Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that during cardiopulmonary resuscitation, chest compression with an unobstructed trachea raises and maintains intrathoracic pressure by collapsing airways and trapping air in the lung, we studied 11 dogs (20-32 kg). An inflatable vest compressed the thorax after induction of ventricular fibrillation. First, tracheal airflow was measured by a pneumotachometer during vest inflation and deflation in nine of the dogs. As expected, during the initial phase of vest inflation of cycles after ventilation, air moved out of the lungs, but then airflow stopped. After vest deflation, however, more air moved out of the lungs in eight of the nine dogs; this occurrence indicated that a portion of the inspired tidal volume was trapped during vest inflation. During cycles without prior ventilation, the amount of air expired by chest compression decreased, paradoxically, at higher peak vest pressure (p less than 0.002); this occurrence indicated that air was trapped at the higher vest pressures. The change in right atrial pressure was higher on cycles after ventilation than on cycles without prior ventilation (79 +/- 12 vs. 67 +/- 12 mm Hg [mean +/- SEM], p less than 0.005), and lung volume was higher on cycles after ventilation (p less than 0.001). Next, a 5-Fr micromanometer was advanced down the airway in eight of the dogs. With the tip of the micromanometer 5-8 cm distal to the carina, a zone of high pressure was noted in seven dogs; this high pressure suggested a zone of airway collapse distal to the carina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Air trapping in the lungs during cardiopulmonary resuscitation in dogs. A mechanism for generating changes in intrathoracic pressure. 279 Dec 29

To study the time course of spontaneous and induced ventricular arrhythmias after myocardial infarction (MI), 20 dogs underwent ligation of the left anterior descending coronary artery and temporary occlusion and reperfusion of the obtuse marginal branch. There were 5 early deaths (less than 24 hours) due to spontaneous ventricular fibrillation (VF). All 15 survivors exhibited spontaneous ventricular tachycardia (VT) up to day 3 with the shortest cycle length occurring at 17 hours after MI (232 +/- 11 msec: mean +/- SEM). The grade of arrhythmia complexity was decreased after day 4 compared to day 1 (p = 0.049), and the number of ventricular premature complexes was reduced after day 6 (1700 +/- 1390/hour) compared to day 1 (9500 +/- 640/hour, p = 0.042). Serial electrophysiologic studies were carried out on days 8, 15, 22, and 29 via an implanted antitachycardia pacemaker using 1 to 3 extrastimuli and rapid ventricular pacing (RVP). On day 8, VT was inducible in 7 dogs (46%), VF in 4 (27%), and 4 dogs (27%) exhibited a negative response. On day 15, 3 more dogs became negative, and all previously negative dogs displayed negative responses. From day 15, the inducibility of VT/VF remained "constant" using RVP. However, inducibility by triple extrastimuli declined week by week until day 29. Stepwise logistic regression analysis of 20 variables selected the mass of the MI as the only independent predictor of inducible VT/VF by multiple extrastimuli and RVP after day 15 (p = 0.049). Thus significant time- and mode-dependent changes in inducibility of VT/VF occur during the early phase after MI.
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PMID:Serial analysis of spontaneous and induced ventricular arrhythmias in a canine model of myocardial infarction. 318 54

The oxygen free radical-induced lipid peroxidative reactions that occur during resuscitation from normothermic cardiac arrest may contribute to the degree of neurologic dysfunction sustained. A blinded, randomized experimental trial was performed to determine whether U74006F, a potent inhibitor of lipid peroxidation, reduces morbidity and 24-hour mortality after 10 minutes of normothermic cardiopulmonary arrest; ventricular fibrillation was induced by electrical stimulation in 24 open-chest, halothane-anesthetized dogs, and circulation was reestablished by direct cardiac compressions, administration of a standardized drug regime, and internal countershocks. When spontaneous circulation was restored, a bolus injection of 1.5 mg/kg U74006F (n = 12) or 25 mM citrate vehicle (n = 12) was infused intravenously in 15 minutes and an infusion was continued at 0.125 mg/kg/hr for the next 12 hours. In the drug-treated group, plasma U74006F concentration averaged 0.13 microgram/ml between 3 and 12 hours after cardiac arrest. By 24 hours after arrest, 10 of 12 (83%) vehicle-treated dogs had died but only four of 12 (33%) U74006F-treated dogs had died (p = 0.017). U74006F-treated dogs survived significantly longer (mean +/- SEM 22 +/- 1 hr) than vehicle-treated dogs (18 +/- 1 hr), with significantly better neurologic function 1, 2, and 24 hours after arrest. Plasma fatty acid hydroperoxide concentrations 12 hours after arrest were 88 +/- 81 pmol/ml in U74006F-treated and 241 +/- 49 pmol/ml in vehicle-treated dogs (p less than 0.05). Vitamin E concentrations were significantly higher in the plasma of U74006F-treated dogs 2, 3, and 6 hours after arrest compared with vehicle-treated dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of the aminosteroid U74006F after cardiopulmonary arrest in dogs. 318 22

Streptozotocin induced diabetic rat hearts were perfused under constant flow conditions with or without 1 x 10(5) U.litre-1 each of superoxide dismutase and catalase (SOD + CAT). Total global ischaemia was produced for 20 min followed by 30 min of reperfusion at pre-ischaemic flow rates. After 5 min of reperfusion, isovolumic LV developed pressure was reduced in diabetic hearts, at 22 (SEM 11)% of baseline v 67(12)% in controls, with increased frequency of ventricular fibrillation (VF) (3/10 v 10/11 hearts). SOD + CAT improved isovolumic LV developed pressure to 67(8)% of baseline during early reperfusion of diabetic hearts but did not affect non-diabetic hearts. SOD + CAT also increased the adenylate energy charge potential in post-ischaemic diabetic hearts to 0.826(0.011) v 0.781(0.012) in diabetic controls, and reduced the incidence and duration of reperfusion induced VF in diabetic hearts. SOD + CAT augmented the production of prostacyclin in coronary effluents during early reperfusion of diabetic hearts, from (baseline) 11.5(1.7) to 18.1(3.0) ng.min-1.g-1 at 2 min, compared with 11.1(1.6) to 12.5(1.9) ng.min-1.g-1 at same interval in diabetic controls. Indomethacin prevented the protective effect of the free radical scavengers on function and VF. In contrast, perfusion with the prostacyclin analogue, iloprost (3 x 10(-8) M), alone completely prevented early post-ischaemic dysfunction and reduced VF from 559(172) to 16(8) s. Oxygen derived free radicals may mediate reperfusion induced contractile dysfunction and VF in acutely diabetic hearts following brief episodes of myocardial ischaemia. The beneficial effects of SOD + CAT appear to be mediated mainly by an increase in prostacyclin production during early reperfusion.
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PMID:Superoxide dismutase plus catalase improves post-ischaemic recovery in the diabetic heart. 325 31

The effects of three anesthetic agents on the inducibility of ventricular tachycardia by programmed stimulation were investigated in dogs with a surgically induced left ventricular infarct. Endocardial catheter electrodes were placed at the right ventricular apex under general anesthesia at least 2 weeks after infarction, and the dogs were allowed to recover for 24 hours before undergoing programmed stimulation in the conscious state on two occasions 2 hours apart. A protocol of programmed stimulation with up to seven ventricular extrastimuli was used. In 15 animals, ventricular tachycardia was inducible on both occasions with 3.4 +/- 0.4 (mean +/- SEM; range, 1-5) extrastimuli. Two hours after baseline conscious induction, the dogs were anesthetized with either halothane, pentobarbital, or a fixed combination of fentanyl-droperidol plus nitrous oxide. Halothane prolonged the PR interval from 99 +/- 4 to 117 +/- 6 msec (p = 0.001) and the ventricular effective refractory period from 140 +/- 4 to 157 +/- 6 msec (p = 0.008). The ability to induce ventricular tachycardia was abolished in five of 10 animals (p less than 0.05). In the animals that remained inducible, the cycle length of tachycardia increased from 153 +/- 10 to 168 +/- 10 msec (p = 0.015), while the number of extrastimuli required was unaltered. Pentobarbital prolonged the PR interval from 104 +/- 6 to 124 +/- 6 msec (p = 0.004) and the QTc interval from 270 +/- 10 to 310 +/- 6 msec (p = 0.006). Ventricular tachycardia remained inducible in only six of 10 dogs (p less than 0.05) with no change in cycle length or the number of extrastimuli required. Ventricular fibrillation was inducible in an additional three dogs with a number of extrastimuli similar to that required to induce ventricular tachycardia before anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of effects of three anesthetic agents on induction of ventricular tachycardia in a canine model of myocardial infarction. 338 5

This study was performed to assess the role of cardiac sympathetic nerves in the in vivo antifibrillatory action of bretylium using the technique of electrically induced ventricular fibrillation. An initial study determined that 3 mg/kg of nortriptyline, an adrenergic amine uptake inhibitor, was sufficient to prevent the adrenergic neuron blockade produced by 5 mg/kg of bretylium in pentobarbital anesthetized dogs. Electrical ventricular fibrillation threshold (VFT) was then determined in two groups of pentobarbital anesthetized dogs using gated trains of increasing current applied to the epicardial surface of the right ventricle during atrial pacing. After determination of an initial VFT in both groups, one group of dogs (n = 8) received 3 mg/kg nortriptyline, the other group received saline (n = 9). The VFT was redetermined in both groups, after which all dogs received 5 mg/kg of bretylium, intravenously, and VFT was then measured at 15 and 90 min after bretylium. In saline-treated dogs, bretylium produced a significant increase in VFT from a control value of 6.9 +/- 1.6 mA (mean +/- SEM) to 31.0 +/- 0.5 mA at 15 min (p less than 0.05) and 45.1 +/- 4.8 mA at 90 min (p less than 0.05). In nortriptyline-treated dogs, however, nortriptyline itself produced an increase in VFT which was reversed by bretylium, and VFT after bretylium was not significantly elevated until 90 min to a value of 25.2 +/- 9.6 mA (control: 5.2 +/- 0.9 mA). These data demonstrate that pretreatment with nortriptyline attenuates and delays the onset of the acute antifibrillatory effect of bretylium and suggests a role for the cardiac adrenergic neuron as a potential target for part of the beneficial effects to be derived from antifibrillatory drugs.
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PMID:Antifibrillatory action of bretylium: role of the sympathetic nervous system. 357 13

The effects of lipoxygenase enzyme inhibitor nafazatrom on infarct size, haemodynamics, and prostanoid release was studied in a canine occlusion-reperfusion model of ischaemic myocardial injury. Treatment was with 10 mg/kg nafazatrom i.d., starting before coronary occlusion, 2 h and 6 h thereafter, and was repeated in 6 h intervals. The left anterior descending (LAD) coronary artery was occluded for 6 h and reperfused for 42 h. Infarct size and anatomic area dependent on the occluded LAD were determined post mortem by the tetrazolium staining technique. Nafazatrom significantly reduced the extent of irreversible myocardial ischaemic damage whether it was expressed as g/100 g left ventricle (24 +/- 4 vs. 46 +/- 6 in controls; p less than 0.01; mean +/- SEM) or as percentage of LAD risk region for infarcting (38 +/- 8 vs. 65 +/- 7% in controls; p less than 0.05). Nafazatrom did not affect peripheral haemodynamics but during drug vehicle treatment and LAD occlusion systemic blood pressure, left ventricular pressure and dP/dtmax decreased while filling pressure, heart rate, and the S-T segments of the ECG increased. The incidence of ventricular fibrillation was 8% during drug treatment and coronary ligature vs. 25% in controls (n.s.). During reperfusion, nafazatrom reduced the incidence of ventricular premature contractions and tachycardia. Ex vivo platelet aggregation in response to collagen was not inhibited by nafazatrom. Prostanoid release (thromboxane B2 and 6-keto-prostaglandin F1 alpha as breakdown products of thromboxane A2 and prostacyclin, respectively) remained unaltered in vehicle controls but nafazatrom treatment elevated prostacyclin release significantly at 4 and 5 h during LAD occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of nafazatrom in an acute occlusion-reperfusion model of canine myocardial injury. 384 82

Closed-chest cardiopulmonary resuscitation (CPR) produces only small pressure differences across the coronary circulation and relatively little coronary blood flow in dogs with ventricular fibrillation. To determine whether coronary flow during experimental resuscitation is sufficient to maintain aerobic myocardial metabolism, we measured left ventricular adenosine triphosphate (ATP) and lactate concentrations before and immediately after a 20 min period of CPR in six fibrillating dogs. The mean aortic-right atrial pressure difference generated during CPR averaged 5.4 +/- 2.6 mmHg (SEM) and 3.2 +/- 2.6 mmHg at the beginning and end of the 20 min period, respectively. Left ventricular myocardial blood flow (measured with radioactive microspheres) averaged 16.7 +/- 5.7% of prearrest values during the first 10 min of CPR, and 8.5 +/- 4.8% of prearrest values during the second 10 min of CPR. Biopsies after CPR contained less ATP (3.3 +/- 0.1 vs 4.7 +/- 0.5 nmol.mg-1, p less than 0.05) and more than seven times more lactate (14.7 +/- 3.1 vs 1.9 +/- 0.2 nmol.mg-1, p less than 0.01) than control biopsies. We conclude that coronary blood flow during CPR is inadequate relative to myocardial oxygen demands during ventricular fibrillation in dogs. The techniques developed in this study provide a potential means of assessing the effects of experimental interventions on myocardial oxygenation during CPR.
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PMID:Metabolic evidence of inadequate coronary blood flow during closed-chest resuscitation in dogs. 401 18

The effects of prostacyclin (PGI2) on ventricular arrhythmias following 20 min of coronary occlusion and release were studied in 34 conscious dogs. We administered PGI2 at 100 ng/kg/min and did not observe significant changes in heart rate, blood pressure, or systemic vascular resistance. During the control period, heart rate was 97 +/- 30 (mean +/- SEM) vs. 99 +/- 28 in the PGI2-treated group. Mean arterial pressure was 115 +/- 26 mm Hg and 109 +/- 10 mm Hg in the control and PGI2 groups, respectively. Systemic vascular resistance declined minimally from 2,985 +/- 221 dyn . s . cm-5 to 2,484 +/- 135 dyn . s . cm-5 during the PGI2 infusion (p = NS). Following coronary occlusion, the frequency of ventricular fibrillation was reduced from 53% (9/17) in the control group to 6% (1/17) in the PGI2 group (p less than 0.01). Overall 80-min postinfarction survival was 64% in the group receiving PGI2 infusion compared to 24% in the control group (p less than 0.05). The effects of PGI2 in preventing ventricular fibrillation following acute coronary occlusion can be ascribed to a direct action of this prostaglandin on the myocardium, rather than to an indirect effect due to a reduction in systemic vascular resistance.
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PMID:Administration of prostacyclin prevents ventricular fibrillation following coronary occlusion in conscious dogs. 618 7

In anesthetized dogs, a silver wire electrode was inserted into the lumen of the circumflex coronary artery (LCX) and myocardial infarction was produced by a temporary 90-minute occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion. Four days later while in the ambulatory state, a 150 microA current was applied to the intimal surface of the LCX of saline (n = 10) and bretylium (n = 10) treated animals. Intimal injury and coronary thrombosis produced ST segment changes at 138 +/- 39 minutes (chi +/- SEM), followed by premature ventricular beats (at 142 +/- 37 minutes), ventricular tachycardia (at 156 +/- 49 minutes), and ventricular fibrillation (at 163 +/- 51 minutes) in 9 of 10 saline-treated animals. In bretylium-treated animals, ST segment changes appeared at 128 +/- 35 minutes, with six animals surviving for 24 hours (p less than 0.03 vs saline). LAD infarction was present in both saline (14.1 +/- 2.3%) and bretylium (15.1 +/- 2.1% of left ventricle) treated animals with only bretylium-treated animals developing LCX infarcts (16.1 +/- 2.1%). Bretylium prevents ventricular fibrillation (VF) resulting from ischemia at a site distant to prior myocardial infarction in the conscious dog and deserves further attention as a potential antifibrillatory agent for prevention of sudden coronary death in man.
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PMID:Prevention of ventricular fibrillation by bretylium in a conscious canine model of sudden coronary death. 684 13


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