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

To clarify the influence of propranolol-and particularly its heart-rate effects-on myocardial ischemia, coronary hemodynamics and metabolism were studied in 15 patients utilizing a protocol to control heart rate. Ten patients had significant coronary narrowing (CAD) and 5 were normal. Systemic pressure, coronary sinus blood flow (CSBF), left ventricular oxygen utilization (LVVO2), ST Segment depression, and myocardial lactate extraction were measured before and after propranolol (10 mg IV), at rest, during pacing-induced tachycardia stress. Propranolol-related reduction in CSBF and LVVO2 at rest was reversed when heart rate was controlled in both patient groups. Propranolol failed to alter heart-rate threshold, tension-time index (TTI), CSBF, or LVVO2 at angina in the CAD patients. Likewise, ischemic-type ST depression, decreases in lactate extraction, and coronary resistance were unchanged compared to values observed during tachycardia stress before propranolol. In normal coronary patients, propranolol also produced no significant change in LVVO2 or coronary resistance when its heart rate effects were controlled. These data imply that a major coronary and metabolic influence of propranolol relates to changes occurring secondary to its influence on heart rate. Furthermore, this agent's anti-ischemic effect is not prominent during tachycardia stress suggesting that this stress test may be clinically useful in patients taking propranolol.
Cathet Cardiovasc Diagn 1977
PMID:Effects of propranolol on coronary hemodynamic and metabolic responses to tachycardia stress in patients with and without coronary disease. 83 33

This study compares the inotropic action of morphine sulfate and ketamine hydrochloride on isolated canine right ventricular trabeculae. The heart was removed from 19 mongrel puppies weighing 5 to 9 kilograms and placed in Krebs-Ringer bicarbonate solution. The bathing solution contained 1.3 mM. of Ca2+ and was bubbled with a gas mixture of 95 per cent oxygen and 5 per cent carbon dioxide. At Lmax (i.e., the peak of isometric force-length curve) morphine even in large concentrations (up to 1 mg. per milliter) produced no significant direct inotropic effect. At the lower concentrations tested there was a minor but not significant increase in contractile performance, whereas at the highest concentration used there was a minor but not significant depression in contractility. In these same muscles lower concentrations of ketamine had a significant positive inotropic action, but a concentration of 200 mug per milliliter, which is approximately equimolecular to 1 mg. per milliliter of morphine sulfate, caused a profound depression in contractile performance. In the presence of a beta-blocking agent and in reserpine-pretreated muscles, low concentrations of ketamine, which had only a positive inotropic action in the normal muscles, now caused depression of contractile performance. The positive inotropic action of ketamine is thus indirect and mediated via adrenergic influences. At each concentration studied the direct inotropic action of ketamine was exclusively negative. Because of this bimodal inotropic action seen when adrenergic mechanisms are intact, we conclude that caution must be exercised when ketamine is given to patients previously treated or still under the influence of drugs having adrenolytic properties. Caution is also necessary when ketamine is used in patients having diminished cardiac adrenergic reserves as in congestive heart failure.
J Thorac Cardiovasc Surg 1976 Jul
PMID:Comparison of the inotropic action of morphine and ketamine studied in canine cardiac muscle. 93 49

In order to evaluate the duration of the biologic effects of propranolol after the drug was discontinued, we evaluated a variety of noninvasively determined hemodynamic parameters. Significant depression was found in the heart rate (18 per cent), cardiac output (13 per cent) (determined echocardiographically), and the triple product of blood pressure, heart rate, and systolic ejection time (16 per per cent) during administration or propranolol (200 mg. per day) to 9 normal volunteers. Significant depression of these parameters was present 12 hours after discontinuing the drug. By 12 hours, serum propranolol levels had returned 90 per cent toward their base line; however, at the same time, the heart rate and cardiac output had returned only 19.4 and 14.3 per cent toward their base-line values, and the triple product had returned 41 per cent toward its baseline. By 36 hours no biologic effect was seen. Thus if propranolol were discontinued 2 days prior to cardiac surgery, no significant biologic effect would remain to complicate the patient's postoperative course.
J Thorac Cardiovasc Surg 1976 Jul
PMID:Persistence of biologic activity after disappearance of propranolol from the serum. 93 53

The effects of aprindine and lignocaine (lidocaine USP) were compared on intracellularly recorded potentials from normal canine conducting tisues. Only aprindine produced marked depression of the maximum rate of rise (Vmax) of action potentials elicited at normal cycle lengths (1000 ms). Both compounds, however, produced enhanced depression of Vmax at short cycle lengths or at short S1-S2 coupling intervals at normal membrane resting potential. Both lignocaine and aprindine shorten the action potential duration (APD) and effective refractory period (ERP) but increase the EPR/APD ratio. These effects are easily reversible upon perfusion with drug-free solution only in the case of lignocaine.
Cardiovasc Res 1976 Mar
PMID:Intracellular electrophysiological alterations in canine cardiac conducting tissue induced by aprindine and lignocaine. 93 91

Despite experimental evidence that myocardial depression resulting from rapid transfusion of ACD blood (citrate binds ionic calcium) is avoidable by simultaneous calcium administration, most hypovolemic patients receive calcium either after transfusion or not at all. Similar iatrogenic hypocalcemic myocardial depression occurs in normovolemic patients with known myocardial damage who are dialyzed for acute uremia when ACD blood prime is used at high initial flow rates (350 c.c. per minute) and when dialysis is performed against low calcium dialysate (2.5 mEq. per liter or less). This study tests the hypotheses that (1) rapid transfusion of as little as one unit of CPD blood causes a significant reduction in ionized calcium, (2) the depressive effect of CPD blood is significant and similar to that of ACD blood, (3) rapid blood transfusion (ACD or CPD) is safe if calcium is given simultaneously, (4) addition of calcium to the extracorporeal heparinized blood prime used in dialysis prevents initial depression, and (5) hemodynamic instability during dialysis is prevented when the dialysate is normocalcemic. From the results of our study, we made the following conclusions: (1) Ionized calcium is reduced significantly by rapid transfusion of CPD blood; (2) acute myocardial depression noted with CPD blood is similar to that previously observed with ACD blood and is prevented during transfusion of either type of blood by simultaneous calcium administration; and (3) hemodialysis in patients who have had cardiac surgery is safe if calcium is added to blood prime and dialysate is made normocalcemic.
J Thorac Cardiovasc Surg 1976 Oct
PMID:Acute clinical hypocalcemic myocardial depression during rapid blood transfusion and postoperative hemodialysis: a preventable complication. 96 82

This investigations evaluates the effects of anticoagulants on platelet function. Fresh human blood from 40 nonmedicated volunteers was anticoagulated with 4.3 units per milliliter heparin and/or acid-citrate-dextrose (ACD) solution 1:9. Retention of platelets from whole blood on glass beads was performed by the method of Bowie. Platelet retention of heparinized blood averaged 88.1 +/- S.E. 1.5 per cent; ACD platelets averaged 24.6 +/- S.E. 2.8 per cent. Platelet retention with citrate-phosphate-dextrose (CPD) and ethylenediaminetetraacetic acid (EDTA) yielded 26.0 +/- S.E. 3.9 per cent and 19.1 +/- S.E. 7.5 respectively. The addition of ACD to heparinized blood decreased platelet retention (19.7 +/- S.E. 3.1 per cent). The addition of heparin to ACD or CPD blood did not alter the original decreased retention. Calcium added, even in excess, to blood containing heparin and ACD did not reverse the depressed retention (29.3 +/- S.E. 4.6 per cent). The substitution of CPD gave similar results. With mixtures of separately collected ACD and heparininzed blood, depression of platelet retention was directly proportional to the amount of ACD blood present. Altering the pH of the ACD blood did not affect its depressed retention of platelets. Neutralizing heparinized blood 50 per cent with protamine or Polybrene also significantly depressed platelet retention 34.6 +/- S.E. 5.8 per cent and 35.5 +/- S.E. 4.0 per cent, respectively. Neither protamine nor Polybrene had any effect upon ACD blood. These data indicate that anticoagulants may play a significant role in the depressed platelt function observed during and following extracorporeal circulation.
J Thorac Cardiovasc Surg 1976 Nov
PMID:The contribution of anticoagulants to platelet dysfunction with extracorporeal circulation. 97 14

Verapamil (Isoptin) caused a dose-dependent peripheral vasodilation, increase in myocardial contractility, and tachycardia in the anaesthetized dog. Propranolol pretreatment blocked the cardiac stimulation following verapamil but the vasodilation was unaltered. Inflation of a thoracic aortic balloon prevented the fall in intravascular pressure and reduced the tachycardia and positive inotropic responses. These experiments suggest that clinical doses of verapamil cause peripheral vasodilation which leads to a sympathetic reflex induced increase in heart rate and myocardial contractility. Verapamil also had a direct myocardial depressant action which became evident at doses above the range used clinically. The drug increased the PR interval in conscious dogs for up to 60 minutes. This effect was partly mediated through cholinergic stimulation and partly through a direct depression on atrioventricular conduction.
Cardiovasc Res 1976 Nov
PMID:Cardiovascular action of verapamil in the dog with particular reference to myocardial contractility and atrioventricular conduction. 99 Nov 62

Pulmonary arterial end-diastolic and mean right atrial pressures were compared in 25 patients with acute myocardial infarction and in one patient with unstable angina. No consistent relationship was observed between these pressures. Simultaneous ventricular function curves relating the stroke work of each ventricle to its respective filling pressure were constructed on 34 occasions, dextran infusion or diuresis being used to alter the filling pressure. The curves from each ventricle were described mathematically by a quadratic (parabolic) function as well as by a straight line function and then compared by canonical correlation analysis. Alterations in the left ventricular function curves occurred with and without depression or right ventricular function curves. These hemodynamic measurements demonstrate that acute myocardial infarction can alter the relationship between left and right ventricular function.
Cathet Cardiovasc Diagn 1976
PMID:Comparison of left and right ventricular function in acute myocardial infarction. 99 Dec 62

Hemodynamics of 12 patients with tetralogy of Fallot were monitored during the first 72 hours after surgical repair. Total immediate repair in 5 patients was followed after 24 hours by a greater decrease in cardiac index than that observed in the group of 4 patients with previous palliative shunt (minus 25 plus or minus 6 vs. minus 1 plus or minus 7 per cent, p smaller than 0.025). This difference disappeared after 48 hours, and the short-term follow-up periods of these two groups were equally smooth. Six patients with pulmonary stenosis requiring the placement of an outflow patch had higher right ventricular filling pressures (after 24 hours 13.8 vs. 10.8 mm. Hg, p smaller than 0.025; 2 to 4 weeks later 9.6 vs. 5.5 mm. Hg, p smaller than 0.05), suggestive of a persistent right ventricular depression. This ventricular depression must be attributed to the induced pulmonary insufficiency and to the presence of akinetic areas. Both these factors should therefore be carefully minimized during the surgical procedure.
J Thorac Cardiovasc Surg 1975 Jul
PMID:Cardiac function early after repair of tetralogy of Fallot. 109 36

Blood coagulation screening profiles were performed in 512 patients who underwent open-heart surgery with extracorporeal circulation. Severe coagulation disorders were found in 29 (5.6 per cent) patients. The most common abnormalities were low one-stage prothrombin time (PT) activities and impaired whole blood clot retractions. In the majority of patients the discrepancy between low PT's and normal or only slightly depressed factor II, V, VII, and X activities was explained by the presence of an inhibitor of the extrinsic system. Eight patients demonstrated the heparin rebound phenomenon but only 1 bled excessively. The pattern of severe hepatic dysfunction was found in 4 and severe depression of vitamin K-dependent factors due to oral anticoagulants in 2. Two had disseminated intravascular coagulation. Seventeen patients with normal coagulation screening profiles bled excessively postoperatively. Of these, 2 had moderate thrombocytopenia associated with a marked platelet functional abnormality. Revision of the wound in 13 revealed a surgical hemostatic defect and in 2 the cause of bleeding could not be determined.
J Thorac Cardiovasc Surg 1975 Jul
PMID:The hemostatic mechanism after open-heart surgery. I. Studies on plasma coagulation factors and fibrinolysis in 512 patients after extracorporeal circulation. 115 4


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