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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of ranitidine and cimetidine on ventricular fibrillation threshold and haemodynamics were studied in pentobarbitone-anaesthetized dogs subjected to acute coronary artery ligation. These drugs did not significantly change the ventricular fibrillation threshold nor haemodynamics before coronary artery ligation, except for remarkable haemodynamic depression by ranitidine 1 mg/kg. Ligation of the left anterior descending coronary artery reduced the ventricular fibrillation threshold, decreased systemic and left ventricular pressures and myocardial contractility, and slightly increased heart rate. Pretreatment with ranitidine 0.25 or 1 mg/kg, or with cimetidine 2 mg/kg, significantly abolished the reductions in ventricular fibrillation threshold, but did not noticeably alter the haemodynamic changes. These findings further support the hypothesis that histamine release may contribute to the increased ventricular vulnerability resulting from acute myocardial ischaemia. However, the role of histamine in the haemodynamic responses to coronary artery ligation remains obscure.
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PMID:Cardiovascular effects of ranitidine and cimetidine during acute myocardial ischaemia in anaesthetized dogs. 287 30

We developed a new method for introducing drugs into the basal cistern of rabbits. With minimal surgical invasion, we used either the opening of the craniopharyngeal duct to access the chiasmatic cistern or the suture between the basisphenoid and basioccipital bones to access the interpeduncular cistern. With our method, 0.5 ml contrast medium injected into three rabbits was determined roentgenographically to remain in the basal cistern; histologically, all the brain tissue remained intact. Intracisternal injection of 0.5 ml physiological saline into five rabbits had no effect on the cardiovascular system. In 23 rabbits, injection of 0.5 ml 0.1% prostaglandin F2 alpha led to a variety of electrocardiographic changes, including sinus bradycardia (in 43.5%), premature atrial contractions (in 17.4%), and premature ventricular contractions (in 39.1%). In 15 rabbits with severe changes, arrhythmia was followed by ST depression (in 30.4%), ST elevation (in 8.7%), T wave inversion (in 4.3%), ventricular tachycardia (in 17.4%), or ventricular fibrillation (in 4.3%). Intracisternal injection of 0.5 ml 1.0% lidocaine into the 23 rabbits was very effective in overcoming bradycardia and arrhythmias. We conclude that the clinical features of electrocardiographic changes seen in patients with subarachnoid hemorrhage are reproducible in this rabbit model.
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PMID:Model of electrocardiographic changes seen with subarachnoid hemorrhage in rabbits. 291 24

The toxicity of local anesthetic agents can be divided into two categories: (1) systemic toxic reactions due usually to an accidental intravascular injection and (2) local tissue toxicity. The systemic toxicity of local anesthetic agents is primarily characterized by CNS excitation and convulsive activity. The cardiovascular system is more resistant to the toxic actions of local anesthetics. However, local anesthetics can exert a negative chronotropic and inotropic action and cause profound peripheral vasodilation. The combination of cardiac depression and peripheral vascular dilation results in irreversible circulatory collapse. The more potent agents such as bupivacaine appear to be more cardiotoxic and may precipitate ventricular arrhythmias and ventricular fibrillation. Local tissue toxicity is rare following the administration of local anesthetics. However, large doses of chloroprocaine solutions administered intrathecally have been associated with prolonged sensory-motor deficits in a few patients due probably to the low pH and presence of sodium bisulfite in the chloroprocaine solutions. In general, local anesthetic agents are relatively safe if administered properly. However, as with any pharmacological agents, local anesthetics may cause severe toxic reactions due to the improper use of these drugs.
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PMID:Toxicity of local anesthetic agents. 317 46

The purpose of this study was to investigate the value and to identify any deleterious effects of antishock trouser use during hypothermic cardiovascular depression. Thirteen mongrels were made hypotensive by cooling to a core temperature of approximately 27 degrees C. Eight dogs had antishock trousers inflated for one hour and five dogs served as controls. Metabolic and hemodynamic variables were measured at regular intervals during cooling, during trouser inflation, and after trouser deflation. No study animal experienced ventricular fibrillation. Neither central temperature, pH, or serum potassium nor mean arterial BP or systemic vascular resistance were significantly affected by trouser inflation or deflation. Antishock trouser use during the early phase of hypothermia before rewarming does not appear to result in a central bolus of cold, acidotic, hyperkalemic blood or the precipitation of ventricular fibrillation. There appears to be no significant hemodynamic benefit of antishock trouser use early in the management of hypotension caused by moderate hypothermia.
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PMID:The effects of antishock trouser inflation during hypothermic cardiovascular depression in the canine model. 317 51

With the increasing application of arrhythmia surgery, intraoperative electrophysiological study is done frequently, although its potential to cause acute depression of cardiac function remains unresolved. This study examines the acute effects of simulated electrophysiological testing on left ventricular function. Seven dogs were anesthetized with sodium pentobarbital and instrumented for measurement of heart rate, mean aortic pressure, cardiac output (CO), and systemic vascular resistance (SVR). Systolic pressure-dimension work loops were analyzed over varying preloads. Contractility was assessed from the end-systolic pressure-dimension relationship (Ees) and from preload recruitable stroke work (PRSW). After the collection of control data, electrophysiological testing was simulated by pacing at 200 beats per minute for 30 seconds, fibrillating for 15 seconds, and finally defibrillating with a 10-J countershock. Data were recorded after 3 and 6 simulations of ventricular fibrillation (VF3, VF6). Mean heart rate and mean aortic pressure did not vary significantly during the course of the experiment. CO decreased from a control value of 2.7 +/- 0.2 L/min (+/- the standard error of the mean) to 2.0 +/- 0.1 (p less than 0.05) after VF3 and remained significantly depressed after VF6. SVR increased from a control value of 3,231 +/- 211 dyne sec cm-5 to 3,976 +/- 305 dyne sec cm-5 after VF3 (p = not significant) and increased further to 4,774 +/- 442 dyne sec cm-5 after VF6 (p less than 0.05). Neither Ees nor PRSW varied significantly even after 6 EP simulations, thereby indicating that contractility was unchanged during the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of simulated intraoperative electrophysiological testing on function of the canine left ventricle. 319 Mar 30

1. Nifedipine and DHM9 (carboxymethyl methyl 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate) were studied for their effects on arrhythmias resulting from regional myocardial ischaemia in conscious rats, and for their effects on left ventricular developed pressure in vitro. 2. Nifedipine possessed antiarrhythmic activity at a high dose of 10 mg kg-1 i.v., but not at 0.5 or 2 mg kg-1. Ventricular fibrillation (VF), tachycardia (VT), and ventricular premature beats (VPB) were all attenuated to a similar degree; nifedipine did not have a selectivity of action for high frequency arrhythmias. 3. Before coronary occlusion, the three doses of nifedipine reduced arterial blood pressure by a similar magnitude, indicating a similar (maximal) degree of systemic vasodilatation. The reductions in blood pressure were accompanied by reflex tachycardia. Heart rate and blood pressure did not correlate with the incidence or severity of arrhythmias. 4. DHM9 had no influence on arrhythmias, haemodynamic variables or the ECG, even at 20 mg kg-1 i.v. 5. Nifedipine concentration-dependently reduced contractility in perfused paced (5 Hz) rat ventricles in vitro. Raising the concentration of K+ in the perfusion fluid from 3 to 10 mequiv.l-1 increased the potency (-log10 EC50) of nifedipine up to four fold, and caused a significant depression in excitability. 6. DHM9 at up to 3 x 10(-5) M had no significant influence on ventricular contractility in vitro. 7. The results provided indirect evidence in support of the hypothesis that calcium antagonists inhibit ischaemia-induced arrhythmias by virtue of inhibition of the slow inward current (Isi) in the ischaemic ventricular myocardium.
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PMID:The mechanism of action of calcium antagonists on arrhythmias in early myocardial ischaemia: studies with nifedipine and DHM9. 320 85

1. Alternate long and short action potential durations, or electrical alternans, has only been sporadically observed in ischaemic myocardium in situ. We systematically studied alternans in the latter to characterize the phenomenon, relate it to ventricular arrhythmia and suggest possible mechanisms. 2. Sixteen Landrace pigs were anaesthetized (Azaperone, N2O and O2), ventilated and the hearts exposed. A branch of the left coronary artery was ligated. Left intraventricular and systemic pressures were monitored. Monophasic action potentials were recorded simultaneously with up to five suction electrodes in and around the proposed ischaemia area. 3. A computer measured the duration of every action potential, at several phases of repolarization, throughout the first hour of ischaemia. This allowed the systematic study of the alternans. Measurements during defined stimulus protocols were also made for the construction of electrical restitution curves. 4. Alternans was found in all recordings within the ischaemic area and in two-thirds of those in the 'border' area. There was no alternans in non-ischaemic areas. 5. The alternans, when action potential duration was plotted for every beat, appeared as an oscillation which was pleomorphic. It could be: (a) stable for hundreds of beats; (b) switched or triggered (by one extraneous beat having a different cycle length) between one stable state with high and one with low or absent alternans; (c) damped; (d) undamped to take a crescendo form, sometimes preceding ventricular fibrillation. 6. The alternans in general showed an ill-defined peak incidence between about 200 to 1500 beats after the onset of ischaemia, and a clearer late peak at about 3000 beats. These periods occurred at about 2-7 min and 15-40 min, corresponding to so-called phase 1A and 1B arrhythmia respectively. Only the late peak was seen with triggered alternans. 7. The electrical restitution curve for the action potential duration during ischaemia when compared with curves, constructed with data from non-ischaemic myocardium, showed a progressive depression in plateau, a reduction in magnitude and was flattened at 1 h. However, there was a reversal or reduction in decline at about 15-45 min. 8. We propose that electrical alternans is a distinctive electrophysiological characteristic of ischaemic myocardium which may be causally related to ventricular arrhythmia and fibrillation, and that at least two mechanisms contribute to the alternans: (i) electrical restitution of the action potential and (ii) changes in intracellular calcium cycling.
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PMID:Electrophysiological alternans and restitution during acute regional ischaemia in myocardium of anaesthetized pig. 323 41

Ventricular arrhythmias occurring consequent to regional disturbances of myocardial perfusion are the most frequent cause of sudden cardiac death. They are related to marked changes of impulse propagation in the ischemic region, which consist of circulating excitation with re-entry. Mapping of the impulse during ventricular tachycardias and ventricular fibrillation shows that the circus movements change their shape and localization from beat to beat. Zones of tissue which block the impulse during one beat may conduct the impulse at a fast rate during the next beat. The main cause underlying this behavior is the depression of the ischemic action potential. This depression is caused by the partial inactivation and the prolonged recovery of the rapid sodium inward current. In addition to the decrease in resting potential, other factors, such as acidosis, contribute to the inactivation of the inward currents generating the upstroke of the action potential. An increase of coupling resistance between myocardial cells and/or an increase of extracellular resistance appear to be less important for explaining conduction disturbances in acute ischemia.
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PMID:Conduction of the impulse in the ischemic myocardium--implications for malignant ventricular arrhythmias. 331 94

The emergency physician's disposition of patients with suspected myocardial ischemia is currently debated; some physicians believe that a subgroup of patients can be managed safely outside the coronary care unit. Clinical predictors are needed in assessing the patient with suspected myocardial ischemia to help identify this subgroup. Through a retrospective cohort study, we investigated the value of the initial emergency department ECG in discriminating between chest pain patients with low and high risk for immediately life-threatening complications. Two hundred eleven initially uncomplicated consecutive coronary care unit admissions with suspected unstable angina or myocardial infarction were studied. Patient outcome, including the incidence of myocardial infarction, complications, and mechanical and pharmacologic interventions, was reviewed. Immediately life-threatening complications included ventricular fibrillation, ventricular tachycardia, shock, 2 degrees and 3 degrees block, and death. Mechanical interventions included electrocardioversion or defibrillation, endotracheal intubation, intra-aortic balloon pump, Swan-Ganz catheter, or pacemaker insertion. Pressors, antiarrhythmics, and vasodilators were the reviewed pharmacologic interventions. A positive ECG was defined by the presence of ST elevation or depression, T wave inversion, left ventricular hypertrophy, left bundle branch block, paced rhythm, or new Q waves. All other ECG interpretations were considered negative. Patients were divided into two groups based on this initial emergency physician ECG interpretation and their complication incidences compared. Of the 211 patients, 96 had a positive ECG; 115 had negative ECGs. Patients with positive ECGs were older, had a greater history and concurrent incidence of myocardial infarction, and more complications and intensive interventions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The emergency department ECG and immediately life-threatening complications in initially uncomplicated suspected myocardial ischemia. 334 14

Out-of-hospital ventricular fibrillation (OHVF) is the most common cause of sudden cardiac death. Of 1,070 patients with OHVF who entered this study, 150 were discharged alive. Of this group, 120 were free of anoxic brain damage. Of these survivors, 67 (57%) had no previously demonstrated anginal symptoms. Treadmill stress testing revealed painless ST depression in 76% of these neurologically intact patients. Exercise ventriculography in a subset of 9 patients without angina before OHVF and in 6 patients with typical anginal symptoms revealed marked left ventricular dysfunction with ST depression in the absence of chest pain in all 15 patients. Sublingual nitroglycerin reversed this evidence of ischemia in the asymptomatic patients. Patients were followed for 6 years after discharge. No statistical difference in mortality could be demonstrated for patients who had previous anginal symptoms vs those who did not, nor was age a predictor of mortality. Women had the same risk of death as men at 2 years after OHVF, but a significantly higher risk by year 6. Myocardial infarction associated with OHVF did not predict lower mortality throughout the study.
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PMID:Six-year survival of patients with and without painless myocardial ischemia and out-of-hospital ventricular fibrillation. 335 59


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