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

The hemodynamic and metabolic changes, during coronary occlusion and during coronary perfusion with non-oxygenated solution, were studied in anesthetized dogs. Coronary perfusion with non-oxygenated Tyrode's solution was performed through a cannula inserted into the left circumflex coronary artery. Left ventricular peak systolic and end-diastolic pressure (LVSP and LVEDP) were measured, and peak LV-dp/dt/IIP calculated. Stroke volume was measured, and the changed of the local myocardial segment length were recorded by a strain gauge arch sutured on that portion of the myocardium perfused through the left circumflex coronary artery. The efflux of lactic acid into the venous blood from the myocardium perfused through the left circumflex coronary artery was calculated. After 10 sec of coronary occlusion, LVSP, SV, and peak LV-dp/dt/IIP declined; LVEDP elevated and a systolic bulge appeared on the local myocardial segment length curve. There was almost no change in these parameters during 3 min of perfusion with non-oxygenated solution. The efflux of lactic acid was more marked during the perfusion with non-oxygenated solution than during coronary occlusion. The delay of the depression of cardiac function during perfusion with the non-oxygenated solution could be related partly to the "wash-out" of metabolites, such as lactic acid, accumulated in the anoxic myocardium.
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PMID:Cardiac function under myocardial ischemia. 88 51

In 100 consecutive patients with acute cerebrovascular accident, due to cerebral thrombosis in 72, cerebral hemorrhage in 12, embolus in 6, and subarachnoid hemorrhage in 10, there were 90 who had electrocardiographic abnormalities during the first three days after admission, compared to 50% in a control group. The patients with cerebrovascular accident had a 7- to 10-fold higher incidence of ST segment depression, prolonged Q-Tc interval and atrial fibrillation, and a 2- to 4-fold higher incidence of T wave inversion, conduction defects, premature ventricular beats and left ventricular hypetrophy. Patients who died had a 2-, 3- and 5-fold higher incidence of electrocardiographic evidence of recent myocardial infarction, atrial fibrillation and conduction defects than those who survived, but these changes occurred in only 5, 21 and 14% of all patients, and other electrocardiographic changes could not be correlated with mortality. During the first three days after admission 29 patients had elevation of serum enzymes which may be derived from cardiac muscle, particularly CPK, which was increased 6-fold, compared to 2-fold increases in HBDH, GOT, and LDH. Only 5 of these patients had electrocardiographic evidence of recent myocardial infarction. Patients with elevated serum CPK had a 2-fold higher incidence of ST segment depression, T wave inversion, conduction defects and atrial fibrillation than those with normal CPK, and a mortality of 66%, compared to 30%. Of 41 patients who died, 49% had elevated serum CPK, compared to 15% of 59 patients who survived. These differences were significant (P less than 0.01). Serum CPK was more frequently helpful than the electrocardiogram in evaluating the extent of cardiac damage and in predicting mortality. Patients with acute cerebrovascular accident should have repeated evaluation of serum CPK and the ECG, and be monitored for arrhythmias.
Stroke
PMID:Electrocardiographic changes and myocardial damage in patients with acute cerebrovascular accidents. 89 40

Retro-placental haemorrhage comes from rupture of patent utero-placental arteries which are neither sclerosed nor thrombosed. This applies whether the form of haemorrhage is minor (simple depression found when the placenta is examined) or grave with utero-placental apoplexy (with complete detachment of the placenta and syndrome of shock). The method by which the arteries rupture depend on the intensity and excessive duration of uterine contractions: --moderate; normal uterine contractions give rise to a prolonged blockage of the return circulation, whereas the arterial flow has not stopped. Rupture occurs because the distended utero-placental arterial wall bursts under the insult of raised pressure during the uterine contraction; --intense; these anomalies come from total blockage, both veinous and arterial, and the arterial rupture is due to anoxaemic necrosis of the utero-placental arterial wall. The rupture of the utero-placental arterial wall, which is normally very fragile because it has no elasticity in its musculature, gives the explanation for the histogenesis of retro-placental haemorrhages.
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PMID:[Intimate mechanism of premature separation of the normally inserted placenta]. 90 73

Haemodynamic and respiratory effects of i.v. morphine (10 mg/70kg body weight) were studied in 10 adults with unimpaired circulatory function. There were significant changes in mean arterial pressure, mean heart rate, respiratory rate and tidal volume, at 10-, 30- and 60-min intervals. Transient changes in mean total systemic resistance and mean stroke volume were also seen at 10 min. The results strongly suggest a peripheral vasodilator response to morphine. Respiratory depression was not demonstrated.
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PMID:Some circulatory and respiratory effects of morphine in patients without pre-existing cardiac disease. 91 92

The importance of certain features of the classification of diseases of the His system for the purpose of planning and conducting permanent cardiac stimulation (PCE). Stability of the conduction disturbance is essential in classifying low stroke volume syndromes as due to sporadic, frequent or habitual disturbance, and the frequency of stimulation should be geared to that of the syndrome. Rehabilitation during PCE also has its psychological side. Indeed, this almost always surpasses the physical side in importance and is dependent on the patient's job, social and economic standing, and the size of his family, as well as on his own emotional blaance and psychological reactions. About 70% of subjects behave in a normal way (rational acceptance of reality and a correct balance between emotiveness and reason), 20% display anxiety and depression, and the remainder show a typical form of euphoria; in many cases, this is clearly hypomaniacal.
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PMID:[Problems of rehabilitation during permanent cardiac stimulation]. 91 38

Records of 11 postmenopausal parkinsonism patients were evaluated in comparison with those of 11 postmenopausal depression patients. None had a history of encephalitis, stroke, drug-induced or toxic extrapyramidal disorders, or active bleeding within six months before admission. There was no significant differences between the two groups with regard to time interval from menopause to onset of symptoms, height, weight, or age at first admission. Both groups showed normal height, hemoglobin, hematocrit, and erythrocyte counts. Parkinsonism patients were underweight and had a shorter interval from menopause to onset of symptoms (12.4 +/- 1.9 vs. 16.8 +/- 2.5 yr.). These findings are compatible with the hypothesis that in parkinsonism, hereditary predisposition to positive body iron balance may be associated with alteration of the blood-brain barrier in parkinsonism.
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PMID:Postmenopausal Parkinsonism: brain iron overload? 93 Jul 48

To determine if depressed myocardial function contributes to the reported decrease in cardiac performance at high altitude, six chronically instrumented, unsedated goats were studied before, during, and after 2-wk exposure to hypobaric hypoxia (PaO2 44 mmHg). Undistorted ventricular pressure wave form was obtained from a miniature transducer implanted in the left ventricular cavity. The relationship between (dP/dt)/28P and P was extrapolated to obtain Vmax as an index of myocardial function. With beta sympathetic blockade (practolol) and pacing to reproduce heart rates, Vmax was uniformly and significantly depressed (P less than 0.01) during chronic hypoxia, and returned to control values following descent to low altitude. Likewise, stroke volume following saline infusion was decreased at high altitude and returned to control values following descent. Acute relief of hypoxia at high altitude by administration of 100% oxygen by mask did not reverse the depressed Vmax. These findings indicate that chronic hypobaric hypoxia produces a depression of myocardial function which is reversible by chronic but not acute relief of hypoxia.
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PMID:Depressed myocardial function in the goat at high altitude. 96 4

The characteristics of left ventricular ejection (velocity and extent of wall shortening) can be analysed in relation to the appropriateness of the matching between afterload and the level of inotropic state (contractility), as modified by the preload (Frank-Starling) reserve. In the normal left ventricle if the preload is not allowed to compensate for an acute increase in afterload, or if the limit of preload reserve is reached, velocity (V CF) and stroke volume will diminish; that is an afterload mismatch occurs. This acute mismatch can be corrected by administration of a positive inotropic agent. In normal conscious animals and in man the ejection phase measures in the basal state (such as ejection fraction, and VCF corrected for heart size) encompass a relatively narrow range, and when the normal heart adapts successfully to a chronic pressure or volume overload such measures remain normal per unit of muscle. These findings provide the basis for their use in detecting a depressed basal level of inotropic state, even in the presence of certain valvular lesions. When there is mild depression of the basal inotropic state, enhanced preload and dilatation can allow full compensation of VCF, but acute pressure loading can allow detection of the the reduced preload reserve by inducing a substantial fall in stroke volume and VCF. When the basal inotropic state is greatly reduced, a mismatch between afterload and contractility, expressed as reduced VCF or ejection function, will become evident in the basal state even if the afterload is normal. Any increase in aortic pressure will then cause a sharp reduction in stroke volume or VCF. Also, under these circumstances therapeutic afterload reduction with agents such as nitroprusside can increase velocity and extent of wall shortening, and the cardiac output, providing the preload is maintained. The concept of afterload mismatch with limited preload reserve provides a framework for understanding the behavior of the normal or depressed ventrile and how it can operate on a "descending limb" of function. It helps to explain why measures of the ejecting phase (which are sensitive to afterload) appear to be more reliable than isovolumic phase indices (which are relatively insensitive to afterload) for detecting depressed basal inotropic state. Finally, the concept allows for interpretation of the responses observed in the clinical setting to acute and chronic increases and decreases in loading conditions on the left ventricle.
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PMID:The concept of afterload mismatch and its implications in the clinical assessment of cardiac contractility. 96 66

Serial invasive and noninvasive (systolic time interval) measurements of left ventricular performance were obtained in six healthy volunteers during general anesthesia employing the following sequence: thiopental induction, succinylcholine (prior to endotracheal intubation), and halothane--100 per cent oxygen at 1.25 and 1.75 MAC. Heart rate (HR), mean pulmonary arterial "wedge" pressure (PAW) and mean systemic arterial pressure (MAP) were measured continuously; cardiac index and systolic time intervals (STI's) were measured during each intervention. At both levels of halothane, MAP and stroke work index decreased (both P less than 0.02), while HR and systemic vascular resistance did not change. At 1.25 MAC halothane PAW was unchanged, but at 1.75 MAC PAW increased from 8 +/- 4 (SD) to 11 +/- 5 torr (P less than 0.02). Preload was altered at 1.25 MAC by administration of 600-1,000 ml lactated Ringer's solution; PAW increased from 9 +/- 4 to 17 +/- 3 torr (P less than 0.01). At 1.75 MAC halothane, volume expansion increased PAW in a similar manner, but the resultant ventricular function curve was depressed compared with 1.25 MAC halothane. In additon, at each level of halothane anesthesia, the ventricular function curve was depressed compared with results obtained in awake normal subjects. Afterload was altered at 1.25 MAC halothane by infusion of phenylephrine sufficient to raise MAP by 30 per cent. This intervention resulted in a greater depression of cardiac performance than that observed at 1.75 MAC halothane alone. Although alterations in STI's were directionally similar to changes observed in invasive hemodynamic measurements, STI's were sensitive to acute alternations in loading conditions. It is concluded that the levels of halothane commonly employed for general anesthesia significantly depress left ventricular performance in normal subjects, as evidenced by abnormal responses to alterations in preload and afterload, and that STI's should not be employed for routine measurement of left ventricular performance during anesthesia unless both the afterload and the preload on the myocardium are known.
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PMID:Alterations of normal left ventricular performance by general anesthesia. 98 77

1 The circulatory effects of labetalol 25 mg intravenously in six patients during 1% halothane anaesthesia were studied. 2Labetalol caused a marked decrease in arterial pressure and a consistent but modest (20%) decrease in cardiac output. Heart rate was slowed and stroke volume did not change significantly. Central venous pressure increased and peripheral resistance decreased. 3 Increasing the halothane concentration of 3% led to marked myocardial depression as evidenced by reduced cardiac output and increased central venous pressure with increasing arterial hypotension. 4 Labetalol may be a suitable drug for controlling induced hypotension under general anaesthesia, although high concentrations of halothane should be used with care.
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PMID:Cardiovascular effects of labetalol during halothane anaesthesia. 99 Jan 59


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