Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEART ARREST”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed1987

Right heart pressure does not equal pericardial pressure in the potassium chloride-arrested canine heart in situ.

Recently proposed concepts of pericardial surface pressure, as opposed to liquid pressure, have advanced our understanding of the relationship between pericardial and heart chamber pressures. However, the subsequent suggestion that right heart intracavitary pressure equals, or nearly equals, pericardial surface pressure is not strictly consistent with the physiology of pericardial constraint. If right heart pressure equals pericardial surface pressure, then transmural right heart pressure equals zero. Because of the difficulty in measuring pericardial pressure directly in the beating heart we designed an experiment in the recently arrested canine heart in situ to measure pericardial pressure indirectly and to test the hypothesis that right heart transmural pressure is zero under reasonably physiologic, static equilibrium conditions. According to a static equilibrium analysis of the pressures acting across the walls of the heart, at a given volume the change in right heart pressure caused by removing the pericardium is equal to the pericardial pressure when the pericardium is intact. We found that this drop in pressure caused by pericardiectomy did not equal right heart pressure and therefore that right heart transmural pressure does not equal zero.

Animals↗
PubMed1987

Left ventricular epicardial deformation in isolated arrested dog heart.

We have developed a method for measuring epicardial deformation in the isolated arrested dog heart. A biplane video system was used to record the motion of discrete epicardial markers at midanterior sites (n = 4 hearts) and midposterior sites (n = 1) during quasi-static left ventricular (LV) filling. Experimental procedures, performed at room temperature, were completed within 20 min, and LV pressure-volume curves were repeatable and within the range of data presented by other authors. To obtain a complete description of local deformation, epicardial displacements derived from the video record were analyzed using homogeneous strain theory. Local epicardial strain was nonuniform; the mean ranges of midanterior major and minor extensions were 0-13.9 and 0-7.2%, respectively, for LV filling pressures of 0-20 mmHg. For the midanterior wall, the mean orientation of the major extension was 28-35 degrees below the LV circumference, compared with an orientation of approximately 62 degrees at the midposterior site. The results demonstrate the value of this preparation for studying passive ventricular mechanics and are not consistent with the predictions of mathematical models of ventricular stress and strain, in which it has been assumed that the material properties of the passive myocardium are isotropic.

Animals↗
PubMed1998

Arresting donor hearts with extracellular-type cardioplegia prevents vasoconstriction induced by UW solution.

The effects of arresting donor hearts with University of Wisconsin solution was investigated. Donor dogs were divided into two groups according to the technique used for arresting the heart. In group I (n = 6) the heart was arrested with University of Wisconsin solution, whereas in group II (n = 6) extracellular-type cardioplegia (K+ = 20 mmol/liter) was used to induce cardioplegic arrest. Aortic root pressure was measured during the infusion of solution at constant flow. In both groups, the hearts were then flushed and stored in cold University of Wisconsin solution for 6 h. The hearts were transplanted orthotopically and disconnected from cardiopulmonary bypass. Left ventricular function was evaluated by pressure-volume relations using a conductance catheter. Peak aortic root pressure during the infusion was significantly higher in group I than in group II, although post-transplant left ventricular function was similar in both groups. Although there was no difference in cardiac function after implantation, donor hearts should be arrested by extracellular-type cardioplegia to prevent coronary vasoconstriction associated with preservation in University of Wisconsin solution.

Adenosine↗
PubMedDate not supplied

Myocardial resistance and tolerance to ischemia: physiological and biochemical basis.

This article is a short review of newer findings concerning the physiological and biochemical bases of the heart's tolerance to ischemia. The following themes are discussed. I. Energy-pool, energy-demand, and efficiency of anaerobic metabolism, the essential determinants of reanimation time and the heart's tolerance to ischemia. II. Experimental results of ischemic heart arrest and the heart arrest induced by a sodium-poor calcium-free, procaine-containing cardioplegic solution, developed by the author. III. Equivalents of function, metabolism and structure during the anaerobic period of the myocardium. IV. The myocardium's capability to recover in dependence on the metabolic state of ischemia and summary of the most important points of gaining a long time of tolerated ischemia. V. Survey and prospects.

Adenosine Diphosphate↗
PubMed1999

Electron microscopic stereology of capillary endothelial cells and cardiomyocytes in artificially arrested canine hearts.

In open heart surgery and transplantation, sufficient structural preservation of the myocardium immediately following cardioplegic arrest is a precondition for overcoming ischemia and for resumption of postischemic function. Therefore, we compared the protective effect of three clinically applied cardioplegic solutions with fibrillating and beating hearts using structural criteria. Left ventricular samples were taken from (1) beating, or (2) fibrillating or arrested hearts following coronary perfu-sion with (3) St. Thomas' Hospital solution, (4) histidine tryptophane ketoglutalate (HTK) (Custodiol), or (5) University of Wisconsin (UW) solution and fixed by immersion. Ultrastructural differences in the swelling of capillary endothelial cells and myocytes were quantitatively evaluated using stereological methods. Endothelial cells were somewhat more swollen after St. Thomas perfusion than those in beating and fibrillating hearts. HTK-arrested hearts showed significantly lower values for cellular edema than beating hearts. UW perfusion resulted in the (significantly) lowest degree of endothelial cell edema. Edematous changes in myocytes were significantly greater in St. Thomas-arrested hearts than in UW- or HTK-arrested hearts. Cardiomyocyte edema in beating and fibrillating hearts was comparable to that in St. Thomas-perfused hearts. Thus, the stereol-ogical analysis revealed significant differences between cardioplegic solutions in structural preservation of myocardial ultrastructure.

Journal Article↗
PubMed1993

Changes in the principal free intracellular amino acids in the Langendorff perfused guinea pig heart during arrest with calcium-free or high potassium media.

OBJECTIVE: Many amino acids have been shown to be cotransported with Na+ in a variety of tissues but evidence for an Na+ dependent efflux in the heart is restricted to taurine. The aim of this study was to determine the intracellular levels of the principal amino acids, alanine, glutamine, glutamate, and aspartate, when the heart was beating at normal or low temperature, during exposure to strophanthidin, and when the heart was arrested with either Ca2+,Mg(2+)-free Tyrode solution (a condition known to raise intracellular Na+) or with a high K+ Tyrode solution. METHODS: Guinea pig hearts, mounted on a Langendorff apparatus, were perfused with a variety of media and the level of amino acids in the ventricles determined using high performance liquid chromatography. RESULTS: During perfusion with normal Tyrode solution a time dependent fall in tissue glutamine, glutamate, and aspartate, but not alanine, was observed. Exposure of the beating heart to strophanthidin (0.2 mM) or cooling to 20 degrees C, which should induce a similar increase in [Na+]i but have opposite effects on metabolism, had different effects on tissue amino acids. Cooling did not affect the level of amino acids whereas strophanthidin produced an effect consistent with an activation of a glutamate-alanine aminotransferase. Arresting the heart with Ca2+,Mg(2+)-free Tyrode solution provoked a marked fall in all amino acids which was associated with their appearance in the effluent. This loss of the amino acids was antagonised by conditions known to reduce the rise in intracellular Na+ concentration and increased by inhibition of the Na+ pump. Comparison of the beating heart with the heart arrested with high K+ Tyrode solution showed no difference in the levels of glutamate or aspartate, with a small fall in alanine and taurine and raised glutamine. CONCLUSIONS: The data from beating or arrested hearts are consistent with the presence of amino acid/Na+ cotransport systems but the levels of amino acids free in the sarcoplasm depend on an interaction between amino acid transport driven by the changes in the Na+ gradient and the effects of metabolism.

Alanine↗
PubMed1985

Computer simulation of cardiopulmonary resuscitation.

Based on recent experiments attributing blood flow in cardiopulmonary resuscitation (CPR) to intra-thoracic pressure variations a computer study of the complete cardiovascular system with an arrested heart is presented. The model is based on a lumped parametric description of the vascular elements subjected to external pressure variations. The blood flow, which is generated in the system, is found to be within the reported experimental findings in similar conditions, and is highly sensitive to valving mechanisms within the heart and the large veins. Optimal conditions for CPR were searched mathematically and found to be consistent with known experimental data. Mechanisms of blood flow in CPR are discussed. The above model thus offers a tool to understand the various mechanisms involved in CPR and the relative importance of different physiological parameters, and may help in the design of an optimal CPR mode.

Animals↗
PubMed2004

Sinoatrial node dysfunction and early unexpected death of mice with a defect of klotho gene expression.

BACKGROUND: Homozygous mutant mice with a defect of klotho gene expression (kl/kl) show multiple age-related disorders and premature death from unknown causes. METHODS AND RESULTS: The kl/kl mice subjected to 20-hour restraint stress showed a high rate (20/30) of sudden death, which was associated with sinoatrial node dysfunction (conduction block or arrest). Heart rate and plasma norepinephrine of kl/kl mice, unlike those of wild-type (WT) mice, failed to increase during the stress. Intrinsic heart rate after pharmacological blockade of autonomic nerves in kl/kl mice was significantly lower than that in WT mice (380+/-33 versus 470+/-44 bpm; n=7). The sinus node recovery time after an overdrive pacing (600 bpm, 30 seconds) in kl/kl mice was significantly longer than in WT mice (392+/-37 versus 233+/-24 ms; n=6). In isolated sinoatrial node preparations, the positive chronotropic effect of isoproterenol was significantly less, whereas the negative chronotropic effect of acetylcholine was significantly greater in kl/kl than in WT mice. There was no degenerative structural change in the sinoatrial node of kl/kl mice. The precise localization of klotho was analyzed in newly prepared klotho-null mice with a reporter gene system (kl(-geo)). Homozygous kl(-geo) mice showed characteristic age-associated phenotypes that were almost identical to those of kl/kl mice. In the kl(-geo) mice, klotho expression was recognized exclusively in the sinoatrial node region in the heart in addition to parathyroid, kidney, and choroid plexus. CONCLUSIONS: In the heart, klotho is expressed solely at the sinoatrial node. klotho gene expression is essential for the sinoatrial node to function as a dependable pacemaker under conditions of stress.

Aging, Premature↗
PubMed1989

Intrathoracic pressures and left ventricular configuration with respiratory maneuvers.

In 12 dogs, we examined the correspondence between esophageal (Pes) and pericardial pressures over the anterior, lateral, and inferior left ventricular (LV) surfaces. Pleural pressure was decreased by spontaneous inspiration, Mueller maneuver, and phrenic stimulation and increased by intermittent positive pressure ventilation (IPPV) and positive end-expiratory pressure (PEEP). To separate effects due to blood flow, we analyzed beating and nonbeating hearts. In beating hearts, there were no significant differences between changes in Pes and pericardial pressures. In arrested hearts, increasing LV pressure by 8 Torr increased pericardial pressures by only 3.6 Torr. With IPPV and PEEP, increases in Pes and pericardial pressures were equal in live hearts and in low-volume arrested hearts (LV pressure = 4 Torr). In high-volume arrested hearts (LV pressure = 12 Torr), the increase in pericardial pressure over the anterior LV surface was less than Pes, whereas that over the lateral and inferior LV surfaces was the same as Pes. At high LV volume, in arrested hearts pericardial pressures decreased less than Pes during negative pressure maneuvers. In another six dogs, external LV configuration and volume were measured. In beating hearts during spontaneous inspiration, Mueller maneuver, and phrenic stimulation (endotracheal tube open), septal-lateral dimension and LV volume decreased by approximately 3% (P less than 0.05). This was also true for PEEP. In arrested hearts, septal-lateral dimension and LV volume decreased only with PEEP. We conclude that 1) the relationship between Pes and pericardial pressures is complex and depends on LV volume, local pericardial compliance, and the means by which Pes is changed, 2) changes in measured pericardial pressures did not completely explain changes in LV configuration, and 3) during different respiratory maneuvers, different forces account for the same observed changes in LV volume and configuration.

Animals↗
PubMed2002

Donor heart contractile dysfunction following prolonged ex vivo preservation can be prevented by gene-mediated beta-adrenergic signaling modulation.

OBJECTIVES: Reperfusion after myocardial ischemia goes together with alteration of the beta-adrenergic (betaAR) signaling. Especially the level and catalytic activity of beta AR kinase (betaARK1) are increased. We hypothesized that myocardial expression of a betaARK1 inhibitor (betaARKct) may protect from post-reperfusion dysfunction. METHODS: Two groups of rabbits were treated by intracoronary delivery of either phosphate-buffered saline (PBS) or a solution of adenovirus carrying the betaARKct transgene (Adeno-betaARKct). At day 5, the hearts were explanted after cold cardioplegic arrest, and preserved at 4 degrees C for 4 h. Reperfusion was hemodynamically standardized on a Langendorff apparatus with oxygenated Krebs solution for 30 min before left ventricular (LV) pressure was recorded using an LV latex balloon connected to a pressure transducer. Non-arrested hearts immediately perfused on the Langendorff apparatus served as controls. RESULTS: LV contractility (LV dP/dt(max), P < 0.05) and relaxation (LV dP/dt(min), P < 0.05) were reduced, and end diastolic pressure (LV EDP) was increased after prolonged exposure to cold preservation solution as compared to normal control hearts, both under basal conditions and when stimulated with the betaAR agonist isoproterenol. However, these parameters remained within a normal range in Adeno-betaARKct-expressing hearts arrested and preserved for 4 h. Biochemical analysis shows a reduced betaAR density and an impaired signaling after reperfusion of hearts arrested for 4 h whereas it is normalized in Adeno-betaARKct-expressing hearts. CONCLUSION: Myocardial gene-mediated inhibition of betaARK1 via betaARKct expression avoids ventricular dysfunction after prolonged preservation. Therefore, this may represent a way of improving early results of cardiac transplantation and perioperative function.

Adenoviridae↗
PubMed2002

Aortic and mitral valve surgery on the beating heart is lowering cardiopulmonary bypass and aortic cross clamp time.

OBJECTIVE: The concept of cardiac surgery on the beating heart is acceptable rationale for the cardiac surgery in the next millenium. Beating heart (off-pump) coronary artery bypass grafting (CABG) techniques have led us to consider the possibility for performing the aortic and mitral valve surgery (mitral valve repairs and replacements - with or without CABG) on the beating heart with the technique of retrograde oxygenated coronary sinus perfusion. METHODS: We used the technique of retrograde oxygenated blood coronary sinus perfusion in 78 patients (Group All) - (36 patients were with extremely low ejection fraction (Group X) - 62% of whom were in New York Heart Association (NYHA) class 4 and 34% of whom were in NYHA class 3). The procedures for the patients were: aortic, mitral and tricuspid valve surgery, in combination with CABG in ischemic patients. CABG was done in all the cases off-pump. In addition, we performed a case match study for 37 patients with good ejection fraction (51.65 +/- 11.88) (Beating Heart Group) operated on the beating heart with most appropriate group of patients (No. 37) operated in our institutions on arrested heart (ejection fraction 51.07 +/- 12.93) (Arrested Heart Group). The case match selection criteria were: gender, left ventricular ejection fraction, atrial fibrillation, hypertension, pulmonary hypertension, and diabetes. The selected beating heart group and selected arrested heart groups were without statistically significant differences for the mentioned criteria. RESULTS: There were statistically significant differences between Beating Heart Group and Arrested Heart Group in the duration of Cardiopulmonary Bypass Time (69.35 +/- 13.52 min. versus 93.59 +/- 28.54 min.), p<0.001, and statistically significant differences in Aortic Cross Clamp Time (46.5 +/- 8.95 min. versus 61.5 +/- 18.34 min.), p<0.001. The values for Creatinin Kinase (CK) and LDH were not statistically different, however the absolute values for Beating Heart Group were lower. There was no statistical difference in complication rate for both the groups for: sternal infection, bleeding, death, atrial fibrillation, AV block and neurological complications. The total early mortality for all the patients was 5.1% (4 out of 78) - for the group X 8.3 % (3 of 36 patients). Two were in-hospital deaths. One patient with triple-vessel disease and acute mitral insufficiency on intra aortic balloon pump (IABP) had been operated on 6 days after acute myocardial infarction (AMI). The cause of the death was systemic meticillin resistant staphylococus aureus (MRSA) infection - (eight days prior to our operation, arthrodesis of the talocrural joint was performed by an orthopedic surgeon). The other death was a female patient who was operated on after previous multiple cerebrovascular infarctions (CVI) (cause of the death was CVI). In addition, one patient died one month after the operation because of prosthetic valve endocarditis (PVE) on aortic and mitral valves (silver-coated silzone aortic and mitral valves were implanted because of chronic latent asymptomatic tibial osteitis). None of these deaths were cardiac related. CONCLUSIONS: We conclude that beating heart valve surgery (any combination) with or without CABG significantly lower the cardiopulmonary bypass and aortic cross clamp time. In addition, the advantages of beating-heart surgery are 1) the perfused myocardial muscle, 2) the heart is not doing any work, 3) no reperfusion injury, 4) the possibility for ablation of atrial fibrillation on the beating heart, and 5) testing of the mitral valve repair is done in real physiologic conditions in the state of left ventricle beating tonus. The procedure could be the procedure of choice for the valve operation or combined operations (valve operation and CABG) in high-risk patients with low ejection fractions. There is no doubt that at present day in cardiac surgery exist at least two major factors for mortality and morbidity after cardiac surgery, which are operation - related, namely cardiopulmonary bypass time and its duration and aortic cross clamp time (ischemic time of myocardium). In the last few years a number of different techniques emerged in the field of cardiac surgery, which were directed toward better results in the selected high risk patients or to minimize the deleterious effects of cardiopulmonary bypass (CPB) on the overall postoperative performance [Calafiore 1996, Tasdemir 1998]. Due to the fact, that the cardiac muscle should be protected at most during the cardiac arrest, retrograde blood cardioplegia was successfully introduced [Buckberg 1990], and more - the warm cardioplegia is being used recently [Kawasuji 1997]. The natural status of the human heart is the beating status, so it is reasonable to try to perform the operations on the beating heart. This has been done recently with the MID - CAB and OP - CAB (off-pump CABG) operations [Tasdemir 1998]. The retrograde warm blood cardioplegia has therefore led us to the premise, that with retrograde oxygenated blood perfusion it would be possible to achieve the operations on the beating heart even in the open heart surgery, such as aortic and/or mitral valve surgery. All will agree that the most damaging effect of the cardioplegia is the reperfusion injury [Allen 1997], and it is obvious that with the technique of retrograde continuous oxygenated blood perfusion this effect will be canceled. In this article, we would like to show the how-to technique for the operations on the beating heart in the case of operations on the aortic valve replacement (AVR) with mitral valve repair (MVR) or replacement MVR and with/without concomitant coronary artery bypass (CABG) surgery. The tricuspid valve repair (PTV) is normally done on the beating heart and there it is realized what problems or technical difficulties may arise during procedures on the mitral valve: the walls of the ventricles are not flattened and the exposure of the mitral valve is challenging task. Furthermore, the free walls of the ventricles with interventricular septum are in the state of the tonus, so every force applied to better expose the aortic or mitral valve is not acceptable

Aortic Valve↗
PubMed1993

Preservation of cardiac myocytes subjected to different preconditions: a comparative morphometric study of beating, fibrillating, and cardioplegically arrested canine hearts.

This study compares the ultrastructure of beating canine hearts with that of hearts subjected to different clinically common forms of cardiac arrest. The contraction state per test field was ascertained according to a specially developed classification. The volume density of myofibrils and the surface to volume ratio of mitochondria were used as parameters for cellular and mitochondrial swelling. Contraction bands were not found in any of the differently pretreated hearts. Following immersion fixation, contractions as well as over- and hypercontractions in beating, fibrillating, and St. Thomas-arrested hearts are significantly more pronounced than in HTK-arrested hearts. Cellular and mitochondrial volumes were similar in beating and fibrillating hearts. St. Thomas-perfusion significantly decreased cellular and mitochondrial volume compared to beating hearts, but these values were in the same range as in fibrillating hearts. Only HTK-solution actually led to a strong reduction of these compartments. Compared to immersion, perfusion fixation after coronary perfusion with cardioplegic solutions led to comparable cellular volumes, but significantly elevated the percentage of relaxed sarcomeres and significantly reduced mitochondrial swelling. The best structural preservation of myocytes was found after HTK-perfusion and perfusion fixation. Such ultrastructural quantitative and morphometrical parameters are powerful tools since results confirm that the degree of myocardial preservation depends on the method of cardiac arrest. This forms the basis for the choice of preconditions for subsequent ischemia. Furthermore, significant alterations of myocardial ultrastructure depend on a combination of the functional state of the heart, the method of cardioplegia, and the technique of fixation.

Animals↗