performed. The results show that the relative intraischaemic volume increase was similar in both cell types after perfusion with histidine-tryptophan-ketoglutarate solution, and significantly less pronounced in capillary endothelial cells after perfusion with University of Wisconsin solution. In hearts arrested with St. Thomas' Hospital solution, a significantly higher volume increase was determined in capillary endothelial cells. Thus, capillary endothelium does not generally show a higher structural preservation than cardiomyocytes during ischaemia. Instead, volume regulation in both types of cells depends on the type of cardioplegic solution used. These results should be taken into consideration in human transplantation medicine.

Adenosine↗
PubMedDate not supplied

Metabolism and structure of the magnesium aspartate-procaine-arrested ischaemic heart of rabbit and man.

The fine structure and the content in energy-rich phosphate compounds, glycogen, and metabolites of the Embden-Meyerhoff-pathway in rabbits hearts or human papillary muscles arrested by magnesium aspartate-procaine are investigated in normothermia and mild or deep hypothermia. In all experimental conditions the break-down of adenine nucleotides and glycogen was distinctly retarded in cardioplegia compared to ischaemic arrest. While e.g. an ATP-content of 3.6 mumole/g wet weight was found after 40 min. at 32 degrees C in the magnesium asparate-procaine arrested heart, it dropped down to 1.3 mumole/g in the ischaemically arrested heart. In cardioplegia after 60 min at 15 degrees C the in vivo contents of ATP and glycogen were determined. The rate in metabolic changes in the magnesium aspartate-procaine arrested human papillary muscle was in the range of that recorded in the arrested rabbit heart. The ultrastructural appearance of the cardioplegically arrested heart did not differ from that of the controls after 20 min at 32 degrees C or 120 min at 15 degrees C. In hearts arrested by cardioplegia 40 min at 32 degrees C first signs of ischaemic lesions e.g. mild swelling of mitochondria and few rarefications in mitochondrial matrix were observed. Because of the significantly improved preservation of the fine structure of the heart and retardation of ischaemically provoked changes in cardiac metabolism, the method of inducing heart arrest by cardioplegia should also clinically be given preference to methods of arresting the heart by ischaemia.

Adenosine Triphosphate↗
PubMed2003

[Experimental study of myocardial protective effect of cardiac arrest versus beating heart during open heart surgery].

OBJECTIVE: To investigate the myocardial protective effects of beating heart versus heart arrest in goats undergoing open heart surgery with cardiopulmonary bypass (CPB). METHODS: Eighteen healthy and homologous goats were randomly divided into three groups: groupI (n=6), with intermittent cold crystalloid cardioplegia; group II (n=6), with continuous warm blood cardioplegia; group III (n=6), with beating heart. Animals in group II and group III were operated with mild hypothermic CPB. The changes in malondialdehyde (MDA) in the myocardium of the right ventricles and atrial natriuretic peptide (ANP) in venous blood were measured respectively. The myocardial tissues were examined for ultrastructural changes. RESULTS: In group I, contents of MDA and ANP rose significantly during CPB, especially when blood was reperfused routinely. While in group II and group III, the levels were lower than those in group I at the same time points. There was no difference in the values between group II and group III. Ultrastructural changes were distinctly seen in group I, while they were mild in group II and group III. CONCLUSION: Continuous warm blood cardioplegia to keep the heart beating during operation can prevent ischemia-reperfusion injury and protect heart better.

Animals↗
PubMed1991

Hypoxic vasodilatation in isolated, perfused guinea-pig heart: an analysis of the underlying mechanisms.

1. The mechanisms underlying hypoxic dilatation of coronary arteries were studied in isolated guinea-pig hearts perfused with physiological salt solution at 37 degrees C. The hearts were perfused at a constant rate of 3-10 ml min-1; coronary perfusion pressure (CPP) and isovolumetric left ventricular pressure (LVP) were measured with piezoresistive transducers. 2. Addition of the K+ channel opener cromakalim (500 nM) to the perfusate caused a maximal vasodilatation in beating hearts, i.e. a decrease in CPP of about 50%. Switching from normal perfusate (partial pressure of O2 (PO2), 650-700 mmHg) to hypoxic perfusate (PO2, 9-10 mmHg) caused a similar vasodilatation. Both of these effects were prevented by 2 microM-glibenclamide, a blocker of ATP-sensitive potassium channels. Hypoxic vasodilatation was accompanied by a marked decrease in LVP, which was reduced by 56 +/- 22% (mean +/- S.D.) in the presence of glibenclamide. 3. In hearts arrested by increasing the K+ concentration of the perfusate to 15 mM, the addition of the adenosine-uptake inhibitor dipyridamole evoked a maximal vasodilatation and this was inhibited by 76 +/- 7% in the presence of glibenclamide. 4. The adenosine antagonist 8-phenyltheophylline (8-PT; 5 microM) inhibited the vasodilatation induced by dipyridamole by 88 +/- 10%. In contrast, hypoxic vasodilatation was unaffected by 5 microM 8-PT. This suggests that hypoxic dilatation of coronary arteries is not mediated by release of adenosine from cardiomyocytes. 5. In order to test whether release of endothelium-derived relaxing factor (EDRF) contributed to hypoxic vasodilatation we blocked EDRF synthesis with N omega-nitro-L-arginine (NNA). When applied at a perfusion rate of 10 ml min-1 to arrested hearts, 10 microM-NNA increased CPP by 35% and prolonged the delay between application of hypoxic solution and half-maximal vasodilatation from 52 +/- 9 to 129 +/- 29 s. 6. Under control conditions the relation between perfusion rate and the CPP measured in the steady state was linear. In the presence of 10 microM-NNA coronary resistance was increased more than twofold at low perfusion rates; at perfusion rates between 4 and 10 ml min-1 coronary resistance decreased progressively. This change in the pressure-flow relationship may be responsible for the alterations in the time course of hypoxic vasodilatation induced by NNA. 7. In order to test whether changes in energy metabolism in coronary smooth muscle cells were responsible for hypoxic vasodilatation we blocked glycolysis by replacing the glucose in the perfusate with deoxyglucose (DOG).(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed1980

[Changes in functional and metabolic characteristics of isolated rat heart during initial phase and long lasting perfusion].

Mechanical performance, tissue content of high-energy phosphates (ATP and CP), glycogen and phosphorylase activity were measured in isolated rat hearts either just after excision (hearts arrested by plunging in ice-cold perfusate) or during long time perfusions (6 h) at 37 degrees C. Arrested hearts exhibited : (1) higher total phosphorylase activity (a + b); (2) higher percentage of phosphorylase a; (3) lower CP content. During perfusion, high energy phosphates appeared well maintained whereas glycogen content and phosphorylase activity decreased with a significant correlation between these two parameters. The validity of this isolated heart model and possible implications of the variations in phosphorylase activity are discussed.

Adenosine Triphosphate↗
PubMed1990

Correlation between cytosolic free calcium, contracture, ATP, and irreversible ischemic injury in perfused rat heart.

The relations between ATP depletion, increased cytosolic free calcium concentration [( Cai]), contracture development, and lethal myocardial ischemic injury, as evaluated by enzyme release, were examined using 19F nuclear magnetic resonance to measure [Cai] in 1,2-bis(2-amino-5-fluorophenoxy)ethane-N,N,N',N'-tetraacetic acid (5F-BAPTA)-loaded perfused rat hearts. Total ischemia at 37 degrees C was induced in beating hearts, potassium-arrested hearts, magnesium-arrested hearts, and hearts pretreated with 0.9 microM diltiazem to reduce but not abolish contractility. In the beating hearts, time-averaged [Cai], which is intermediate between the systolic and the basal [Cai], was 544 +/- 74 nM. In contrast, in the potassium- and magnesium-arrested hearts, the time-averaged values are lower than in beating hearts (352 +/- 88 nM for potassium arrest, 143 +/- 22 nM for magnesium arrest). During ischemia, ATP depletion, contracture, and a rise in [Cai] are delayed by cardiac arrest, but all occur more rapidly in the potassium-arrested hearts than in the magnesium-arrested hearts. The diltiazem-treated hearts were generally similar to the magnesium-arrested hearts in their response to ischemia. Under all conditions, contracture development was initiated after tissue ATP had fallen to less than 50% of control; invariably, there was a progressive rise in [Cai] during and following contracture development. Reperfusion with oxygenated perfusate shortly after peak contracture development resulted in a return of [Cai] to its preischemic level, resynthesis of creatine phosphate, no significant enzyme release, and no substantial loss of 5F-BAPTA from the heart. The data demonstrate that an increase in [Cai] precedes lethal myocardial ischemic injury. This rise in [Cai] may accelerate the depletion of cellular ATP and may directly contribute to the development of lethal ischemic cell injury.

Adenosine Triphosphate↗
PubMed1997

cAMP-mediated c-fos expression in pressure-overloaded acceleration of protein synthesis in adult rat heart.

OBJECTIVES: The aim was to determine whether proto-oncogene c-fos expression and acceleration of protein synthesis by acute pressure overload to the heart were coupled with a cAMP- and protein-kinase-A-dependent system in adult rat heart. METHODS: Isolated adult rat hearts were perfused as Langendorff preparations at a constant aortic pressure of 60 mmHg. In the pressure-overloaded group, aortic pressure was raised from 60 to 120 mmHg for the time indicated. Agents that increase cAMP were added to the perfusate at an aortic pressure of 60 mmHg. Furthermore, a selective protein kinase A inhibitor (H-89) or a selective protein kinase C inhibitor (calphostin C) was administered before the elevation of aortic pressure or the addition of the agents. cAMP content or rates of protein synthesis were measured by RIA or the incorporation of [14C]phenylalanine into total heart protein, respectively. c-fos mRNA expression was determined by Northern blot analysis. RESULTS: Elevation of aortic pressure in beating hearts and arrested hearts increased cAMP content at 2 min of perfusion by 36 and 41%, induced c-fos mRNA expression at 30-60 min of perfusion by 4.8- and 2.0-fold, and accelerated rates of protein synthesis during the 2nd hour of perfusion by 39 and 41% over control levels, respectively. Glucagon, forskolin or IBMX mimicked increases in these parameters by elevated aortic pressure. H-89 prevented these changes by elevated pressure overload or exposure to forskolin or IBMX in arrested hearts. On the other hand, calphostin C prevented the pressure-induced increases in c-fos expression and protein synthesis rates in arrested hearts. CONCLUSIONS: These results suggest that c-fos expression induced by acute pressure overload may be coupled with increased cAMP content and protein kinase A activity in addition to increased protein kinase C activity in adult rat heart.

1-Methyl-3-isobutylxanthine↗