BACKGROUND: In cardiac surgery, hypothermia is associated with a number of major disadvantage, including its detrimental effects on enzymatic function, energy generation and cellular integrity. Warm cardioplegia with normothermic cardiopulmonary bypass cause three times more incidence of permanent neurologic deficits than the cold crystalloid cardioplegia with hypothermic cardiopulmonary bypass. Interruptions or inadequate distribution of warm cardioplegia may induce anaerobic metabolism and warm ischemic injury. To avoid these problems, tepid blood cardioplegia was recently introduced. MATERIAL AND METHOD: To evaluate whether continuous tepid blood cardioplegia is beneficial in clinical practice during valvular surgery, we studied two groups of patients matched by numbers and clinical characteristics. Warm group(37degree C) consisted of 18 patients who underwent valvular surgery with continuous warm blood cardioplegia. Tepid group(32degree C) consisted of 17 patients who underwent valvular surgery with continuous tepid blood cardioplegia. RESULT: Heartbeat in 100% of the patients receiving continuous warm blood cardioplegia and 88.2% of the patients receiving continuous tepid blood cardioplegia converted to normal sinus rhythm spontaneously after removal of the aortic cross clamp. There were no differences between these two groups in CPB time, ACC time, the amount of crystalloid cardioplegia used and peak level of potassium. During the operation, the total amount of urine output was more in the warm group than the tepid group(2372+/-243 ml versus 1535+/-130 ml, p<0.01). There were no differences between the two groups in troponin T level measured 1hr and 12hrs after the operation. CONCLUSION: Continuous tepid blood cardioplegia is as safe and effective as continuous warm blood cardioplegia undergoing cardiac valve surgery in myocardial protection.
Cardiopulmonary Bypass ; Heart Arrest ; Heart Arrest, Induced* ; Heart Valves ; Heart* ; Humans ; Hypothermia ; Incidence ; Metabolism ; Neurologic Manifestations ; Potassium ; Thoracic Surgery* ; Troponin T

Cytosolic Ca2+ concentration of rat ventricular cells was measured under varying experimental conditions by using a fluorescent Ca2+ indicator, Fura-2. Resting [Ca2+]i of rat myocyte was 150 +/- 30 nM (n = 39), and this value was compatible with others. The Perfusion of cardioplegic solution significantly increased [Ca2+]i, and this effect was further augmented by hypothermia (p<0.05). Application of nifedipine (5 x 10(-7) M) to the perfusate or pretreatment of caffeine (10 mM) had no apparent effect on this cardioplegia-induced [Ca2+]i change. But Ni2+ (5 mM), an antagonist of Na+/Ca2+ exchange mechanism, prevented the [Ca2+]i change during cardioplegia (p<0.05). Magnitude of cardioplegia-induced [Ca2+]i increase was also dependent on the Ca2+ concentration of cardioplegic solution. These results suggest that Na+/Ca2+ exchange may play an important role in cardioplegia-induced [Ca2+]i change. To rule out the possibility whether the protective effect of hypothermic cardioplegia is due to the preservation of high-energy phosphate store or decreasing the transmembrane ionic fluxes by phase transition, we exhausted a energy store of cardiac cell by application of 2,4 dinitrophenol to the bath and measured its effect on [Ca2+]i change during cardioplegia. Hypothermic cardioplegia delayed the onset of [Ca2+]i increase and decreased its amplitude compared to those of normothermic cardioplegia. From the above results, hypothermic cardioplegia may protect the cardiac cells from ischemic insult by preserving a high-energy phosphate store. Application of Ni2+ to the cardioplegic solution or reduction of external Ca2+ concentration also had some protective effect, since it prevented [Ca2+]i increase during cardioplegia.
Animal ; Calcium/*metabolism ; Cytosol/metabolism ; *Heart Arrest, Induced ; Heart Ventricle/metabolism ; Hypothermia, Induced ; Myocardial Ischemia/metabolism/*prevention & control ; Myocardium/*metabolism ; Rats ; Support, Non-U.S. Gov't

OBJECTIVETo study the effects of cold autoblood cardioplegia on oxygen free radicals in the myocardium in infants who underwent cardiopulmonary bypass and to explore the possible mechanism of myocardial protection of autoblood cardioplegia.

METHODSThirty infants with acyanotic congenital heat disease (CHD) (weight< or =8 kg) were randomized to receive cold crystalloid, cold blood or cold autoblood cardioplegia (n=10 each group) during cardiopulmonary bypass. The biopsy samples were taken from the right atrium just before heart arrest and after heart self-recovery for the measurement of malonaldehyde (MDA) and superoxide dismutase (SOD) contents. The time and the rate of the heart self-recovery to sinus rhythm, and the incidence of ventricular fibrillation were recorded during operation. The cardiac index (CI) and the dependence of positive inotropic drugs were monitored after operation.

RESULTSBefore the operation, there were no significant differences in myocardial MDA (0.87+/-0.14, 0.88+/-0.11 and 0.86+/-0.15 nmol/mg prot, respectively) and SOD contents (61.3+/-3.4, 69.2+/-3.1 and 64.4+/-4.2 U/g, respectively) among the crystalloid, the blood and the autoblood cardioplegia groups. After operation, the myocardial MDA content increased (3.12+/-0.21, 2.93+/-0.27 and 1.67+/-0.15 nmol/mg prot, respectively) and SOD content (42.6+/-2.3, 44.6+/-3.1 and 57.7+/-2.1 U/g, respectively) decreased significantly in the three groups (P<0.05 or 0.01). The autoblood cardioplegia group had lower myocardial MDA content and higher SOD content than the crystalloid and the blood cardioplegia groups (P<0.05). The time of heart self-recovery was shortened and the dependence of positive inotropic drugs were reduced in the autoblood cardioplegia group compared with the crystalloid and the blood cardioplegia groups (P<0.05). Post-operational CI in the autoblood cardioplegia group was significantly higher than that in the blood and the crystalloid cardioplegia groups. There were significant differences in the time of heart self-recovery, the dependence of positive inotropic drugs and the CI between the blood and the crystalloid cardioplegia groups (P<0.05 or 0.01).

CONCLUSIONSCold autoblood cardioplegia reduces oxygen free radicals in the myocardium, thus providing myocardial protections in infants undergoing cardiopulmonary bypass.

Cardiopulmonary Bypass ; Female ; Heart Arrest, Induced ; Heart Defects, Congenital ; surgery ; Humans ; Infant ; Male ; Malondialdehyde ; analysis ; Potassium Compounds ; Superoxide Dismutase ; metabolism

To investigate the changes of myocardial glucose metabolism in rabbit cardiac arrest models and the effect of hydrogen intervention by 18F-fluroro-2-deoxyglucose (18F-FDG) positron emission tomography (PET) imaging.
 Methods: Fifteen male New Zealand white rabbits were randomly divided into a hydrogen group (n=6), a control group (n=6) and a sham group (n=3). Cardiac arrest (CA) was induced by intravenous injection of potassium chloride. Conventional cardiopulmonary resuscitation (CPR) was initiated after five-minutes CA. The hydrogen group and the control group were mechanically ventilated into mixed gas with 4% hydrogen+96% oxygen and pure oxygen, respectively, for 30 minutes after CPR. Rats in the sham group was performed the same surgical procedure and was injected adrenaline and potassium chloride but did not induce CA. The vital signs at basic state and 30 min after return of spontaneous circulation (ROSC) were recorded in each group. The parameters of CPR were recorded in two CA groups. Myocardial glucose metabolism was assessed by positron emission tomography (PET) at basic state, 2 h and 24 h after ROSC. The maximum standardized uptake value (SUVmax) of 18F-FDG was measured.
 Results: There were no significant differences in the basal body weight and vital signs among the three groups. There was no significant difference in the blood glucose level before PET examination. The 18F-FDG SUVmax in the sham group at three time points was not significantly changed. In the hydrogen group and the control group, the 18F-FDG SUVmax at 2 h after ROSC were significantly higher than the basic level (1.89±0.47 vs 3.47±1.24 and 1.90±0.36 vs 4.26±0.80, respectively). Compared with the control group, the 18F-FDG SUVmax in the hydrogen group was lower at the point at 2 h after ROSC. The 18F-FDG SUVmax in the 2 CA group were down to the basic level at 24 h after ROSC (hydrogen group 2.02±0.64, control group 2.07±0.61).
 Conclusion: Myocardial glucose metabolism in CA rabbits was increased significantly after ROSC, and hydrogen intervention can reduce the degree of glucose metabolism.
Animals ; Cardiopulmonary Resuscitation ; Glucose ; metabolism ; Heart Arrest ; physiopathology ; surgery ; Male ; Myocardium ; metabolism ; Positron-Emission Tomography ; Rabbits ; Random Allocation ; Rats

This study investigated the feasibility and effects of organ bath to be used for detection of bronchial function of non-heart-beating donor (NHBD) lung after 1-h warm ischemia. Sixteen Swedish pigs were divided into two groups randomly: heart-beating donor (HBD) group and NHBD with 1-h warm ischemia (NHBD-1 h) group. The bronchial rings whose lengths and inner diameters were both 1.5 mm were obtained from isolated left lungs of all the pigs. Acetylcholine, arachidonic acid natrium and papaverine were used to test and compare the contractile and relaxant function of bronchial smooth muscles and epithelium-dependent relaxation (EpiDR) response between HBD and NHBD-1 h groups. The results showed that there was no significant difference in the values of bronchial precontraction between HBD and NHBD-1 h groups (5.18+/-0.07 vs 5.10+/-0.11 mN, P>0.05). No significant difference in the values of EpiDR responses between HBD and NHBD-1 h groups (1.26+/-0.05 vs 1.23+/-0.07 mN, P>0.05) was observed either. During the process of EpiDR induction, the rings had no spontaneous relaxation in two groups. In addition, papaverine solution completely relaxed the bronchial smooth muscles of all bronchial rings. It was concluded that after warm ischemia for 1 h, the contractile and relaxant abilities of bronchial smooth muscles, and the epithelium-dependent adjustment both kept intact. Organ bath model could be a liable and scientific way to evaluate the bronchial function of NHBD lung.
Biological Factors/metabolism ; Bronchi/metabolism ; Bronchi/*physiology ; Heart Arrest/*metabolism ; Heart Arrest/physiopathology ; Lung Transplantation ; Models, Biological ; Muscle Relaxation/physiology ; Organ Preservation/*methods ; Random Allocation ; Reperfusion Injury/prevention & control ; Swine ; Tissue and Organ Procurement ; Warm Ischemia/*methods

Cardiac dysfunctions such as myocardial functional failure and ventricular arrhythmia have been largely attributed to intracellular Ca2+ overload. One of the mechanisms of intracellular Ca2+ overload involves a rapid influx of Ca2+ via Na(+)-Ca2+ exchange during the reperfusion which utilizes the accumulation of Na+ in myocytes during ischemic cardiac arrest. Possible sources of the intracellular Na+ accumulation include Na+ channel, Na(+)-H+ exchange, Na(+)-Ca2+ exchange, and Na+ background current. In this study, we studied the role of the Na+ background current in intracellular Na+ accumulation during the cardiac arrest by measuring the Na+ background current in guinea pig ventricular myocytes with whole cell clamp method and evaluating the effects of cardioprotective drugs on the Na+ background current. The results were as follows: (1) The Na+ background inward current at -40 mV membrane potential was larger at Ca2+ free solution than 1.8 mM Ca2+ solution. (2) The Na+ background current was not affected by verapamil. (3) 2 microM O-(N, N-hexamethylene)-amiloride (HMA) decreased the Na+ background current at negative membrane potential. (4) The new cardioprotective drug, R 56865, decreased the Na+ background current. These results suggest that the Na+ background current plays a role in increasing the intracellular Na+ activity during high K+ cardioplegia and the blocking effect of myoprotective drugs, such as R 56865, on the Na+ background current may contribute to myocardial protection after cardioplegia.
Amiloride/pharmacology ; Animal ; Guinea Pigs ; Heart/*drug effects ; Heart Arrest, Induced ; Myocardium/metabolism ; Piperidines/pharmacology ; Potassium/pharmacology ; Sodium/*metabolism ; Support, Non-U.S. Gov't ; Thiazoles/pharmacology ; Verapamil/pharmacology

It is important that the clinical anesthetist pay attention to the interaction of anesthetic induction agents and succinylcholine chloride(S,C,C) on the elctrolyte level especially the plasma potassium ion concentration. For instance succinylcholine chloride has a marked effect upon specific conditions such as severe burns, multiple injury, deabetes insipidus and myopathy. Also secondary plasma changes may bring about non synchronous depolarizing action on the muscle and cause cardiac arrhythmai and even cardiac arrest by the increase of potassium concentration in the plasma. With this in mind the author has randomly selected 30 patients who belong to class l physical status by the classification of the American Society of Anesthesiologist had no abnormal symptoms in respiration, circulation or endocrine and metabolism defects. This paper covers the period from the 10th of April 1979 to the 10th of May 1980 in the Department of Anesthesiology, Hanyang University Hospital. The 30 subjects were divided into 3 groups: a) propanidid with S.C.C. b) thiopental sodium with S.C.C. c) diazepam with S.C.C. The plasma concentration of potassium, sodium and calcium were observed and compared in the pre-induction (control group) and two minute post-induction(study group). The results are follows: 1) The plasma potassium ion concentration showed no any significant changes in the whole group. 2) The plasma sodium and calcium ion concentration also showed no any significant changes in the whole group.
Anesthesiology ; Burns ; Calcium* ; Classification ; Diazepam ; Heart Arrest ; Humans ; Metabolism ; Multiple Trauma ; Muscular Diseases ; Plasma ; Potassium ; Propanidid ; Respiration ; Sodium* ; Succinylcholine* ; Thiopental

Phosphate is essential in regulating human metabolic processes, and severe hypophosphatemia can induce neurologic and hematological complications and result in respiratory failure and cardiac dysfunction. Therefore, correction of severe hypophosphatemia can be pivotal in the management of diabetic ketoacidosis (DKA). We report the case of a 14-year-old female who was diagnosed with type 1 diabetes and referred to our institute for treatment of DKA. Although the patient received fluid and continuous insulin administration according to the current DKA treatment protocol, generalized tonic seizures and cardiac arrest developed. After cardiopulmonary resuscitation, the patient recovered and was stable. Within 16 hours after DKA treatment, the patient developed respiratory failure with severe hypophosphatemia that required mechanical ventilation. Concurrent neurologic evaluation revealed no specific abnormalities. The patient recovered without any complications after correcting the hypophosphatemia. We suggest vigilant monitoring of the phosphate level in DKA patients and active replacement when required.
Adolescent ; Cardiopulmonary Resuscitation ; Clinical Protocols ; Diabetic Ketoacidosis* ; Female ; Heart Arrest ; Humans ; Hypophosphatemia* ; Insulin ; Metabolism ; Respiration, Artificial ; Respiratory Insufficiency* ; Seizures

OBJECTIVETo study the application of positron emission tomography (PET) in detection of myocardial metabolism in pig ventricular fibrillation and asphyxiation cardiac arrest models after resuscitation.

METHODSThirty-two healthy miniature pigs were randomized into a ventricular fibrillation cardiac arrest (VFCA) group (n=16) and an asphyxiation cardiac arrest (ACA) group (n=16). Cardiac arrest (CA) was induced by programmed electric stimulation or endotracheal tube clamping followed by cardiopulmonary resuscitation (CPR) and defibrillation. At four hours and 24 h after spontaneous circulation was achieved, myocardial metabolism was assessed by PET. 18F-FDG myocardial uptake in PET was analyzed and the maximum standardized uptake value (SUVmax) was measured.

RESULTSSpontaneous circulation was 100% and 62.5% in VFCA group and ACA group, respectively. PET demonstrated that the myocardial metabolism injuries was more severe and widespread after ACA than after VFCA. The SUVmax was higher in VFCA group than in ACA group (P<0.01). In VFCA group, SUVmax at 24 h after spontaneous circulation increased to the level of baseline.

CONCLUSIONACA causes more severe cardiac metabolism injuries than VFCA. Myocardial dysfunction is associated with less successful resuscitation. Myocardial stunning does occur with VFCA but not with ACA.

Animals ; Asphyxia ; physiopathology ; Cardiopulmonary Resuscitation ; Gene Expression Regulation ; Heart Arrest ; etiology ; metabolism ; therapy ; Myocardium ; metabolism ; Positron-Emission Tomography ; methods ; Random Allocation ; Swine ; Ventricular Fibrillation ; metabolism

BACKGROUNDMorbidity and mortality after resuscitation largely depend on the recovery of brain function. Ventricular fibrillation cardiac arrest (VFCA) and asphyxial cardiac arrest (ACA) are the two most prevalent causes of sudden cardiac death. Up to now, most studies have focused on VFCA. However, results from the two models have been largely variable. So, it is necessary to characterize the features of postresuscitation cerebral metabolism of both models.

METHODSForty-four Wuzhishan miniature inbred pigs were randomly divided into three groups: 18 for VFCA group, ACA group, respectively, and other 8 for sham-operated group (SHAM). VFCA was induced by programmed electric stimulation, and ACA was induced by endotracheal tube clamping. After 8 min without treatment, standard cardiopulmonary resuscitation (CPR) was initiated. Following neurological deficit scores (NDS) were evaluated at 24 h after achievement of spontaneous circulation, cerebral metabolism showed as the maximum standardized uptake value (SUVmax) was measured by 18 F-fluorodeoxyglucose positron emission tomography/computed tomography. Levels of serum markers of brain injury, neuron specific enolase (NSE), and S100β were quantified with an enzyme-linked immunosorbent assay.

RESULTSCompared with VFCA group, fewer ACA animals achieved restoration of spontaneous circulation (61.1% vs. 94.4%, P < 0.01) and survived 24-h after resuscitation (38.9% vs. 77.8%, P < 0.01) with worse neurological outcome (NDS: 244.3 ± 15.3 vs. 168.8 ± 9.71, P < 0.01). The CPR duration of ACA group was longer than that of VFCA group (8.1 ± 1.2 min vs. 4.5 ± 1.1 min, P < 0.01). Cerebral energy metabolism showed as SUVmax in ACA was lower than in VFCA (P < 0.05 or P < 0.01). Higher serum biomarkers of brain damage (NSE, S100β) were found in ACA than VFCA after resuscitation (P < 0.01).

CONCLUSIONSCompared with VFCA, ACA causes more severe cerebral metabolism injuries with less successful resuscitation and worse neurological outcome.

Animals ; Asphyxia ; complications ; physiopathology ; Brain ; metabolism ; Cardiopulmonary Resuscitation ; Heart Arrest ; metabolism ; pathology ; therapy ; Positron-Emission Tomography ; Swine ; Ventricular Fibrillation ; metabolism ; pathology ; therapy