Disease relevance of Heart Arrest, Induced

• Myocardial protection through cold cardioplegia with potassium or diltiazem. Experimental evidence that diltiazem provides better protection even when coronary flow is impaired by a critical stenosis [1].
• Rat heart reduced glutathione levels decreased 32% as a consequence of cardioplegia and ischemia [2].
• The particular protective procedures that will be described involve the combined use of hypothermia and nifedipine (50 micrograms/l), with and without K+-induced chemical cardioplegia [3].
• Addition of DIDS or substitution of HCO3 at pHo 7.4 had the same effects as acidosis per se, i.e. shortened contractile activity and increased incidence of arrhythmias during anoxia, prolonged cardioplegia and provoked arrhythmias at reoxygenation [4].
• Thus adenosine cardioplegia caused rapid cardiac arrest and improved postischemic recovery when compared with potassium cardioplegia and with a combination of these two agents [5].

High impact information on Heart Arrest, Induced

• Since the introduction of cold potassium chloride cardioplegia, significantly less regional contraction-band necrosis (19 of 79) (24%) was found than before (80 of 157) (51%) [6].
• Peroxynitrite, the breakdown product of nitric oxide, is beneficial in blood cardioplegia but injurious in crystalloid cardioplegia [7].
• In the present study, we tested the hypothesis that ONOO(-) is cardiotoxic in crystalloid cardioplegia but cardioprotective in BCP in ischemically injured hearts [7].
• BACKGROUND: Laboratory evidence supports the use of adenosine-supplemented cardioplegia [8].
• CONCLUSIONS: Despite promising experimental data, adenosine supplementation of warm blood cardioplegia did not demonstrate any statistically significant benefit in patients undergoing elective coronary artery bypass graft surgery [8].

Chemical compound and disease context of Heart Arrest, Induced

• In contrast, the adenosine level in the PS-PTx group was significantly (p < 0.05) augmented during global ischemia (from 0.50 +/- 0.13 microM to 63.16 +/- 28.08 microM) and cardioplegia infusion (to 15.26 microM +/- 5.61 microM) [9].
• To test the role of lactate as an aerobic energy substrate postischemia in vivo, we employed the cardiac-arrest-induced transient global cerebral ischemia (TGI) rat model and the monocarboxylate transporter inhibitor alpha-cyano-4-hydroxycinnamate (4-CIN) [10].
• Isolated, retrograde-perfused rabbit hearts received multidose cardioplegia containing increasing concentrations of glucose, from 0 to 88 mmol/L, and underwent 120 minutes of "warm" 34 degrees C global ischemia [11].
• Potassium or potassium verapamil cardioplegia, 10 ml per kilogram of body weight, was administered after application of the aortic cross-clamp and at 30-minute intervals during the 90-minute arrest [12].
• In the hypothermia plus cardioplegia group postischemic aortic flow recovered to more than 50% of its preischemic control value, myocardial energy phosphate content returned to near preischemic control levels, and creatine kinase leakage was moderate [13].

Biological context of Heart Arrest, Induced

• Low hemoglobin low flow warm blood cardioplegia increased myocardial oxygen consumption and coronary sinus blood flow after cross clamp release, and also decreased lactate consumption [14].
• Recovery of ventricular function was significantly lower with low-dose nifedipine than with potassium cardioplegia [15].
• CONCLUSIONS: We concluded that administration of histidine-containing cardioplegia promotes anaerobic glycolysis and improves recovery of high-energy phosphates and contractile function in hypertrophied myocardium [16].
• Experiments were designed to evaluate function of the endothelium and smooth muscle of coronary arteries following storage of hearts in cardioplegia containing an inhibitor of lipid peroxidation (H 290/51, cis-7-methyl-9-methoxy-5,5a, 6,10b tetrahydroindeno [2,1-b] indole) [17].
• 1 In order to understand mechanisms that limit the safe ischaemic time of donor hearts, this study evaluated NO/cyclic GMP biosignalling in the recovery of function after cardioplegia and hypothermic storage [18].

Anatomical context of Heart Arrest, Induced

• The initial 10 minutes of reperfusion in groups 2-4 was modified by aspartate/glutamate-enriched leukocyte-depleted blood cardioplegia (group 2, n = 7), leukocyte depletion alone (group 3, n = 9), and aspartate/glutamate-enriched blood cardioplegia alone (group 4, n = 6) [19].
• The cardioprotective effects of cardioplegia and the calcium channel blocker verapamil appear to be due to a reduction of myocardial work rather than to any specific direct action on calcium fluxes across the myocardial cell membrane [20].
• The role of red blood cells during cold blood cardioplegia was studied using an intravital microscope in 13 isolated canine hearts perfused with diluted blood containing potassium chloride [21].
• CONCLUSION: Nitecapone added to cardioplegia solution reduces cardiac neutrophil accumulation and transcoronary neutrophil activation during clinical cardiopulmonary bypass [22].
• Glucose transport over the capillary endothelium is considered rate limiting for its uptake in the working heart but not during cold potassium cardioplegia despite the glucose deprivation following perfusion of glucose-free cardioplegic solution [23].

Associations of Heart Arrest, Induced with chemical compounds

• Higher dose nifedipine resulted in a return of function, which was no different than with potassium cardioplegia [15].
• CONCLUSIONS: Nicorandil (100 micromol/L and 1 mmol/L) significantly improved functional recovery compared with control and was as effective as KCl cardioplegia [24].
• Phorbol-12,13-dibutyrate and pinacidil cardioplegia. Novel forms of myoprotection [25].
• Hearts in group 3 were perfused with 3 mmol/L L-arginine in the cardioplegia solution [26].
• Intermittent cold cardioplegia inhibited mitochondrial function but prevented the degradation of adenine nucleotides [27].

Gene context of Heart Arrest, Induced

• Increased levels of IL-6 (P = 0.013), TNF-alpha (P = 0.0272), and IL-10 (P = 0.0008) were measured after cardioplegia [28].
• Protection by superoxide dismutase and catalase in the isolated rat heart reperfused after prolonged cardioplegia: a combined study of metabolic, functional, and morphometric ultrastructural variables [29].
• In the group receiving blood cardioplegia, no significant differences in CD11b, CD18, or L-selectin expression were found [30].
• Because increased expression of TGF-beta has been correlated with accelerated CAV, the use of blood/insulin cardioplegia may help to decrease the extent of endothelial damage and attenuate the progression of CAV [31].
• Effect of ischaemia-reperfusion on glutathione peroxidase, glutathione reductase and glutathione transferase activities in human heart protected by hypothermic cardioplegia [32].

Analytical, diagnostic and therapeutic context of Heart Arrest, Induced

• This study suggests that there is no statistically significant difference between any of the three cardioplegia and reperfusion techniques for either ATP or MDA; the three reperfusion techniques limit the free radical activity but do not prevent the fall in high energy phosphates [33].
• Warm retrograde cardioplegia produced a breakdown of ATP to inosine and hypoxanthine, small molecules that accumulated during the cross-clamp period and were not washed out, perhaps because of inadequate perfusion with retrograde delivery [27].
• RESULTS: The postoperative thoracic drainage at 6 hours, 24 hours, and at the time of chest tube removal in the high-dose adenosine cardioplegia group was 68%, 76%, and 75% of the placebo and low-dose adenosine cardioplegia group (p < 0.05) [34].
• Regional cardioplegia and cardioprotection during transluminal angioplasty, which role for nifedipine [35]?
• The cyclic GMP levels decreased in the control group during ischaemia from 100 +/- 6 after induction of cardioplegia to 47 +/- 3 pmol g-1 dry wt. at the end of ischaemic duration [36].

References