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)

Cardiac beriberi is considered a rare disease in western society. A patient with fulminant Shoshin-type beriberi was studied in the acute phase and found to have severe metabolic acidosis, high output biventricular failure, and markedly low systemic vascular resistance. Red blood cell transketolase activity was abnormally low. Following treatment with thiamine, diuretics, digitalis and oxygen, all abnormalities disappeared. The historical background of the disease is reviewed along with a discussion of pathophysiologic mechanisms responsible for the hemodynamic profile and lactic acidosis. Angiographic and hemodynamic data on the patient presented suggest relative depression of left ventricular function in the acute phase of beriberi. Since beriberi is uncommonly encountered, emphasis is placed on diagnostic and therapeutic implications of the disease which may not be widely appreciated.
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PMID:Fulminant beriberi heart disease with lactic acidosis: presentation of a case with evaluation of left ventricular function and review of pathophysiologic mechanisms. 67 49

A cumulative dose--response curve for metocurine based on body weight was determined in 30 infants and children during halothane (1.2 per cent inspired), nitrous oxide and oxygen (60/40 per cent) anesthesia. The mean and range of twitch depression and time for recovery from maximal neuromuscular blockade were not significantly different over an age range from newborn to 7 years. Metocurine is twice as potent as d-tubocurarine in children, and their requirement is more than that for adults. The rate of recovery from metocurine in children was the same as that from d-tubocurarine. In another 30 children, use of metocurine at a large dose (0.5 mg/kg) for endotracheal intubation caused no significant change in blood pressure or pulse rate. Cardial arrhythmias were not seen.
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PMID:Metocurine in infants and children: neuromuscular and clinical effects. 69 81

Pressure plethysmographic measurement of ventilation and electromyographic measurement of diaphragm activation in unanesthetized suckling opossums revealed spontaneous episodes of obstructive apnea. To better understand this phenomenon, intact animals were tested under different conditions of respiratory drive and during activation of pulmonary reflexes. Results showed that obstructed breaths were usually initiated with the lungs at or near the end-inspiratory level, and they occurred more frequently during air or oxygen breathing as compared with inhalation of hypercapnic or asphyxiant test gases. The latter two gas mixtures caused increases in ventilation; but depression of breathing resulting from pentobarbital anesthesia was not accompanied by obstructed breaths. It was initially considered that a reflex laryngeal response with changes in lung volume or lung irritation might trigger obstructive apnea; but pulmonary inflation and deflation as well as ammonia inhalation did not typically produce such an effect. The results indicate that mechanisms for obstructive apnea in the suckling opossum must account for the limited incidence of obstructed breaths during both ventilatory chemostimulation and anesthetic respiratory depression.
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PMID:An obstructive apnea in the suckling opossum. 70 85

Unanesthetized rats put in the hermetic chamber breathed with a gas mixture containing 10.5% of oxygen in nitrogen during 30 and 60 min (moderate hypoxia), and 3.5% of oxygen in nitrogen for 30 min (severe hypoxia). The circulating blood volume increased in moderate hypoxia but was rather reduced in severe hypoxia. Mobilization of blood from the liver occurred in moderate hypoxia after 30 min, becoming less obvious after 60 min or in severe hypoxia. Redistribution of blood in the myocardium, skeletal muscles of the head and neck occurred in moderate hypoxia. Severe hypoxia led to depression of the regional circulating blod redistribution and the signs of pathological accumulation of the blood in the liver, small intestine, colon and testicles.
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PMID:[Regional blood filling in hypoxic hypoxia]. 72 45

Tissue energy metabolism was examined in posterior (ischemic) and anterior ("control") regions of canine ventricles after 5 and 10 minutes of left circumflex coronary artery occlusion. When compared to identical regions of normal hearts, the following changes were found: (1) decreases in glycogen and phosphorylase activity in the anterior and posterior regions, (2) depressed state 3 rates of oxygen consumption of isolated mitochondria in both anterior and posterior regions, (3) shifts in optimum substrate concentrations for palmityl-CoA (+ carnitine) oxidation by mitochondria in the anterior and posterior regions, and (4) decreases in the apparent zero order and first order rates of mitochondrial palmitylcarnitine production. These changes correlated with a marked decrease in developed tension in the posterior regions. Depression in tension development in the posterior regions of the heart still was present after 30--60 minutes of reperfusion following a 10-minute period of occlusion. Glycogen content in the reperfused areas was significantly decreased after 60 minutes of reperfusion when compared to normal areas and to control hearts perfused for 70 minutes. After reperfusion, mitochondrial function appeared to return toward "normal." However, the slow restoration of contraction of the ischemic area suggests that cellular mechanisms operative in vivo to restore pump function still might be abnormal.
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PMID:Biochemical and morphological correlates of acute experimental myocardial ischemia in the dog. IV. Energy mechanisms during very early ischemia. 75 32

Hypotension may be expected to produce less perturbation of metabolism in the brain when cerebral metabolic rate is lowered by deep anesthesia. Male Wistar rats having unilateral carotidartery ligation were exposed to mean arterial pressure (MAP) of 40 torr for 22 min by an intravenous infusion of trimethaphan during anesthesia with halothane, 0.6 or 2 per cent, in oxygen. Cortical tissue metabolite levels on the side of the ligated carotid artery were more abnormal in rats receiving halothane, 0.6 per cent, than in those receiving halothane, 2 per cent. Values at halothane, 0.6 per cent, were adenosine triphosphate (ATP), 1.71 +/- 0.05 (+/-SEM) mumol/g, phosphocreatine (PCr) 1.97 +/- 0.07 mumol/g. and lactate 16.5 +/- 5.1 mumol/g; corresponding values at halothane, 2 per cent, were ATP 2.27 +/- 0.02, PCr 4.02 +/- 0.23, and lactate 4.75 +/- 0.9 mumol/g. ATP and PCr values were significiantly lower (P less than 0.05) and the lactate value was significantly higher with halothane, 0.6 per cent, than with halothane 2 per cent. Cerebral oxygen consumption decreased 47 per cent in rats anesthetized with halothane, 2 per cent. Preservation of cortical metabolite levels in deeply anesthetized animals suggests a protective effect of cerebral metabolic depression.
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PMID:Cerebral energy levels during trimethaphan-induced hypotension in the rat: effects of light versus deep halothane anesthesia. 76 Jun 1

Propranolol and practolol were tested in patients with repeated daily occurrence of spontaneous angina. Twenty-one showed ST segment depression (type I) and 15 ST segment elevation (type II) during angina. The efficacy of the treatment was evaluated in subjective (number of reported episodes of pain) and objective terms (number of episodes of electrocardiographic abnormalities documented during periods of continuous recording): practolol was fully effective in 42 per cent and propranolol in 38 per cent of type I cases; in type II angina 73 per cent of the cases fully responded to propranolol, none of the patients in this group given practolol improved. The study also showed that: (a) the effects on angina are strictly dose-dependent, and optimal results are achieved at individualized doses; (b) within the same subject the response may be preferential to one beta-blocker as opposed to the other; (c) propranolol is more effective in type II angina; (d) the occurrence of heart failure is uncommon even with high doses of beta blockers;(e) the relief of angina is due to prevention of ischaemia and not to a placebo or anaesthetic effect; (f) the prevention of ischaemia is not adequately explained by reduction of the mechanical effort and the oxygen need of the myocardium; (g) the antianginal effect is possibly dissociated from the beta blockade of the heart. The hypothesis that beta-blocking agents influence the conronary vasomotion is discussed.
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PMID:Treatment of spontaneous angina pectoris with beta blocking agents. A clinical, electrocardiographic, and haemodynamic appraisal. 77 91

Propranolol is known to decrease ischaemic damage in developing myocardial infarction. Besides acting on mechanical parameters which help determine the balance of oxygen supply and oxygen demand in the ischaemic tissue, propranolol decreases the myocardial uptake of free fatty acids and increases that of glucose. It is suggested that propranolol may favourably alter developing myocardial infarction in dogs by altering the supply of substrates reaching the ischaemic zone. However, propranolol also decreases enzyme release from isolated rat hearts with coronary ligation at a relative constant arterial free fatty acid concentration. Propranolol causes more marked depression of mechanical function and of heart rate in hearts perfused with free fatty acids than with glucose. It is suggested that the glucose-promoting and anti-lipolytic actions of propranool might be important not only in decreasing infarct size but also in helping to prevent undesirable side effects in hearts with experimental myocardial infarction.
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PMID:Propranolol and experimental myocardial infarction: substrate effects. 78 52

The activity and responsiveness of the peripheral ventilatory chemoreflex were assessed by the transient depression of ventilation following two breaths of oxygen in air-breathing subjects, and the differing times of onset of the ventilatory response to i.v. sodium bicarbonate in subjects breathing either air or oxygen. In patients premedicated with pethidine, in whom anaesthesia was induced with thiopentone, it was found that halothane, in an inspired concentration of 0.7-0.8%, reduced the activity and responsiveness of the peripheral ventilatory chemoreflex markedly. When halothane was discontinued and anaesthesia was maintained wtih intermittent injections of thiopentone (0.2 mg/kg/min) evidence of peripheral chemoreceptor activity and responsiveness returned.
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PMID:The effect of halothane and thiopentone on ventilatory responses mediated bythe peripheral chemoreceptors in man. 79 11

Coma and other neurologic abnormalities are present in patients with either diabetic ketoacidosis (DKA) or nonketotic coma (NKC), and the cause of such phenomena are not known. Patients with NKC also manifest seizures and focal neurologic changes. Treatment of diabetic coma with insulin may induce cerebral edema by as yet undefined mechanism(s). In patients with DKA, cerebral oxygen utilization is impaired, and there is hyperviscosity of the blood. A substantial part of the brain's energy source is derived from ketones, which in themselves can depress sensorium. Extracellular hyperosomolality is present, which may also contribute to the genesis of coma. In addition, most ketoacidotic patients have associated medical conditions, which may further impair consciousness. Biochemical changes in the brains of animals with DKA include impairment of both phosphofructokinase activity and pyruvate oxidation, and accumulation of citrate. The net effect upon sensorium in ketoacidotic patients probably represents the interaction of most of the above factors and differs markedly among individuals. Patients with NKC manifest not only depression of sensorium, but also focal motor seizures, hemiparesis, and other neurologic changes, such as aphasia, hypereflexia, sensory defects, autonomic changes, and brainstem dysfunction. Most of the aforementioned changes revert to normal after correction of hyperosomolality. Gamma amino butyric acid, which has been shown to elevate the seizure threshold, is normal in brains of ketoacidotic animals, but may be low in nonketotic coma. Also, hyperosomolality per se may produce seizures. Cerebral edema may complicate the treatment of either DKA or NKC. The available experimental evidence suggests that many of the commonly held theories for the production of such brain swelling probably do not occur. There is no breakdown of the sodium pump, sorbitol or fructose do not accumulate in brain, and brain glucose is only about 25 percent of that in plasma; Cerebral edema is probably produced largely by a direct action of insulin on brain at a time when plasma glucose is approaching normal values. Cerebral edema can thus theoretically be avoided by stopping insulin when plasma glucose has been lowered to values approaching normal.
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PMID:Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain. 80 37


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