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

A model of partial thickness ischemia has been developed using subendocardial S-T elevation without epicardial S-T elevation to detect partial thickness ischemia which is sufficient to cause subsequent necrosis. Subendocardial blood flow in this model (measured with radioactive microsphere techniques) may be reduced to 25 percent of normal (P less than 0.001) by coronary stenosis and tachycardia while subepicardial flow remains normal. Epicardial S-T depression seems to indicate reciprocally subendocardial S-T elevation as long as a layer of nonischemic epicardial muscle is present, but when ischemia becomes transmural, epicardial S-T elevation occurs. Regional pressure-flow relations were determined as distal coronary pressure was reduced at a constant aortic pressure, heart rate and cardiac output. These relations revealed remarkably effective autoregulation of epicardial blood flow concomitant with progressive subendocardial ischemia.
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PMID:Significance of subendocardial S-T segment elevation caused by coronary stenosis in the dog. Epicardial S-T segment depression, local ischemia and subsequent necrosis. 90 35

The correlation between the three ischemia indicators angina pectoris (AP), ST-segment depression (ST) and excessive pulmonary wedge pressure rise (PCP) during exercise, and the coronary angiographic findings, were analysed in 293 patients without previous transmural myocardial infarction. This patient material consisted of 253 men and 40 women between the age of 20 and 65 years, the mean age being 48. The exercise tests were performed on a bicycle ergometer in supine position and in relatively steady state conditions. Pulmonary wedge pressure was measured by means of a Swan-Ganz floating catheter. The essential findings were: 1. If all three ischemia indicators were positive, the incidence of a positive angiographic finding i.e. a greater than or equal to 50% stenoses in at least one main coronary artery was 96.3%. 2. If only the two classic ischemia indicators were evaluated and positive, the incidence of a positive angiographic finding was only 86.1% (24). This difference is mainly due to false positive results of AP and ST in women. 3. If all three ischemia indicators were negative, the incidence of a negative angiographic finding was 89.2%. 4. If only the two classic ischemia indicators were evaluated and negative the incidence of a negative angiographic finding was as high (87,6% [24]). This lack of difference is due to the fact that patients with a previous intramural infarcion can be free not only of AP and ST but also of PCP during exercise. 5. The combination of AP and PCP, or ST and PCP, is equally reliable in predicting coronary morphology as the classic combination of AP and ST. It follows that PCP measurement is recommended, if one of the classic ischemia indicators cannot be properly evaluated.
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PMID:[Can predictability of coronary angiographic findings be improved by additional measurement of pulmonary wedge pressure during exercise? (author's transl)]. 91 74

In 35 open chest anesthetized dogs coronary and aortic blood flow were measured with electromagnetic flowmeters while aortic and distal coronary blood pressure and an epicardial ECG were recorded. A fixed amount of stenosis (60-80%) was produced in the coronary artery by an externally applied plastic cylinder. In 24 of the 35 dogs the coronary blood flow showed cyclical reductions to near zero, with a sudden spontaneous return to near control levels. During reduced flow the epicardial ECG showed ST-segment depression suggestive of ischemia, and ventricular premature beats were often noted. Six animals died acutely during episodes of reduced flow. After 35 mg/kg of aspirin were given intravenously the cyclical reductions in coronary blood flow were abolished and the in vitro platelet aggregations were reduced from a control of 62.1 +/- 15 units (Born technique) to an average of 23.7 +/- 12 units. Histologic sections of the narrowed coronary artery obtained when coronary flow was reduced show an amorphous mass in the lumen which was thought to be a platelet aggregate. Perhaps a similar process of platelet aggregation occurs in the stenosed coronary arteries in man, producing acute coronary obstruction, ischemia, and sudden death.
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PMID:Platelet aggregation in partially obstructed vessels and its elimination with aspirin. 94 67

Functional reserves of the cardiovascular system during sharp depression of the cardiac output in the postreanimation period after 15-minute cardiac arrest were studied in experiments on dogs (by loading with different fluid volumes). Acute hypervolemia did not produce any circulatory decompensation. Reinforcement of venous return and changes in the peripheral circulation due to polyglucine loading augmented the CVP temporarily, and produced a stable increase of the AP, of the cardiac output, systolic volume, the work of the left cardiac ventricle and of the total oxygen consumption by the organism. Meanwhile there was a decrease of the peripheral vascular resistance. In model experiments on dogs, which sustained 20-minute isolated compression ischemia the syndrome of low cardiac output developed too. This indicated the relation of this phenomenon to the disorders in the neuro-humoral regulation of blood circulation.
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PMID:[Pathogenesis of the low cardiac output syndrome in postreanimation states]. 95 32

Older people often describe their headaches as starting with vague neck discomfort and eventually moving to the temples and forehead. These are muscle-tension headaches, by far the most common type in the elderly. Although cervical osteoarthritis often is at fault, depression can be a significant factor, patricularly when headaches are chronic. There is no sure cure for tension headache, and often, several of the many remedies-ethyl chloride spray, moist heat, massage, antidepressant drugs, analgesics, local anesthetics, etc.-must be tried before an effective one is found. But just as important to successful therapy are concern, compassion, and a willingness to listen on the part of the physician. True migraine headaches are rare in the elderly. More prevalent is the type of vascular headache associated with giant cell arteritis, which is severe and resistant to any form of analgesic except the strongest narcotics. Vascular headaches also may result from congestive heart failure (which produces venous congestion in the cranial cavity), transient ischemia, increased intracranial pressure, and a variety of metabolic disturbances.
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PMID:The types of headache that affect the elderly. 95 13

Ajmaline, a rauwolfia derivative, has been found to possess potent antiarrhythmic effects. The present study has been designed to define the cardiovascular effects of this drug. Hemodynamic studies performed in anesthetized and conscious dogs demonstrated no significant changes in measured hemodynamic parameters at doses equal to or less than 2 mg. per kilogram. Studies in isolated papillary muscle demonstrated no negative inotropic effects until concentrations of 1 X 10(-4). Disparate results were obtained with regard to heart rate reflecting the state of autonomic tone. Electrophysiologic studies in both anesthetized and conscious dogs demonstrated a significant depression of intraventricular conduction with no significant effect on AV nodal conduction; ventricular automaticity was not affected. Ajmaline did not alter digitalis-induced AV nodal conduction prolongation. However, ajmaline dramatically altered or abolished ventricular arrhythmias secondary to acute ischemia. In conclusion, these studies demonstrate that ajmaline specifically depresses intraventricular conduction, suggesting that this drug would be particularly effective in the treatment of re-entrant ventricular arrhythmias.
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PMID:Cardiovascular effects of ajmaline. 96 88

From Wistar rats, data are presented which indicate that inbred females a) have a greater ability to clear particulate matter from the blood stream than do males of the same strain; b) are significantly more resistant to two different forms of lethal circulatory stress (e.g., intestinal ischemia and whole-body trauma) than are males; and c) exhibit a greater resistance to undergo reticuloendothelial system (RES) phagocytic depression after both forms of lethal trauma than do males. Estradiol treatment of males, using either acute, massive (1 or 10 mg/kg) or multiple, low dose (10 or 100 mug/kg) regimens, confers trauma resistance on such animals. Such estradiol treated male rats exhibit hyperactive RES's. These estradiol-treated males, when subjected to either lethal ischemia or trauma, fail to demonstrate the early RES phagocytic depression seen in untreated controls. Untreated female as well as estradiol-treated male rats exhibit significantly higher arterial blood pressures post-trauma than do untreated male rats. Direct microscopic observation of rat mesenteries indicr whole-b0dy trauma, the untreated females as well as the estradiol-treated males exhibit significantly less dilatation of microscopic capacitance vessels (i.e., venules) than do untreated male rats. The data reported herein could be used to suggest that estrogenic hormones may play pivotal roles in a) the amelioration of an organism's reaction to systemic stress; and b) control of macrophage and peripheral vascular functions.
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PMID:Sex and estrogens in protection against circulatory stress reactions. 97 Apr 65

In order to assess the relative significance of precordial ST-segment elevations and depressions, 32 patients with anterior transmural myocardial infarction were studied utilizing serial 49-lead precordial maps. Theoretically, zones of ST-segment depression adjacent to major zones of ST-segment elevation might represent border areas of mild ischemia, and hence could be more readily amenable to intervention therapy. As expected, an extensive zone of ST-segment elevation was observed precordially in each of these patients. However, zones of ST-segment depression in adjacent areas were noted to occur inconsistently, were limited in distribution and magnitude, and bore no fixed relationship to zones of ST-segment elevation. Thus, mapping of precordial ST-segment depression in anterior transmural infarction probably has a limited role in assessing evolution of ischemic injury or therapy in these patients. This finding does not, however, vitiate the significance of ST-segment depressions in angina, intermediate coronary syndrome, or non-transmural infarction, conditions which may deserve further study using mapping techniques.
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PMID:Precordial ST-segment mapping. 4. Experience with mapping of ST-segment depression in anterior transmural myocardial infarction. 97 82

The effects on myocardial function, metabolism and ultrastructure of 60 minutes of reperfusion, instituted after 30, 60 and 90 minutes of occlusion of the left anterior descending coronary artery, were studied in 48 dogs. Twelve sham-operated dogs served as controls. Coronary occlusion for 60 or 90 minutes caused significant depression in the first derivative of left ventricular pressure (dP/dt) (P less than 0.05) that could not be reversed by reperfusion. Upon reperfusion, creatine phosphate stores in myocardium made ischemic for 30 and 60 minutes, but not for 90 minutes, returned toward control levels, but stores of adenosine triphosphate (ATP) and total nucleotides and the ATP/adenosine diphosphate ratio of myocardium subjected to 60 and 90 minutes of ischemia were further decreased. After 60 and 90 minutes of ischemia, swelling of the sarcoplasmic reticulum and mitochondrial damage (swelling, decreased matrix density and partial loss of cristae) were seen. Myofibrils were relaxed in all these groups. Reperfusion produced gross contraction of myofibrils and aggravated these changes in mitochondria and sarcoplasmic reticulum. In the hearts subjected to 90 minutes of ischemia these changes were gross. The levels of creatine phosphokinase, glutamic oxaloacetic transaminase and lactic dehydrogenase in the coronary sinus blood increased dramatically (P less than 0.05) upon reperfusion after 60 or 90 minutes of occlusion, indicating severe impairment of cell membranes. This secondary rise in serum enzyme activity during reperfusion should be taken into consideration when estimating the size of a myocardial infarct from enzyme changes alone. It appears that 60 and 90 minutes of ischemia cause severe myocardial damage that is not reversed by reperfusion maintained for 1 hour although longer periods of reperfusion may be beneficial.
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PMID:Alterations in energy metabolism and ultrastructure upon reperfusion of the ischemic myocardium after coronary occlusion. 108 Mar 52

The mechanism of elevation of left ventricular end-diastolic pressure during acute global ischemia was evaluated by examiniation of the relative contributions of a decrease in contractility and an alteration of the pressure-volume relationship. The external circumference (mercury-in-silastic gauge) pressure relationship, as an index of the pressure-volume relationship, was studied in beta adrenergic and ganglionic blocked, open chest dogs on right heart bypass at constant heart rate ane aortic pressure. Ischemia of one and two hours' duration was produced by reducing total coronary blood flow in cannulated left and right coronary arteries until left ventricular end-diastolic pressure rose significantly. At a constant stroke work, left ventricular end-diastolic pressure rose from 5.0 +/- 0.5 to 15.0 +/- 0.5 cm H2O in the experiments of one hour of ischemia, and from 7.0 +/- 1.0 to 17.0 +/- 1.0 cm H2O in experiments of two hours of ischemia. Ischemia was followed by one hour of restoration of coronary blood flow. Ischemia produced a marked depression of ventricular function: stroke work, considered at a left ventricular end-diastolic pressure of 15 cm H2O, decreased from 21.0 +/- 3.0 to 3.5 +/- 0.5 gm-m, and from 15.0 +/- 2.0 to 2.5 +/- 0.5 gm-m, in the experiments of one and two hours, respectively. Neither ischemia nor reflow changed the pressure-volume relationship. Thus, the elevation of left ventricular end-diastolic pressure during ischemia in an otherwise normal canine myocardium is due to a decrease in systolic performance of the heart rather than to an alteration of the pressure-volume relationship.
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PMID:Left ventricular end-diastolic pressure volume relationships with experimental acute global ischemia. 108 86


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