A new technique for producing myocardial infarction using coronary artery balloon occlusion.

Many techniques for producing myocardial infarction have required the potential physiological altering effects of a thoracotomy. Previous techniques have used the variable and therefore unpredictable effects of coronary artery injection of occlusive agents, intravascular plugs, and externalized coronary balloon catheters. Previous investigators have reported a survival rate of 50-70%. In the present study a new closed chest dog technique was used in which a catheter with an inflatable detachable balloon was placed in the aorta via the carotid artery. The catheter could be readily lodged into any portion of the right, left anterior, or circumflex coronary artery. The proximal left anterior descending and circumflex arteries were occluded in 15 dogs. This new coronary artery balloon occlusion technique may be used to produce a chronic myocardial infarction with a high survival rate of 90% through the use of short acting anaesthesia and rapid reversal of the effect of morphine with naloxone hydrochloride. The rapid recovery of the dog permits earlier study of haemodynamic variables and arrhythmia due to myocardial infarction in the best physiological state.

Predictive value of the ECG in determining cardiac resuscitation outcome in a canine model of postcountershock electromechanical dissociation after prolonged ventricular fibrillation.

The purpose of our study was to determine if the surface ECG in postcountershock electromechanical dissociation (EMD) is of value in predicting return of effective myocardial contractile function during CPR. Nine dogs were subjected to five minutes of ventricular fibrillation (VF) without CPR followed by countershock and closed-chest CPR. Intravascular pressures, coronary perfusion pressure, and coronary sinus flow were measured during conventional CPR. After countershock, and before CPR, the frequencies of the following ECG variables were assessed: the presence or absence of P waves, an abnormal QRS duration (greater than 100 ms), a prolonged QTc (greater than 430 ms), and a bradyarrhythmia (QRS rate less than 60/min). Twenty-three episodes of postcountershock EMD were studied. Countershock after prolonged VF without CPR was always followed by EMD. The mean values of ECG variables were not significantly different (P greater than .05) between animals successfully resuscitated and those that were not. The sensitivity, specificity, and predictive values of individual ECG variables in estimating successful cardiac resuscitation exhibited a wide range of values. The QTc had the highest sensitivity (1.00), but the lowest specificity (0.08). The presence or absence of P waves had the highest specificity (0.62), but a sensitivity of only 0.40. QRS rate had the greatest positive predictive value (0.48) but a negative predictive value of 0.46 for successful cardiac resuscitation. The QTc had the greatest negative predictive value (1.00) but a positive predictive value of only 0.45. Multiple regression analysis using the study ECG variables as independent variables demonstrated that ECG variables were not related to outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

The pathogenesis of experimental bluetongue virus infection of calves.

Eleven seronegative calves were intravenously inoculated with bluetongue virus (BTV) serotype 10, and two calves were inoculated with a placebo. Cellular association of BTV during viremia was investigated in three of the calves by titrating virus present in plasma and different blood cell fractions at weekly intervals after infection. Viremia persisted 35 to 49 days in individual calves. Virus was transiently isolated from blood mononuclear cells and plasma collected from two of the calves but was consistently isolated from erythrocytes throughout infection of all three animals. Titers of BTV present in the erythrocyte fraction were comparable to those of the unseparated blood cell fraction. Tissue tropism of BTV was determined by viral isolation from tissues collected from calves euthanatized at 1, 2, 3, 4, 5, 7, 14, 28, 42, and 56 (2 calves) days after inoculation with BTV. Tropism was also determined by immunohistochemical staining of selected tissues with an avidin-biotin complex immunoperoxidase staining procedure using three BTV-specific monoclonal antibodies. The BTV infected calves remained healthy throughout the study. Virus was isolated from at least one tissue collected from calves euthanatized at 1 through 28 days after inoculation, but not thereafter. High titers of BTV were present in the lungs, prescapular and mesenteric lymph nodes, thymus, and spleen of calves euthanatized at 1 to 4 days after inoculation, whereas BTV was either not isolated or isolated in low titer from bone marrow collected from these animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Postcountershock pulseless rhythms: hemodynamic effects of glucagon in a canine model.

Defibrillation after prolonged ventricular fibrillation (VF) is frequently followed by asystole or electromechanical dissociation (EMD) which are usually fatal. We studied the effects of glucagon, a known inotropic and chronotropic agent, during 19 episodes of postcountershock asystole/EMD in nine dogs. Systolic and diastolic aortic (Ao), left ventricular, pulmonary arterial, and right atrial (RA) pressures were recorded as was the instantaneous Ao-RA difference (coronary perfusion pressure) and coronary sinus blood flow (CSF) during closed-chest CPR. VF was induced electrically; 2 min later, a 400-J transthoracic shock was given. Countershock was always followed by asystole (n = 12) or EMD (n = 7). Conventional closed-chest CPR with a mechanical device was begun 30 to 60 sec after countershock and continued for 2 to 3 min. If a perfusing rhythm did not occur, glucagon (1 mg) was given iv and CPR continued for 2 to 3 min more. Glucagon had no significant effect on intravascular pressures, the coronary perfusion gradient, or CSF when compared to CPR alone. However, in 14 or 19 postcountershock episodes unresponsive to CPR alone, glucagon restored effective spontaneous circulation, i.e., successful cardiac resuscitation, due to its effects on the intrinsic pacemaker discharge rate. Glucagon has been previously shown to stimulate myocardial adenyl cyclase via nonadrenergic mechanisms. We conclude that when postcountershock asystole/EMD occurs, glucagon has a direct and favorable effect on cardiac resuscitation outcome due to its effects on pacemaker discharge rate which is not mediated by changes in myocardial blood flow or coronary perfusion pressure.

Enhancement of mitochondrial oxidative phosphorylation capability by hypoperfusion in isolated perfused rat heart.

To define alterations in myocardial mitochondrial function due to hypoperfusion, oxidative phosphorylation was simultaneously studied in 17 control (stable perfusion pressure) rat hearts and 17 hypoperfused isolated rat hearts. Hypoperfusion for 30 minutes was achieved by a reduction in coronary perfusion pressure from 77.8 +/- 1.2 mm Hg (mean +/- SEM) to 20.2 +/- 1.8 mm Hg in the experimental group (control perfusion pressure after 30 minutes 75.6 +/- 1.2). Hypoperfusion caused a reduction in left ventricular developed pressure to 20.5 +/- 1.5 mm Hg (versus control 74.8 +/- 3.3, p less than 0.0001), a reduction of coronary flow rate to 4.9 +/- 0.3 ml/min (versus control 19.4 +/- 1.2, p less than 0.0001), and a drop in myocardial oxygen consumption to 0.06 +/- 0.005 ml O2/min (versus control 0.17 +/- 0.01, p less than 0.0001). Myocardial lactate production was increased by hypoperfusion (3.0 +/- 0.6 mumol/min) compared with controls (0.7 +/- 0.5, p less than 0.02), but myocardial creatine kinase release was similar in the hypoperfused and control groups. Hypoperfusion was associated with an augmentation of state 3 mitochondrial respiration with glutamate and malate as respiratory substrates (448.8 +/- 14.0 ng atoms O/min/mg mitochondrial protein versus controls 290.7 +/- 13.4, p less than 0.001). When rates were normalized for mitochondrial malate dehydrogenase (MDHm), state 3 respiration was still increased in hypoperfused hearts (24.1 +/- 2.1 ng atoms O/min/IU MDHm) compared with controls (15.5 +/- 1.6, p less than 0.02). The rates of dinitrophenol-uncoupled electron transport were similar to the rates of state 3 respiration in both the hypoperfused and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Postcountershock pulseless rhythms: response to CPR, artificial cardiac pacing, and adrenergic agonists.

Clinically, countershock of ventricular fibrillation (VF) may result in asystole or a pulseless rhythm in more than 50% of attempts. We conducted a study to assess the effects of immediate artificial pacing, CPR, and adrenergic drug therapy in the management of postcountershock pulseless rhythms. Thirty-four episodes of VF followed by countershock were studied in eight anesthetized dogs. Transducer-tipped catheters were positioned in the ascending aorta (Ao) and right atrium (RA). A bipolar pacing catheter was advanced to the apex of the right ventricle and a catheter for measurement of coronary sinus blood flow (CSQ) (continuous thermodilution technique) was positioned in the coronary sinus. VF was induced electrically and a countershock at 400 J was given two minutes later; CPR was not performed during VF episodes. Countershock was followed by asystole or a pulseless rhythm in all animals. Immediate endocardial pacing (0.1 to 5 mA) of bradyarrhythmias produced electrical capture but did not result in arterial pressure pulses in any animal. After pacing, CPR was performed for two minutes or until restoration of spontaneous circulation (ROSC). During CPR, the diastolic coronary perfusion gradient (Ao-RA) was 20 +/- 7 mm Hg (mean +/- SD) and CSQ was 14 +/- 7 mL/min/100 g (53% +/- 43% of control). ROSC followed CPR of less than two minutes duration in 24% of VF study episodes. If ROSC did not follow two minutes of CPR, 1 mg epinephrine, or 50 micrograms or 100 micrograms isoproterenol was given IV.(ABSTRACT TRUNCATED AT 250 WORDS)