Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results from recent studies suggest that the endogenous opioid beta-endorphin (beta-E) is related to pain modulation. Therefore, plasma beta-E levels were studied in 23 patients with essential hypertension (EH) and in 7 patients with coronary artery disease (CAD) during asymptomatic ischemic events and in 5 patients with CAD during symptomatic ischemic events. Blood samples for beta-E were taken at the moment of silent ST depression, pointed with alarm by the real time ECG monitor "Q Med Monitor" (USA). Control blood samples were taken under the same conditions without ischemic events. Control plasma beta-E levels were significantly higher (p less than 0.01) in patients with EH as compared to that in both groups of patients with CAD (22.9 +/- 4.0 vs 7.0 +/- 1.9 and 4.5 +/- 1.6 pmol/l). At the time of silent ischemia, beta-E showed a significant increase in patients with EH (+10.1 +/- 2.1 pmol/l, p less than 0.01) and in patients with CAD (+10.7 +/- 1.3 pmol/l, p less than 0.05) as compared to the control levels. However, plasma beta-E showed no increase (+1.0 +/- 0.6 pmol/l, p greater than 0.1) during symptomatic ischemia as compared to the control levels. Thus, differences in the circulating levels of beta-E may be associated with the presence or absence of pain during myocardial ischemia.
 ...
PMID:[Plasma beta-endorphin level in "silent" myocardial ischemia during Holter ECG monitoring]. 140 1

We correlated the effects of high volumes of K+ cardioplegic solution on myocardial structure and function in 16 dogs following open-heart surgery. Eight animals received high volume potassium cardioplegic solution (25 cc/kg body weight, every 30 min) during 90 min of ischemic arrest (HVK-C group). The others received sufficient cardioplegic solution to maintain complete electrical arrest as defined by voltage monitoring criteria (VM group). Cardiac index (CI), left ventricular stroke work index (LVSWI), and myocardial contractility (dp/dt) were determined before arrest and after 90 min of ischemia and 45 min of reperfusion. Biopsies were taken for EM ultrastructure and ATP estimation. Morphometric analysis of EM micrographs found increased volume of damaged mitochondria (DMR) (p less than 0.025), damaged myofibrils (DMF) (p less than 0.001), intermyofibrilar edema (p less than 0.005), T-tubule and sarcoplasmic reticulum (p less than 0.05) in the HVK-C group. Left ventricular (LV) function was more depressed in animals receiving HVK-C. CI decreased by 1.8 +/- 0.4 l/min/square meter (p less than 0.01), LVSWS fell by 3.3 +/- 0.8 gm-m/beat/Kg (p less than 0.01), dp/dt decreased by 684 +/- 135 (p less than 0.0025). ATP decreased by 26% in HVK-C and by 12% in VM group (0.1 less than p less than 0.05). Structural damage (scores of injured volume of mitochondria and myofibrils) correlated with post-ischemic depression of LV function (Cardiac output and myocardial contractility), r = -0.72 and -0.66 (p less than 0.001 and 0.004).
 ...
PMID:Morphometric analysis on myocardial injury related to the use of high volume potassium cardioplegic solution during ischemic arrest. 140 9

The TQ segment depression and the ST segment elevation in the electrocardiogram during acute myocardial ischemia are caused by flow of injury current. This current flows between potential gradients across the ischemic border. The initial change is the TQ segment depression, which is brought about by a positive shift of the resting membrane potential of the ischemic cells. After 1 to 2 minutes ST segment elevation develops as a consequence of the action potential shortening and loss of plateau. The loss of potassium ions and ensuing extracellular K+ accumulation is the major cause of the alterations in action potential. After 15 to 20 minutes of ischemia, electrical cell-to-cell uncoupling occurs and interrupts the flow of injury current (decrease of TQ segment depression and ST segment elevation), producing conduction block.
 ...
PMID:[Elevation of the ST-segment in the electrocardiogram and ischemic injury current]. 141 Sep 97

Liver and spleen phagocytic clearance of blood-borne microparticulate tissue debris and products of intravascular coagulation after trauma and surgical injury is an important mechanism to limit the deposition of debris in the pulmonary vascular bed. Plasma fibronectin (pFn) modulates this clearance process. We evaluated the effect of a localized peripheral ischemia and reperfusion injury on liver and spleen phagocytic function. Male rats (250 to 350 g) underwent 4 hours of tourniquet-induced bilateral hindlimb ischemia, followed by 18 hours of reperfusion after release of the tourniquet. Rats subjected to ether anesthesia alone or anesthesia followed by groin incision without ischemia were the control and sham groups, respectively. Reticuloendothelial (RE) phagocytic function was assessed at 15 minutes and 18 hours after the start of reperfusion by the in vivo liver and spleen removal of blood-borne iodine 125 (125I)-test microparticles, which were coated with gelatin (denatured collagen) to enhance their interaction with pFn. Liver and spleen particle uptake in control and sham rats was similar. In contrast, after 4 hours of ischemic injury with 15 minutes of reperfusion, we observed a 30% to 40% decrease (p less than 0.05) in liver and spleen particle uptake as compared with sham controls with partial restoration of this removal mechanism by 18 hours. This depression in liver and spleen phagocytic function was associated with a significant (p less than 0.05) increase in the deposition of the 125I-test particles in the lung. RE depression was not due to a deficiency of pFn; indeed, a marked elevation (588 +/- 12 micrograms/mL versus 1,083 +/- 40 micrograms/mL) of pFn was observed by immunoassay over the 18-hour reperfusion interval. Comparative bioassay of humoral (opsonic) versus cellular (Kupffer's cell) activity revealed that Kupffer's cells in livers from controls or ischemia-reperfusion rats exhibited normal phagocytic function when incubated in plasma harvested from either control or 4-hour ischemic rats. The opsonic activity of plasma harvested after ischemia and reperfusion was also more than adequate, consistent with the immunoassay analysis. Thus, the impaired liver and spleen clearance mechanism after peripheral ischemia and reperfusion injury did not appear to be due to either a macrophage cellular deficit or a lack of pFn. This clearance depression may be mediated by splanchnic malperfusion, which is known to develop after peripheral ischemia and reperfusion and associated soft tissue injury.
 ...
PMID:Liver and spleen phagocytic depression after peripheral ischemia and reperfusion. 141 24

Clinicians often fail to detect intraoperative ischemic electrocardiographic (ECG) changes when viewing oscilloscopes. Automated ST-segment monitors promise to increase the detection of such ECG changes. We investigated the capacity of two commercially available ST-segment monitors to detect intraoperative myocardial ischemia in patients at high risk for developing intraoperative myocardial ischemia during vascular and other noncardiac procedures. The ST-segment monitors were compared with two reference monitors: (a) printed eight-lead ECGs, as interpreted by a cardiologist, and (b) the presence of segmental wall motion abnormalities and thickening abnormalities detected by transesophageal echocardiography (TEE). We also examined the capacity of the printed ECG to diagnose myocardial ischemia when compared with TEE. We studied 44 patients who underwent TEE, printed multilead ECG, oscilloscope monitoring of leads V5 and II, and measurement of ST-segment deviation from the baseline using an automated Hewlett Packard ST-segment device. The sensitivities for the Hewlett Packard system were 40% for TEE-diagnosed myocardial ischemia and 75% for ECG-diagnosed ischemia. Comparison of the printed ECG with TEE revealed that ST-segment changes in the printed ECG, as analyzed by a cardiologist, were 25% sensitive and 62% specific for the detection of TEE-diagnosed myocardial ischemia. When T-wave inversions were added to ST-segment depression as a criterion for the diagnosis of myocardial ischemia by the printed ECG, the sensitivity of ECG for the detection of intraoperative myocardial ischemia, as determined by TEE, was 40% and specificity was 58%. Twenty-three of the 44 patients were simultaneously monitored in leads I, II, and V5 with an automated Marquette ST-segment monitor.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:A comparison of methods for the detection of myocardial ischemia during noncardiac surgery: automated ST-segment analysis systems, electrocardiography, and transesophageal echocardiography. 141 32

The anti-ischemic effect of a 4% proxanol solution (intravenous injection in a dose of 10 ml/kg 60 min after occlusion) was compared with that of a salt solution in experimental acute ischemia of dog myocardium, induced by partial occlusion of the anterior descending branch of the left coronary artery. Overall estimation of the effect of SAS infusion has demonstrated that this drug has a beneficial effect on hemorheology (decreases blood viscosity and vascular resistance, increases coronary blood flow), stabilizes oxygen supply of the myocardium and lowers the extent of its ischemia-induced damage (eliminates ST segment depression). However, the cardiodepressive action of proxanol does not allow for compensation of the ischemia-induced decrease in myocardial contractility and pump function of the heart.
 ...
PMID:[The effect of the surface-active substance proxanol on the ischemic myocardium]. 142 46

The association of verapamil with halothane causes ischaemic-like myocardial dysfunction. Using an isolated rat heart model perfused with a radiolabelled fatty acid (123I-labelled iodohexadecenoic acid) as a sensitive marker of ischaemia this study investigated whether or not this dysfunction is of ischaemic origin. Hearts were perfused with a control solution or with solutions containing either 1% of halothane or 150 ng ml-1 of verapamil or the association of 0.75% halothane + 120 ng ml-1 verapamil. The ischaemic group was perfused at a reduced perfusion rate (-50%). Intracellular fate of IHA was assessed, and its esterification ratio computed. Ischaemia and the drugs induced a similar depression of haemodynamics. The esterification ratio in the ischaemic group was significantly higher (0.723 +/- 0.04) than in controls (0.0526 +/- 0.03) and than in the treated groups: halothane (0.533 +/- 0.06), verapamil (0.411 +/- 0.027) or the association halothane+verapamil (0.408 +/- 0.05), suggesting a non-ischaemic origin for the dysfunction caused by halothane-verapamil.
 ...
PMID:Comparative effects of halothane associated with verapamil and ischaemia on myocardial metabolism in isolated perfused rat hearts. 142 13

We studied 12 patients with stable effort angina in a randomized, double-blind, cross-over and placebo-controlled trial to compare the different antianginal efficacy of "acute" and "chronic" (after reaching a steady-state level) gallopamil therapy. Efficacy was assessed using treadmill exercise testing (Bruce protocol) after a 50 mg single-dose and at the end of a nine-dose course of 50 mg of gallopamil (given three times a day). Three daily exercise tests were performed the first, second, fifth and eighth day of the study protocol at 8, 12 and 16 h. Four hours after a single-dose of gallopamil 50 mg both angina-free exercise time and time to 1 mm ST segment depression increased by a mean value of 78 s (p < 0.003) and 53 s (p < 0.03), respectively, with respect to placebo values. Under steady-state conditions exercise time and time to 1 mm ST segment depression increased by a mean value of 59 s (p < 0.009) and 46 s (p < 0.015), respectively, 4 h after the last dose. The duration of the anti-ischemic effects was no longer present after 8 h for both treatment schedules. Furthermore no significant differences were observed on parameters of ischemia after a single dose as compared to "chronic" therapy. The results of this study reveal that, in accordance with the pharmacodynamic properties of the drug, the anti-ischemic efficacy of 50 mg of gallopamil remains for approximately 4 h. Reaching a steady-state condition does not imply a prolongation of the anti-ischemic effect.
 ...
PMID:Comparison of acute and steady-state conditions of gallopamil therapy in stable angina pectoris. 142 94

The goal of cardiac rehabilitation is to optimize function through attention to the patient's medical needs, risk factors for recurrent events, physical reconditioning, and psycho-social needs. Medical needs include beta-adrenergic blocking agents and aspirin unless contraindicated, angiotensin converting inhibitors for left ventricular dysfunction, and relief of residual ischemia. Smoking, lipid abnormalities, physical inactivity, and hypertension remain important predictors of reinfarction and death and must be controlled. Obesity must be addressed because it exacerbates these problems. Therefore, the principles of behavior change should be applied to help patients control their risk factors and adopt healthy lifestyles. Smoking cessation and appropriate dietary behaviors can be adopted by the patient while in the hospital. Physical reconditioning can also begin with twice-daily exercises. After discharge from hospital and after an initial submaximal exercise evaluation, the patient will benefit from three sessions per week of outpatient cardiac rehabilitation for six to eight weeks. These sessions should last about an hour and raise the patient's heart rate as much as 30 beats per minute. Along with physical reconditioning, the cardiac rehabilitation program provides an opportunity to address risk factor modification, return to work, return to sexual activity, management of depression and anxiety, and the presence of risk factors in the patient's family. The patient should attend reinforcing sessions every three months for the first year and as necessary after that to control risk factors and reinforce the necessity for physical fitness.
 ...
PMID:Cardiac rehabilitation 1992. 143 5

Tissue levels of inorganic phosphate (iP-) and lactate (lac) increase during cerebral ischemia and cortical spreading depression (SD). Since cell membranes become leaky during these insults, iP- and lac were expected to leak into the extracellular space (ECS). In order to find out whether this occurs or does not, a microdialysis (MD) fiber was implanted into the cortex of anesthetized rats and extracellular lactate (lac(e)) and extracellular iP- (iPe-) were determined during various insults. Extracellular lactate increased to about the same extent during ischemia and SD. In contrast, iPe- increased during ischemia but not during SD. Instead, iPe- started to rise after SD and reached its maximum about 45 min later. The distinct pattern of iPe- in comparison to lac(e) during the above mentioned insults points to a qualitative difference of the underlying mechanisms: whereas lac appears within the ECS at any stressful situation, elevation of iP- within the ECS indicates depletion of energy stores in parallel to the lack of control of ion homeostasis.
 ...
PMID:Extracellular changes of inorganic phosphate are different during spreading depression and global cerebral ischemia of rats. 143 48


<< Previous 1 2 3 4 5 6 7 8 9 10