Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathodynamics of lethal intoxication in rats and mice by i.v. administration of enterotoxin of Clostridium perfringens type A was studied using whole animals and isolated organs. A lethal i.v. dose (50 micrograms/kg) of enterotoxin killed anesthetized rats and mice within 4-15 min. Rapid changes of ECG pattern suggestive of hyperpotassemia, rapid fall of blood pressure and transient hyperpnea followed by respiratory depression were observed. Analysis of plasma levels of cations revealed hyperpotassemia in both animal species. On the other hand, enterotoxin (up to 100 micrograms) showed little direct cardiotoxicity on the isolated heart. ECG changes produced by i.v. injection of KCl (0.5 ml of 50 mM) mimicked the ECG changes observed in the intoxicated rats injected with a lethal dose of enterotoxin. Perfusion of rat isolated organs showed that potassium concentration in the eluent from the liver (but not lungs or lower extremities) increased markedly within 1-2 min after the administration of enterotoxin. The amount of potassium liberated from a rat liver was about 133 mumoles, which is sufficient to increase the plasma level of potassium to more than 10 mM. In addition to potassium, cytoplasmic enzymes, such as glutamate oxalacetate transaminase, glutamate pyruvate transaminase and lactate dehydrogenase, were also liberated from the intoxicated liver, indicating that potassium was liberated from hepatocytes by the change in membrane permeability produced by enterotoxin. It is concluded that hyperpotassemia elicited by the cytotoxic action of enterotoxin on hepatocytes caused cardiac failure leading to the death of the intoxicated animals.
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PMID:Pathodynamics of intoxication in rats and mice by enterotoxin of Clostridium perfringens type A. 192 76

Patients randomized to placebo in the encainide and flecainide arms of the Cardiac Arrhythmia Suppression Trial (CAST) have been found to have a relatively low 1-year mortality rate of 3.9% in comparison with previous studies of patients in the postmyocardial infarction period. To determine the comparability of CAST with previous studies, baseline variables were examined in the 743 patients randomized to placebo in the flecainide and encainide arms of CAST. Twenty-three baseline characteristics were correlated with major outcome events: arrhythmic death (16 events), total mortality (26 events) and congestive heart failure (51 events). On multivariate analysis the risk of new or worsening congestive heart failure was significantly associated with diuretic use, diabetes, high New York Heart Association functional class, age, prolonged QRS duration and low ejection fraction. The risk of arrhythmic death or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, history of heart failure, use of digitalis, diabetes and prolonged QRS duration. Total mortality or resuscitated cardiac arrest was significantly associated with an index Q wave myocardial infarction, diabetes, ST segment depression, high functional class, prolonged QRS duration and low ejection fraction. The variables at baseline associated with mortality from all causes or arrhythmic death or resuscitated cardiac arrest and heart failure in the CAST placebo-treated patients are similar to those identified in previous postmyocardial infarction studies. Thus, the observation of increased mortality in CAST associated with the administration of encainide and flecainide for suppression of ventricular premature depolarizations is probably applicable to any comparably defined group of patients in the postmyocardial infarction period.
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PMID:Events in the cardiac arrhythmia suppression trial: baseline predictors of mortality in placebo-treated patients. 193 43

A new cardioselective beta 1-adrenergic receptor agonist xamoterol (Corwin) has been developed for the treatment of heart failure. To study the acute hemodynamic effects of xamoterol, 24 patients, 39-70 years old, with mild-to-moderate postinfarction left ventricular dysfunction entered a double-blind, between-patient comparison of a single 5-minute intravenous infusion of xamoterol (0.2 mg/kg) and placebo. The acute hemodynamic effects of xamoterol were measured at rest and during two multistaged symptom-limited supine bicycle exercise tests (Ex-T), a control Ex-T followed by an Ex-T with either xamoterol or placebo. Compared with placebo, xamoterol significantly increased left ventricular contractility (Vmax and positive [+] dP/dt) and enhanced relaxation (dP/dt- and time constant relaxation) at rest and at the 25% and 50% levels of maximum exercise. The heart rate, the frequency and time to onset of anginal symptoms, the magnitude of exercise-induced ST segment depression, the left ventricular end-diastolic and peak systolic pressures, the mean pulmonary artery pressures, the cardiac index, the left ventricular stroke-work index, and the epinephrine and norepinephrine plasma levels at rest and during exercise did not differ significantly between placebo xamoterol groups. Thus, xamoterol can be a useful addition for the treatment of left ventricular dysfunction because of long-term ischemic heart disease.
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PMID:Improvement of left ventricular contractility and relaxation with the beta 1-adrenergic receptor partial agonist xamoterol at rest and during exercise in patients with postinfarction left ventricular dysfunction. A placebo-controlled randomized trial. 196 62

Within the health care of the elderly with prevention, diagnosis, therapy, rehabilitation, nursing care and social service, diagnostic procedures are of great importance to avoid under- and over-diagnosis. Many diagnostic difficulties exist in elderly patients such as changed reference values, changed normal values and changed signs and symptoms. Well-known examples of conditions which are likely to be under-diagnosed include depression and urinary incontinence. Examples are given from the cardiopulmonary field where e.g. dyspnoea showed to be very common, but in only 36% of males and 52% in females related to cardiac failure or pulmonary disease. The most common symptom of acute myocardial infarction in elderly patients was shown to be dyspnoea, whereas chest pain occurred in only one fifth of the cases. In another study of patients with ulcer disease loss of appetite and weight, nausea and anemia were more common than abdominal pain and heartburn. In peritonitis patients, abdominal pain was observed in only just more than half of the cases and guarding and/or abdominal rigidity in about one third. In patients with suspect age dementia a detailed investigation showed the prevalence of organic dementia to be 89% whereas 3% had treatable dementia and 8% non-dementia conditions. In geriatric long-term patients the mean hearing loss in the speech area was about 50 dB, in spite of the fact that only about 10% of the patients had hearing aids. The need for nursing diagnosis is also obvious. It is concluded that a detailed multidisciplinary diagnostic investigation procedure is very important in geriatric medicine.
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PMID:The importance of diagnostic procedures to ensure quality of health care in geriatric medicine. Examples from recent studies. 198 60

The autonomic components of the baroreflex control of heart rate were evaluated in conscious mongrel dogs before and after 4-6 weeks of ventricular pacing (250 beats/min). Arterial baroreflex sensitivity (BRS) was determined by the slopes of linear regression of pulse interval versus the preceding systolic arterial pressure in response to bolus injections of either phenylephrine or nitroglycerin. BRS was significantly depressed in the heart failure state [nitroglycerin slope, 5.0 +/- 2.7 (mean +/- SD) versus 16.6 +/- 5.1 msec/mm Hg, p less than 0.005; phenylephrine slope, 15.0 +/- 14.8 versus 32.0 +/- 26.7 msec/mm Hg, p less than 0.005]. There was no depression in BRS in dogs that were used as time controls or were acutely paced for 30 minutes. After beta 1-adrenergic blockade with metoprolol, the resting heart rate in the heart failure state was depressed more than in the normal state (-17.0 +/- 5.0% versus -3.2 +/- 3.4%, p less than 0.001). Atropine significantly increased resting heart rate more in the normal state than in the heart failure state (115.8 +/- 36.7% versus 25.4 +/- 14.5%, p less than 0.005). Thus, dogs in the heart failure state appear to have high resting cardiac sympathetic tone and low resting vagal tone. For nitroglycerin administration, metoprolol depressed BRS by 47.6 +/- 26.3% in the normal state and by 63.6 +/- 58.5% in the heart failure state. Atropine decreased the BRS by 86.7 +/- 7.8% in the normal state and by 39.5 +/- 30.2% in the heart failure state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Analysis of baroreflex control of heart rate in conscious dogs with pacing-induced heart failure. 198 84

We have observed that many spontaneously hypertensive rats (SHR) between the ages of 18 and 24 mo develop findings suggestive of heart failure, including pleural and pericardial effusions, left atrial thrombi, and right ventricular hypertrophy. Isolated left ventricular papillary muscle function was studied in these animals (SHR-F), in age-matched SHRs without evidence of heart failure (SHR-NF), and in nonhypertensive controls (WKY). Preparations from SHR-F showed depression of active tension development (3.58 +/- 1.75 g/mm2, means +/- SD) compared with both SHR-NF (7.17 +/- 0.94) and WKY (6.17 +/- 1.00) (P less than 0.01). Shortening velocity was also depressed in SHR-F (0.95 +/- 0.38 lengths/s) compared with SHR-NF (1.60 +/- 0.30; P less than 0.05) and WKY groups (2.15 %/- 0.48; P less than 0.01). Depression of muscle function was not found before 18 mo of age. Thus the aging SHR is a model in which one can observe the transition from chronic stable left ventricular hypertrophy to overt heart failure. Furthermore, left ventricular papillary muscles from SHRs with heart failure show evidence of significant contractile dysfunction, suggesting that impairment of intrinsic myocardial function underlies the development of heart failure.
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PMID:Impaired myocardial function in spontaneously hypertensive rats with heart failure. 199 92

The study objective was to describe the clinical, biologic, and hemodynamic features of adult overwhelming meningococcal purpura and to examine the prognostic factors by multivariate analysis at the time of admission to the intensive care unit. Thirty-five patients (greater than or equal to 13 years of age) with meningococcal infection, circulatory shock, and generalized purpuric lesions of abrupt onset were recorded in eight intensive care units from 1977 to 1989. The patients were young (mean age, 26.6 years; range, 13 to 68 years) and had been previously healthy. The female-to-male ratio was 3:1. Mortality was 54.3%, with most deaths occurring within the first 48 hours, usually secondary to irreversible shock with multiple organ failure. Ischemic complications (eight cases), prolonged heart failure (seven cases), and secondary septicemia (five cases) were the chief complications among survivors. Initial hemodynamic study after volume loading showed low stroke volume index (mean +/- SD, 29.4 +/- 13 mL/m2) and tachycardia (mean +/- SD, 138 +/- 16 beats per minute), a profile suggesting a greater myocardial depression than usually observed in gram-negative bacillary septic shock. Univariate prognostic analysis showed that four variables at the time of admission were associated with fatal outcome: a plasma fibrinogen level of 1.5 g/L or less, a factor V concentration of 0.20 or less, a platelet count lower than 80 x 10(9)/L, and a cerebrospinal fluid leukocyte count of 20 x 10(6)/L or less. Stepwise regression analysis showed that low fibrinogen level (less than or equal to 1.5 g/L) was the sole adverse prognostic variable (odds ratio = 2, 95% confidence interval, 1.5 to 2.7). Adult overwhelming meningococcal purpura is still associated with high mortality and morbidity. Low fibrinogen level at time of admission may permit early recognition of the most severely ill patients.
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PMID:Adult overwhelming meningococcal purpura. A study of 35 cases, 1977-1989. 199 58

We have previously demonstrated a decrease in baroreceptor discharge sensitivity in dogs with experimental heart failure. In the present study, we determined the sensitivity of the carotid sinus baroreceptor reflex in dogs with pacing-induced heart failure. The carotid sinus baroreceptor reflex sensitivity was determined by pressurizing one carotid sinus with all other baroreceptor and cardiopulmonary receptor inputs removed. The data were analyzed by plotting carotid sinus pressure-mean arterial pressure curves and carotid sinus pressure-renal sympathetic nerve activity curves in the two groups of dogs. The peak arterial pressure during carotid hypotension was significantly depressed in dogs with heart failure compared with normal dogs (107.1 +/- 5.7 versus 139.8 +/- 7.0 mm Hg, p less than 0.001). Mean arterial pressure range, renal sympathetic nerve activity range, and peak slope were significantly decreased in the heart-failure group. To determine if this depression was completely due to depression of baroreceptor discharge per se, or to alterations in central or end-organ responsiveness, similar experiments were performed by stimulating the carotid sinus nerve and evaluating frequency, voltage, and duration of stimulation on the resultant mean arterial pressure and renal sympathetic nerve activity. As was the case with carotid sinus pressurization, electrical stimulation caused a significantly smaller change in mean arterial pressure in heart-failure dogs compared with the normal dogs. However, there was no significant difference between normal and heart-failure dogs for the renal sympathetic nerve activity-electrical stimulation curves. These data strongly suggest that the depressed carotid sinus baroreceptor reflex in heart failure is not solely the result of depressed baroreceptor responsiveness but may be related to poor end-organ responses and normal central control of renal sympathetic outflow.
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PMID:Carotid sinus baroreceptor reflex in dogs with experimental heart failure. 201 93

Among the clinical manifestations of ischemic heart disease, right coronary artery (RCA) disease offers a wide variety of right and left ventricular ischemic involvement, including prevalent right ventricular dysfunction and severe cardiac failure. Whether the right ventricular impairment is dependent primarily on ischemia of the right ventricle or requires a concomitant left ventricular dysfunction remains debatable. To assess the pathophysiology and clinical relevance of RCA-related ischemia, a systematic study of patients with single RCA disease (either vasospastic angina at rest or typical stable angina) was undertaken by radionuclide ventriculography. A high incidence of ischemia-induced right ventricular dysfunction was observed (93% and 95% in angina at rest and on effort, respectively), either alone or associated with left ventricular impairment. These results were compared with those obtained in a control population with isolated left anterior descending artery disease and either primary or secondary angina pectoris. We infer that the impairment of the right ventricle was related primarily to right ventricular ischemia and that left ventricular dysfunction alone did not cause an important depression of right ventricular systolic function. In conclusion, the clinical manifestations of RCA disease can be protean; the right ventricle can be the target of ischemia, and recognition of its impairment poses diagnostic problems. Radionuclide ventriculography and two-dimensional echocardiography, together with stressors of coronary flow reserve, are reliable techniques for assessing RCA-related ischemia.
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PMID:Right coronary artery disease. Pathophysiology, clinical relevance, and methods for recognition. 202 49

Many of the newer antiarrhythmic agents are said to cause minimal myocardial depression, but their hemodynamic effects have not been invasively evaluated and compared in patients with severe chronic heart failure. In a randomized, crossover study, the hemodynamic responses to single oral doses of procainamide (750 mg), tocainide (600 mg), and encainide (50 mg) given to 21 patients with severe chronic heart failure were compared. Cardiac performance decreased with all three drugs, but the magnitude of deterioration differed among the three agents. Stroke volume index decreased with procainamide (-5 +/- 1 ml/m2, p less than 0.001), tocainide (-7 +/- 1 ml/m2, p less than 0.001), and encainide (-8 +/- 1 ml/m2, p less than 0.001), but the decline was significantly greater with encainide than with procainamide (p less than 0.05). Similarly, left ventricular filling pressure increased with tocainide and encainide (+4 +/- 1 and +5 +/- 2 mm Hg, respectively; both p less than 0.05), but not with procainamide; the increase was significantly greater with tocainide and encainide than with procainamide (p less than 0.001). These deleterious hemodynamic effects were accompanied by worsening symptoms of heart failure in six patients with encainide and seven patients with tocainide but in only two patients with procainamide. Serum levels for all drugs were in the therapeutic range. In conclusion, although the three type I antiarrhythmic agents tested may all adversely affect left ventricular function in patients with heart failure, encainide and tocainide are more likely than procainamide to cause hemodynamic and clinical deterioration.
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PMID:Comparative hemodynamic effects of procainamide, tocainide, and encainide in severe chronic heart failure. 210


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