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Results for “HEART ARREST”

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At least 37 records · Page 2Linked to original sources
PubMed1983

Effect of temperature on the arrested heart exposed to a 4-hour ischemia during blood potassium cardioplegia. An experimental study.

This study was undertaken to evaluate the optimal myocardial temperature during a 4-hour ischemia induced by blood potassium cardioplegia (PC). Heart-lung preparations with work load circuit were used as experimental model. 24 mongrel dogs were divided into four groups and two myocardial temperatures (moderate hypothermia, deep hypothermia) and two perfusates (PC with blood, PC without blood) were tested. Parameters used to evaluate the myocardial protection include the coronary sinus blood pH of the initial reperfusion and left ventricular stroke work after resuscitation. In blood PC at moderate hypothermia, deleterious acid metabolites were minimally produced as evidenced by the coronary sinus blood pH (7.221 +/- 0.122) at initial reperfusion, and cardiac function was best recovered in this group. Blood PC at moderate hypothermia allows the heart to tolerate 4 h ischemia without an excessively elevated coronary perfusion pressure during cardioplegic infusion.

Animals↗
PubMed1984

Effects of reperfusion after acute coronary occlusion on the beating, working heart compared to the arrested heart treated locally and globally with cardioplegia.

To determine whether acutely ischemic myocardium could be more effectively salvaged by reperfusion on cardiopulmonary bypass (CPB) in the cardioplegia-treated heart than with reperfusion in the beating, working heart, 52 greyhound dogs underwent 3 hours of left anterior descending (LAD) occlusion and were randomly assigned to one of four groups. In Group I (19 dogs) the LAD occlusion was released at 3 hours and reperfusion continued in the beating, working heart for an additional 3 hours. Group II (six dogs), Group III (14 dogs), and Group IV (13 dogs) were placed on CPB and underwent 45 minutes of hypothermic ischemic arrest protected by aortic root potassium cardioplegia. In Group II, only aortic root potassium cardioplegia was given; in Group III, the ischemic area was perfused with potassium cardioplegic solution via a graft from the internal mammary artery (IMA) to the LAD. In Group IV, blood cardioplegic solution via the IMA-LAD graft was used. After the cross-clamp and local occlusion were removed, CPB was discontinued after an additional 45 minutes and reperfusion was continued off CPB for an additional 1 1/2 hours (total 6 hours). The ischemic area at risk was determined by injecting monastryl blue dye via the left atrium while the LAD was briefly reoccluded. After the animal had been sacrificed and the left ventricle had been sectioned, the area of myocardial necrosis was determined by nonstaining with triphenyltetrazolium chloride (TTC). For each group, the ratios of area of necrosis/area at risk (AN/AR) were calculated and postreperfusion arrhythmias were documented. Postreperfusion arrhythmias were noted in 11 of 12 animals in the beating, working heart group and only two of 24 in the combined CPB groups. The mean AN/AR was 66% +/- 2% in the beating, working heart (Group I), 59% +/- 6% after infusion of potassium cardioplegic solution into the aortic root (Group II), 57% +/- 6% with blood cardioplegia (Group IV), and 38% +/- 6.5% after global and local application of the potassium cardioplegic solution into the ischemic area (Group III). This study suggests that the reperfused ischemic myocardium will sustain less necrosis and less postreperfusion arrhythmias when the heart is protected by global and local cold potassium cardioplegia on CPB.

Acute Disease↗
PubMed1978

[Myocardial potassium and H-ion loss during normothermic, ischemic heart arrest].

Arterial and venous [K+] and [H+] concentrations were determined during normothermic ischemic arrest in cat hearts intermittently perfused without resuscitation. The slight loss in [K+] was taken as evidence of a stable membrane potential. The decrease in [H+] activity appearing in the perfusate correlated well with the previously described increase in coronary resistance. This was interpreted as a sign of restricted coronary perfusion and not as evidence for reduced anaerobic metabolic activity. Thus the functional impairment of the coronary system was confirmed to be a limiting factor when resuscitating ischemically arrested hearts.

Animals↗
PubMed2004

Preventive mechanism of genistein on coronary endothelial dysfunction in ovariectomized rats: an isolated arrested heart model.

The effects of genistein on coronary endothelial dysfunction in bilateral ovariectomized rats were examined. Female Wistar rats were subjected to a bilateral ovariectomy (OVX rat). The animals were divided into three groups: sham treated with vehicle (DMSO 100 microl/day, Sham-DMSO), OVX treated with vehicle (DMSO 100 microl/day, OVX-DMSO), and OVX treated with genistein (0.25 mg/kgBW/day, OVX-genistein). Mean arterial pressure (MAP), heart rate (HR), body weight (BW), uterine weight and plasma E2 were monitored at 4- and 10-week after the treatment. We investigated the endothelium-dependent and -independent vasorelaxation by using acetylcholine (Ach 10(-5) M) and sodium nitroprusside (SNP 10(-7) M), respectively. The experimental results indicated that the uterine weights of all OVX rats were significantly decreased as compared to the sham groups. HR and MAP of both OVX-DMSO and OVX-genistein on 4 and 10 weeks were no significantly increased as compared to the Sham groups. The present coronary vasodilatation responses demonstrated only the significant decrement of endothelium-dependent, not for endothelium-independent, in OVX rats. The treatment of genistein could significantly attenuate this abnormality (% changes of vessel diameter obtained after Ach 10(-6) M: Sham-DMSO(10-wk) = 10.96 +/- 1.2%, OVX-DMSO(10-wk) = 3.2 +/- 0.77%, OVX-genistein(10-wk) = 11.45 +/- 1.85%), (% changes of vessels diameter obtained after SNP 10(-7)M: Sham-DMSO(10-wk) = 16.05 +/- 2.82%, OVX-DMSO(10-wk) = 12.73 +/- 2.72%, OVX-genistein(10-wk) = 16.4 +/- 4.71%) (p < 0.05). However, the lipid profiles monitored from all groups of 4 and 10 weeks did not demonstrate any significant changes. Therefore, it implied that endothelial dysfunction was not primarily cause by the lipid profiles changing in ovariectomized rats. Moreover, such effects of estrogen lacking on coronary endothelial-dependent vasodilatation could be attenuated by genistein supplementation. The present findings suggest that genistein might be used as an therapeutic agent for preventing the menopausal vascular complications.

Analysis of Variance↗
PubMed2004

Beating versus arrested heart coronary revascularization: evaluation by cardiac troponin I release.

BACKGROUND: This prospective randomized study aimed to compare beating and arrested heart revascularization in patients undergoing first elective coronary artery bypass graft, with cardiac troponin I release used to evaluate myocardial injury. METHODS: Seventy patients were randomly assigned to a beating or arrested heart revascularization group. Cardiac troponin I concentrations were measured in serial venous blood samples drawn preoperatively in both groups: after aortic unclamping at 6, 9, 12, and 24 hours in the arrested heart group and after the last anastomosis at 6, 9, 12, and 24 hours in the beating heart group. Analysis of covariance with repeated measures was performed to test the effect of group and time on cardiac troponin I concentration. RESULTS: The total amount of cardiac troponin I released was higher in the arrested heart revascularization group than in the beating heart revascularization group (8.25 +/- 6.16 vs 3.18 +/- 4.75 microg, p < 0.0001). Cardiac troponin I concentrations were significantly higher in the arrested heart group at hours 6, 9, 12, and 24 than in the beating heart group (p < 0.0001). CONCLUSIONS: The lower release of cardiac troponin I in the beating heart revascularization group indicates that conventional coronary artery bypass graft with cardioplegic arrest causes more damage to the heart than off-pump myocardial revascularization.

Aged↗
PubMedDate not supplied

Metabolism and fine structure of the Mg++-procaine-arrested perfused heart.

Arrested rabbit hearts were perfused in normothermia for up to two hours by a cardioplegic erythrocyte-containing solution having an increased Mg++-, procaine-, and a reduced NaCl-content. After this time, hearts did not reveal any sign of anoxic or toxic damage in their metabolic pattern, in their ultrastructural picture, and in their functional capacity after reanimation. Despite a small loss in adenine nucleotide content, the ATP/ADP ratio and the PC content were raised. The contents of glycogen and glycolytic intermediates were normal or slightly reduced. After two hours of perfusion mitochondria showed no swelling, their membrane structure was unaltered. The myofibrils were well aggregated. The number of glycogen granules was increased. Hearts were reanimated after two hours of cardioplegia and could be loaded by pressure and volume.

Adenosine Diphosphate↗
PubMedDate not supplied

[The potentials for therapy of the postresuscitation process using regulatory peptides after 10 and 15 minutes of heart arrest].

The therapeutic effect of a single systemic injection of regulatory peptides was assessed in experiments oil white rats exposed to 10- and 15-min heart arrest. The effect of regulatory peptides was found to depend on the initial body resistance to hypoxia and on the duration of heart arrest. Positive effects of thyrotropin-releasing factor, ACTH4-10 and substance P on the recovery of cerebral function grew weaker as the duration of heart arrest increased, whereas the effects of oxitocin and somatostatin were unchanged, and that of taftsin even increased. In animals nonresistant to hypoxia cardiopulmonary resuscitation and survival of 50% of animals after 15-min heart arrest was provided by injection of thyrotropin-releasing factor at the beginning of resuscitation and of somatostatin 30 min later.

Animals↗