| Cardiac arrest (CA) is a dangerous and common clinical situation. Though many progresses in concepts and methods of cardiopulmonary resuscitation (CPR) have been made, but the success rate remains low. Precordial compression combinated with artificial respiration and electrical defibrillation, have rescued tens of thousands of human victims. But the artery blood flow produced by precordial compression is less than 20% of normal cardiac blood flow. Moreover, it deteriorates consistently along with time. Laboratory study has found that mean arterial pressure and coronary perfusion pressure in CPR played a key role in the restoration of spontaneous circulation. In the process of CPR vasoconstrictor ( Epinephrine,Vasopressin) may increase coronary perfusion pressure, shorten the time of spontaneous circulation recovery, contributes to retrieve patient's life and improve life quality after recovery. However, in some patients with delayed CPR or cardiac arrest time more than 8 minutes, precordial compression is often inefficient, even over- dose of Vasoconstrictor is given.Heart rebeating after cardiac arrest needs oxygenated blood flow reperfusion, which may be achieved by CPR to reconstruct breathing and circulation in a short time after cardiac arrest. Artificial respiration and mechanical ventilation can reconstruct respiration. However, the blood circulation is not easy to recover. The pump function of heart reduced gradually during CPR process. It may be related with decreased myocardial compliance. This paper is aim to investigate the changes and its mechanism of myocardial contractility and compliance after cardiac arrest.Experiment is divided into three parts: (1) discussing the risk factors related to outcome of 27 rats' asphyxial cardiac arrest in order to establish stable model of cardiopulmonary resuscitation; (2) making cardiac arrest model used suffocation, observing the general change of heart during cardiac arrest, elucidating whether cardiac contracture takes place in the first six minutes of cardiac arrest; (3) researching the change and influence of CPR outcome pretreated with Diltiazem before cardiac arrest, to determine the role of L-calcium channel opening of myocardial cell in ischemic myocardial contracture .In the first part of experiments, 27 Wistar rats were enrolled. They experienced different total asphyxial time by the method of clipping trachea to asphyxia, then accepted cardiopulmonary resuscitation. The risk factors, like nonintervention interval (the interval of untreated cardiac arrest without chest compression), total asphyxial time, and so on, were tested by the methods of Binary Logistic regression analysis. It is found that nonintervention interval is the most important factor related to CPR outcome. It indicates that a stable model of cardiopulmonary resuscitation should be established according to time of nonintervention interval.In the second part of the experiments, we used suffocation to make cardiac arrest model. In the early stage of cardiac arrest, we found all the heart of rats is in rounded and full shape with fresh red color. There are still weak beating in atria and ventricle. With the extension of time, the heart volume gradually decreaded, especially for the left ventricle. The color of left ventricle changed from fresh red to pink. Right ventricle also got narrowed, but the color changed to dark red. After 4 to 6 minutes of cardiac arrest, heart surface shrinkage. Because the left ventricle and right ventricle do not contracture synchronously, the heart become distorted.By measuring the length and width of the heart of rats, we found that the length of rat heart in the initial stages of cardiac arrest is 1.747±0.010 cm, reduced to 1.418±0.061cm 6 minutes later. The width reduced from 1.324±0.021cm to 1.058±0.032 cm accordingly. By multiple comparisons, we also found that the changes of cardiac length between 4th minute and 6th minute after cardiac arrest have no significant difference (P=0.182), which suggested that the left ventricular contraction has reached the limit in the end of 4 minutes after the cardiac arrest. Thus, we concluded that 4-6minutes after the cardiac arrest, the heart of Wistar rats experienced serious ischemic myocardial contracture, excessive contraction of myocardial cells make heart look like stone. The left ventricular volume sharply reduce. In this period, the blood flow produced by closed chest compression be hampered seriously, traditional cardiopulmonary resuscitation methods can not product sufficient forward blood flow, even if Vasoconstrictor is used, there will not have satisfactory recovery outcome.The last part of the experimental study is to investigate the mechanism of myocardial overcontraction by pretreating rat with Diltiazem, a kind of myocardial cells L-calcium channel blocker, and to observe the influence on cardiopulmonary resuscitation outcome of rats. Diltiazem as a selective L-calcium channel blocker can reduce the calcium inflow into myocardial cells when cell depolarizes. During the pulseless electric activity after cardiac arrest, it can make the cells depolarized rhythmically, the L-calcium channel on the surface of cell opened, so that calcium can flow into the cell. If the L-calcium channel be blocked, the ischemic contracture of cadiocyte may be reduced consequently, the success ratio of cardiopulmonary resuscitation maybe increased. Experimental rats were divided into two groups: Diltiazem-pretreated group and physiological saline control group, eight Wistar rats used in each group. Waiting for 10 minutes after Diltiazem or physiological saline administration, cardiac arrest caused by asphyxia continued for 4 minutes before recovery, then CPR was practiced. The results shows that the rats in Diltiazem-pretreated group have no significant difference with control group in heart rate (HR) and mean arterial blood pressure (MAP) before suffocation. The outcome of CPR were absolutely different between the two groups. In Diltiazem-pretreated group, spontaneous circulation of 8 rats were restored, and survived over 24 hours; in the control group only 3 rats restored spontaneous circulation, 2 rats survived over 24 hours. Restoration rate of spontaneous circulation and 24-hour survival rate have significant differences between the two group: P=0.007 and P=0.002. The results suggest that Diltiazem may reduce the amount of calcium inflow to myocardial cells during cardiac arrest, improved myocardial compliance, and weakened ischemic myocardial contracture. It indicate that the reduction of pump function after cardiac arrest is related to myocardial overcontraction induced by intracellular calcium overload during CPR.
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