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)

Little information is available regarding left ventricular (LV) functional recovery from treadmill exercise. Accordingly, we used a recently described ultrasound index of LV function, the isovolumic index (IVI), to assess LV performance before and after exercise in 9 normal middle-aged men and 12 male patients with coronary artery disease (CAD). The IVI was measured at rest and at each minute for at least 10 min after completion of the Bruce protocol; normals had maximal tests and CAD patients had symptom limited studies. At rest the IVI value for normals was 26.2 +/- 2.1 (SD) and it was 43.5 +/- 8.2 for CAD patients (p less than 0.001); isovolumic times were longer in CAD patients (137 +/- 26 vs. 89 +/- 8 ms, p less than 0.001). The rate of recovery from exercise did not differ between normals and CAD patients. We conclude that despite depression of resting LV performance in CAD patients, the time course of functional recovery of the left ventricle from exercise is not different from normal subjects.
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PMID:Left ventricular functional recovery from exercise in normals and patients with coronary heart disease. 356 49

Addition of diltiazem (0.0, 0.95, 2.5 or 7.5 microM) to isolated working rat hearts before and during ischemia, produced a concentration-dependent increase in recovery of contractile function. Recovery of post-ischemic pressure-rate product showed a strong relationship with depression of pre-ischemic pressure-rate product, primarily from decreased heart rate before ischemia and increased pressure development following reperfusion. Increased recovery in treated hearts was associated with higher ATP and adenine nucleotide levels (ADN), but no relationship was observed between energy levels and degree of recovery of function or concentration of diltiazem. Hearts made ischemic for 20 min without reperfusion had increased ATP and decreased lactic acid accumulation when treated with 7.5 microM diltiazem. The results indicate contractile-dependent mechanisms of action of diltiazem in global ischemic hearts which can only be partly explained by preservation of ATP and ADN, but also are associated with reduced lactic acid accumulation.
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PMID:Effects of diltiazem upon globally ischemic rat hearts. 362 15

Transient global amnesia has been explained by epileptic mechanisms or transient ischemic attacks affecting the hippocampus. None of these two mechanisms appear likely. The animal experimental phenomenon entitled spreading depression of cortical electrical activity (SD) or spreading depression of Leao has been implicated in migraine pathogenesis and may be relevant to transient global amnesia. In experimental animals, SD in the hippocampus causes a temporary functional ablation lasting minutes to hours with full functional recovery. Glutamate, which is present in large amounts in the hippocampus, may experimentally elicit spreading depression, and strong emotional events may possibly liberate glutamate and bring about this reaction in human patients.
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PMID:Leao's spreading depression in the hippocampus explains transient global amnesia. A hypothesis. 370 31

Magnesium-diltiazem cardioplegia was evaluated in the intact, perfused rat heart to determine whether the joint administration of these agents would adversely affect myocardial contractile and high-energy phosphate recovery following intermittent, normothermic global ischemic arrest. Sequential metabolic and functional analyses were performed on isolated perfused rat hearts during each phase of the experimental protocol: control (10 min), normoxic cardioplegia (10 min), intermittent global ischemic arrest (two 15-min periods separated by 2 min infusion of the normoxic cardioplegic perfusate), and normoxic postischemic control reperfusion (60 min). Four different cardioplegic solutions were evaluated: 30 mM KCl, 30 mM KCl with 2 mg diltiazem/liter, 20 mM MgCl2, and 20 mM MgCl2 with 2 mg diltiazem/liter. Myocardial phosphatic metabolite levels and intracellular pH were analyzed nondestructively in the intact hearts by phosphorus-31 NMR spectroscopy. Corresponding measurements of peak left intraventricular pressure, rate of peak pressure development (dP/dt), and contraction frequency were performed at the midpoint during each 5-min interval of 31P NMR signal averaging. Magnesium plus diltiazem-treated hearts were distinguished from all other groups by a marked delay in postischemic functional recovery consisting of a prolonged depression in contractility (34% of control, P less than 0.01) that persisted throughout the first 50 min of postischemic reperfusion. Diltiazem in combination with magnesium cardioplegia was detrimental to postischemic functional recovery, despite a rapid restoration of high-energy phosphate stores. The apparent adverse interactive effects of excess magnesium and diltiazem suggest that elective ischemic arrest with magnesium cardioplegia in combination with diltiazem may be contraindicated clinically. The mechanistic basis and drug specificity of this response require further clarification. The present findings appear to exclude ATP and PCr production, and structural causes as the basis for the observed aberrant functional recovery from global ischemia of magnesium plus diltiazem-arrested hearts.
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PMID:Sustained postischemic cardiodepression following magnesium-diltiazem cardioplegia. 371 20

Acute myocardial infarction causes depression of left ventricular function, but the capacity of the ventricle to recover from such an injury remains unknown. This problem was explored by measuring left ventricular function in eight intact conscious dogs before, 1 hr after, and again 6-8 days after myocardial infarction. Acute myocardial infarction was produced using a technique which entails gradual inflation over an average period of 1 hr of a balloon cuff previously implanted around the left anterior descending coronary artery. Occurrence of anterior wall infarction was detected electrocardiographically and later confirmed by postmortem examination. Left ventricular function was evaluated from the relationship between left ventricular developed pressure (left ventricular peak systolic pressure minus left ventricular end-diastolic pressure) and left ventricular end-diastolic pressure during transient aortic occlusion with a balloon catheter. Left ventricular function curves were obtained by plotting left ventricular-developed pressure at increasing left ventricular end-diastolic pressures up to 50 mm Hg. Acute myocardial infarction caused marked depression of left ventricular function measured 1 hr after onset of infarction, but 1 wk later all eight animals showed improvement with return of function toward the control levels. A small but significant descending limb was noted at left ventricular end-diastolic pressures above 35 mm Hg. Quantitatively, the descending limb was similar before, 1 hr after, and 1 wk after myocardial infarction. Hemodynamic data revealed evidence of left ventricular failure in all animals, but variability in individual hemodynamic parameters was noted. The data indicate that the marked depression of left ventricular function observed immediately after experimental acute myocardial infarction undergoes considerable resolution within 1 wk, but that functional recovery remains incomplete.
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PMID:Experimental myocardial infarction. II. Acute depression and subsequent recovery of left ventricular function: serial measurements in intact conscious dogs. 540 8

Initiation of 60 min ischaemia to rat isolated hearts produced a depression in developed tension and heart rate. Subsequent reperfusion caused a greatly exacerbated creatine phosphokinase (CPK) efflux and limited functional recovery. Sulphinpyrazone (100 ng ml-1 and 1 microgram ml-1) significantly reduced CPK release, particularly after reperfusion, the lower concentration being more effective. A reduction in the mechanical depression during ischaemia and enhanced recovery after reperfusion were seen only with 100 ng ml-1 sulphinpyrazone. Heart rate and coronary perfusion pressure were unaffected by drug treatment. The reduction in reperfusion-induced CPK efflux by 100 ng ml-1 sulphinpyrazone was maximal when the drug was present throughout the perfusion period although some protection was evident when sulphinpyrazone was present either during ischaemia or reperfusion only. An enhanced recovery in contractility was seen only when the drug was present throughout all phases of perfusion. It is suggested that sulphinpyrazone exerts a direct protective effect on the heart particularly during reperfusion. The degree of protection is critically dependent on the concentration of sulphinpyrazone.
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PMID:A direct protective effect of sulphinpyrazone on ischaemic and reperfused rat hearts. 648 90

Spontaneous recovery of function occurs in the syndrome of hemisensory neglect in monkeys. We produced this syndrome in 13 macaques by unilateral operative resection of the frontal polysensory association cortex. Using standardized behavioral measures, we documented severe acute neglect and followed the course of its improvement. Using the 2-deoxy[14C]glucose autoradiographic method, we studied animals in the acute phase of neglect and found decrements in local glucose utilization in subcortical structures, but not in cortical regions with known frontal connections. After spontaneous behavioral recovery, mild local glucose utilization decrements remained, but only in nucleus medialis dorsalis of the thalamus. The findings suggest that acute behavioral symptoms are based on widespread depression of neuronal activity in uninjured structures with synaptic relations to damaged cortex, and that return of neuronal activity in those structures is accompanied by restitution of behavioral function.
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PMID:Recovery from unilateral neglect. 688 82

The insulinoprivic influence of acute severe streptozotocin diabetes on liver regeneration in rats was evaluated by determining liver weights as well as hepatocyte and Kupffer cell functional capacities. Functional capacities were assessed by bromosulfophthalein uptake for hepatocytes and carbon phagocytosis for Kupffer cells. Evaluation immediately after partial hepatectomy revealed a 66% reduction of liver mass, a 63% decrease in hepatocyte bromosulfophthalein removal, and a 65% decline in Kupffer cell carbon phagocytosis. Per cent recovery at 48-hr posthepatectomy was considerably greater for carbon phagocytosis than for bromosulfophthalein removal by regenerating livers. This apparent difference in functional recovery was likely due in part to enhanced non-Kupffer cell carbon phagocytosis. No significant differences of the three regeneration indices were noted for untreated streptozotocin-diabetic rats compared to nondiabetic animals. However, insulin administration to fasted streptozotocin diabetics significantly stimulated liver regeneration above that of untreated fasted rats and almost equivalent to that of pair-fed animals. Fasted rats had in general slower liver regeneration than pair-fed animals as expected. Furthermore, insulin administration to fasted nondiabetic rats after partial hepatectomy caused severe hypoglycemia and resulted in a further depression of liver regeneration.
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PMID:Hepatocyte and Kupffer cell functions during liver regeneration in streptozotocin-diabetic rats. 703 Sep 5

Twenty-one immature piglets (< 3 weeks old) underwent 30 minutes of aortic clamping with hypocalcemic glutamate/aspartate blood cardioplegia. Six piglets underwent hyperoxemic cardiopulmonary bypass and blood cardioplegia without preceding hypoxemia (control). Fifteen piglets became hypoxemic (oxygen tension about 25 mm Hg) for up to 2 hours by decreasing ventilator fraction of inspired oxygen to 6% to 7% before cardiopulmonary bypass. Of these, six piglets underwent 5 minutes of abrupt hyperoxemic uncontrolled reoxygenation by starting cardiopulmonary bypass at oxygen tension of about 400 mm Hg before they received oxygen tension of about 400 mm Hg blood cardioplegia. Nine others underwent controlled cardiac reoxygenation by starting cardiopulmonary bypass at ambient oxygen tension (about 25 mm Hg) followed 5 minutes later by 30 minutes of cardiopulmonary bypass at normoxemic oxygen tension (about 100 mm Hg) before raising oxygen tension to about 400 mm Hg. Myocardial function after cardiopulmonary bypass was evaluated from end-systolic elastance by conductance catheter, oxidant damage was estimated by measuring transcoronary conjugated diene levels to detect lipid peroxidation, and antioxidant reserve capacity was determined by measuring malondialdehyde produced from myocardium incubated with the oxidant t-butylhydroperoxide. Hyperoxemic cardiopulmonary bypass and blood cardioplegia preserved myocardial function and produced no oxidant damage in nonhypoxemic piglets. In contrast, uncontrolled reoxygenation at oxygen tension about 400 mm Hg, followed by blood cardioplegia, resulted in marked conjugated dienes production (42 +/- 4* vs 3 +/- 1) A233 nm/min/100 g during blood cardioplegic induction, reduced antioxidant reserve capacity malondialdehyde at 4 mmol/L t-butylhydroperoxide; 1342 +/- 59* vs 958 +/- 50 nmol/g protein) and caused profound myocardial dysfunction; end-systolic elastance recovered only 21% +/- 2%* despite a blood cardioplegic regimen that was cardioprotective in nonhypoxemic piglets. Conversely, controlled cardiac reoxygenation reduced lipid peroxidation (conjugated dienes production was 2 +/- 1**), restored antioxidant reserve capacity (malondialdehyde at 4 mmol/L t-butylhydroperoxide; 982 +/- 88**), and allowed near-complete (83 +/- 8%**) functional recovery. We conclude that reoxygenation of the hypoxemic immature heart by initiating conventional hyperoxemic cardiopulmonary bypass causes oxidant damage characterized by lipid peroxidation, reduced antioxidant reserve capacity, and results in functional depression that nullifies the cardioprotective effects of blood cardioplegia. These changes can be reduced by starting cardiopulmonary bypass at the ambient oxygen tension of the hypoxemic subject and delaying subsequent reoxygenation until blood cardioplegic induction by controlled cardiac reoxygenation (*p < 0.05 vs control; **p < 0.05 vs uncontrol reoxygenation) and analysis of variance.
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PMID:Studies of hypoxemic/reoxygenation injury: with aortic clamping. XII. Delay of cardiac reoxygenation damage in the presence of cyanosis: a new concept of controlled cardiac reoxygenation. 747 78

Local cerebral lesions may cause depression of function in remote areas of the brain presumably by a transneural mechanism; it has been called "diaschisis". In the present study, to investigate the relationship between motor function and "diaschisis" regional brain blood flow in hypertensive right putaminal hemorrhage was studied in 33 patients (mean age, 55 years; 22 men, 11 women). The hematoma was treated conservatively in 8 patients, aspirated stereotaxically in 9 patients, and evacuated through a craniotomy in 16 patients. The regional blood flow in the right motor cortex and the left cerebellar hemisphere was measured by a single photon emission CT with N-isopropyl-p- (123 I) iodo-amphetamine intravenous injection method, and was evaluated by the RI count on early image/the decay-corrected RI count on delayed image (E/D) value. The time during which regional brain blood flow was measured ranged from 29 to 35 days from the onset. There was a positive correlation between the grade in the motor function in the subacute stage and the regional blood flow in the right motor cortex and the left cerebellar hemisphere. There was also a positive correlation between the Barthel index in the chronic stage (mean follow-up periods: 40 months) and the regional blood flow in the right motor cortex and the left cerebellar hemisphere. The results of the present study suggest that in right putaminal hemorrhage the flow reduction in areas remote from the primary lesion, i.e., "diaschisis", may reflect not only the degree of functional abnormalities of the internal capsule, but also the possibility of functional recovery.
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PMID:[Diaschisis in right putaminal hemorrhage: correlation with motor function]. 784 7


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