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

In healthy, closed-chest dogs, dose-dependent depression of ventricular function was produced by the anesthetics halothane, methoxyflurane, and fluroxene, as evidence by decreases in left venticular stroke volume, stroke work, dP/dt, and an increased enddiastolic pressure. Myocardial blood flow and oxygen consumption decreased concomitantly and were correlated with aortic blood pressure decreases. There was no change in myocardial lactate extraction with halothane and methoxyflurane, suggesting that myocardial oxygenation was adequate in spite of the decrease in blood flow. However, even with marked increases in arterial lactate concentration during fluroxene anesthesia, extraction did not chance and, in fact, tended to decrease. The hemodynamic effects of halothane and methoxyflurane are similar to those previously reported in man, but those of fluroxene are different. Consequently, clinical speculation from these results is not justified at this time.
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PMID:Effects of inhalation anesthetics on cardiac function and metabolism in the intact dog. 0 33

Cardiac performance was assessed in 33 lambs less than 1 to 5 days of age by means of left ventricular function curves. Performance was quantified by determining stroke volume ejected at end diastolic pressure 10 cm H2O (SV10) with constant afterload. Coronary flow, myocardial O2 consumption (MVO2), blood gas tensions and pH were determined. Measurements were obtained before and at 30 min intervals following hemorrhage to 30 mm Hg arterial pressure, and in controls (arterial pressure 75 mm Hg). Effects of metabolic acidosis, hypercapnia and beta-blockade were determined. In control lambs acidosis and hypercapnia failed to reduce SV10 after two hours. In hemorrhaged animals both factors sharply reduced SV10 and lambs with prior beta-blockade showed no greater reduction. MVO2 fell following hemorrhage but did not differ with metabolic conditions and did not relate to SV10. It is concluded that beta-adrenergic function is critically important in preserving left ventricular performance in newborn exposed to acidosis or hypercapnia. With sustained hemorrhage this mechanism fails leading to a significant depression of ventricular function. MVO2 was not a determining factor in these studies.
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PMID:Cardiac function and metabolism following hemorrhage in the newborn lamb. 1 55

As shown previously, the electrical function of the brain is critically dependent on cerebral blood flow in the sense that reduction beyond an ischemic threshold of approximately 15 ml/100 gm per minute (approximately 35% of control) in the baboon leads to complete failure of the somatosensory evoked response. This study tests the hypothesis that electrical failure in ischemia may be directly associated with a massive release of intracellular K+ or with a critical degree of extracellular acidosis. By microelectrode techniques, measurements of blood flow, extracellular activity of K+ and H+ as well as evoked potential were made in the baboon neocortex. Reductions in blood flow were obtained by occlusion of the middle cerebral artery and depression beyond the ischemic threshold of electrical function achieved by a reduction of systemic blood pressure which, in the ischemic zones, changed local cerebral blood flow proportionally. Abolition of evoked response could not be explained by depolarization by release of intracellular K+, nor was it critically dependent on cortical pH. However, the massive release of intracellular K+ was by itself critically dependent on cortical blood flow and occurred at 18 greater than 6 greater than 2 ml/100 gm per minute (median with 5% confidence limits). Thus a dual threshold in ischemia for neuronal function is described, the threshold for release of K+ being clearly lower than the threshold for complete electrical failure. Further, the findings support the concept of an ischemic penumbra during which the neurons remain structurally intact but functionally inactive. That neurons can survive for some time in this state of lethargy is evidenced by the observations that an increase in rCBF, if sufficient, can restore evoked potential and normalize extracellular K+ activity as well as pH.
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PMID:Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia. 1 21

The studies were undertaken to determine whether isoflurance inhalation is associated with a degree of beta-adrenergic action that is potentially important in clinical situations, and to compare the circulatory tolerance to isoflurane and halothane in dogs following beta blockade. We measured arterial and pulmonary artery pressure, left and right ventricular filling pressure, heart rate and cardiac output, and derived stroke volume and systemic and pulmonary vascular resistances in 13 mongrel dogs. The haemodynamic response to 1 MAC and 2 MAC isoflurane was studied in seven dogs and was similar before and after propranolol 0.1mg/kg i.v. In six dogs, propranolol 0.5mg/kg caused no significant changes in the circulatory response to 1 MAC and 2 MAC isoflurane or 1 MAC halothane. However, in three dogs, administration of 2 MAC halothane after propranolol 0.5mg/kg resulted in such profound circulatory depression as to preclude further study. These data suggest that (a) isoflurane possesses no clinically important beta-adrenergic stimulating activity; (b) there is no adverse drug interaction upon the circulation with the combination of isoflurane and propranolol; (c) in the presence of moderated profound beta-adrenergic blockade, 2 MAC isoflurane may be tolerated better than 2 MAC halothane.
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PMID:Lack of beta-adrenergic activity of isoflurane in the dog: a comparison of circulatory effects of halothane and isoflurane after propranolol administration. 1 56

The cardiovascular effects of total hip placement were evaluated in 10 surgical patients, aged 55 to 82, while receiving fluroxene-N2O-O2 anesthesia. The anesthetic regimen caused mild cardiovascular depression. The placement of the acrylic cement into the acetabulum and femoral shaft also induced mild cardiovascular depression, but these changes were not significant at p less than 0.05. In one 67-yr-old woman, there were significant reductions of cardiac output and stroke volume 2 min after the insertion of acrylic into the femoral shaft, despite careful replacement of intravascular loss and careful anesthetic management. Methylmethacrylate (1 X 10(-6) to 1 X 10(-4), v/v) was administered to 24 isolated perfused rabbits hearts. These concentrations of methylmetacrylate are of the same order as measurable blood levels in surgical patients. There was a dose-dependent depression of left ventricular dP/dt correlated with a depression of the spontaneous heart rate. When the bradycardia was prevented by electrically pacing the hearts or the administration of atropine, the depressed dP/dt rose to control levels. Reduction in myocardial temperature and heart rate by means of reduction in perfusate temperature of the isolated hearts reduced the myocardial depressant effect of methylmethacrylate.
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PMID:Cardiovascular effects of total hip placement in man. With observations on the effects of methylmethacrylate on the isolated rabbit heart. 1 17

The haemodynamic effects of a new beta-adrenergic blocking agent KO.1366 (bunitrolol) were assessed in 10 males admitted to hospital for investigation of chest pain. Measurements were made at rest, during atrial pacing at 100 beats/min, and during hand grip exercise, before and afterintravenous administration of KO.1366 at a dosage of 0.05 mg/kg body weight. There was a 12% (p less than 0.01) slowing in resting heart rate and alpha 4% (p less than 0.05) slowing in exercise heart rate after drug administration. Resting left ventricular end diastolic pressure rose by 2.2 mm Hg (p less than 0.01) following the drug, but there was no significant change during pacing or exercise. Left ventricular systolic pressure and its first derivative did not change significantly. Cardiac output rose slightly, and stroke volume at rest and during exercise showed a considerable increase. In the dosage used, KO.1366 has an important chronotropic effect on the heart without causing significant myocardial depression.
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PMID:Haemodynamic observations with KO. 1366 (bunitrolol), a new beta-adrenergic blocking agent. 2 26

A seven-year follow-up in 1973 of a prospective cardiovascular study of 1820 initially, healthy, middle-aged Chinese men of 40-59 years of age identified 1745 (95.9%) known survivors, 49 (2.7%) interim deaths, and 26 (1.4) who could not be traced. Of the survivors, 1462 (83.8%) were re-examined, 292 (16.7%) had another treadmill test of maximal exercise, and 283 (16.2%) failed to return for re-examination. On the basis of interim surveillance of hospital admissions, questionnaires and re-examination, a greater incidence of noncardiovascular events (338 or 18.6%) than evidence of cardiovascular disease (220 or 12.1%) was found while the majority (1021 or 56.1%) remained healthy. Total mortality was 0.29 for men under 50 and 0.76 per 100 person-years for men of 50 or more years of age. Only nine, or 18.4% of the deaths were due to cardiovascular causes, and unexpectedly for this population sample, only three were attributed to stroke. When cardiovascular morbidity was related to presence of ST depression after maximal exercise, to hypertension at rest by WHO criteria, to both findings, or to absence of either on initial intake examination, incidence increased from 2.3% for NEITHER group, to 5.7% for ST group, to 11.9% for HT group, and to 25.0% for BOTH groups. Re-examination revealed more evidence of cardiovascular disease than did surveillance of hospital admissions. Additional to effects of aging and mild adiposity, longitudinal changes in blood pressure and ST depression, increasing in the NEITHER group, but less frequent in the other groups, showed some evidence of regression toward the mean, as well as emerging disease and the confounding effects of uncontrolled treatment of hypertension in many. The potential for prediction of subsequent cardiovascular morbidity or mortality appeared stronger for hypertension than for postexertional ST depression, although the two were additive in this population, which is more prone to hypertension and stroke but now is developing clinical manifestations of coronary heart disease more frequently.
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PMID:Seven-year follow-up of cardiovascular study and maximal exercise of Chinese men. 12 87

To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 +/- 8 mm Hg) showed significant cardiac hypertrophy (44 +/- 1% increased ratio of heart weight to body weight, P less than 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 +/- 0.8 vs. 4.7 +/- 0.4 mm Hg). We evaluated cardiac function by recording left ventricular end-diastolic pressure, stroke volume (SV), and cardiac output (CO) (by electromagnetic flowmeter) during rapid alteration in venous return. Analysis of variations of stroke volume vs. left ventricular end-diastolic pressure showed that renal hypertension is accompanied by a significant decrease in ventricular performance [SV = 0.0190 + 0.0509 LVEDP - 0.0025 (LVEDP)2 + 0.0001 (LVEDP)3] compared to the normotensive group [SV = 0.0430 + 0.0644 LVEDP - 0.0040 (LVEDP)2 + 0.001 (LVEDP)3]. The alterations in stroke volume and cardiac output were associated with a lack of significant changes in the work performed at matched end-diastolic pressures. The data indicate that chronic renal hypertension is accompanied by a depression of cardiac reserve which is not revealed by measurements of cardiac output and left ventricular end-diastolic pressure at rest. This impairment in cardiac function might be related to either diminished cardiac contractility or reduced left ventricular compliance; the latter possibility is in accord with our finding of a 2-fold increase in the hydroxyproline content (P less than 0.001) and a significant decrease in the DNA concentration of ventricular tissue.
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PMID:Cardiac performance in rats with renal hypertension. 13 Oct 7

Stupor in patients with nonketotic hyperglycemia has been ascribed to hyperosmolarity, but the cause of depressed consciousness in patients with ketoacidosis has been puzzling. In this study, blood pH, serum glucose and sodium concentrations, and serum osmolality were measured in eighty-five consecutive episodes of diabetic ketoacidosis and forty-seven of nonketotic hyperglycemia. In the acidotic patients, as in those with nonketotic hyperglycemia, stupor closely paralleled hyperosmolarity and not the severity of acidemia. Indeed, the mean elevations of serum osmolarity were almost the same in the ketotic and in the nonketotic patients who were deeply obtunded. It seems likely that depression of consciousness in patients with severely uncontrolled diabetes mellitus, if not due to a nonmetabolic disorder, such as acute stroke, is attributable to hyperosmolarity, whether or not ketoacidosis is present.
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PMID:Hyperosmolar nature of diabetic coma. 23 99

In man, high doses of the "group 1" inhalation anesthetics (diethylether, cyclopropane, and fluroxene) produce relatively minor depression of ventricular function, although it is possible to depress the heart if the dose is great enough. The "group 2" drugs (halothane, methoxyflurane, etc.) produce dose-related depression in cardiac function, but reasonable caridac outputs and blood pressure can be maintained at light anethetic levels. Much the same can also be said for the intravenous barbiturates and other hypnotics. If ventilation is supported and hypovolemia avoided, large doses of the narcotic analgesics appear to produce minimal cardiac effects. The only intravenous drug which stimulates the heart is the dissociative anesthetic ketamine, and this is probably an autonomic, reflex phenomenon (as with group 1 inhalation anesthetics). Regional anesthesia and the neuromuscular blocking drugs appear to have relatively little effect on ventricular function. Most of the work in man on the effect of anesthetics has been in healthy patients or volunteers. The effects on patients with severe heart or other systemic disease may well be different. In fact, low concentrations of fluroxene have been shown to produce significant depression of stroke volume in patients with aortic vavular disease in contrast to the effects on healthy volunteers. All potent central nervous system depressant drugs possess the potential for significant cardiac depression. If such depression is undersirable in a particular patient, the only safe way to administer anesthesia is by careful titration of the dose against the best measurement of cardiac function which is available. At the present time, this would mean measuring at least direct arterial pressure, central venous pressure, and a continuous electrocardiogram. The optimal management would prpbably include recording systolic time intervals, pulmonary capillary wedge pressure, and some measure of cardiac output as well. All the skill and pharmacologic knowledge available connot substitute for vigilant monitoring and carful tiration of drug dose in the clinical situation.
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PMID:Effect of anesthetics on the heart. 24 Nov 24


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