Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe constriction of the suprarenal abdominal aorta of 3-kg rabbits to 3.7+/-0.2 mm2 and maintenance of a daily sodium intake of 10 mE q by infusion of 0.9% sodium chloride resulted in a progressive increase in central ear arterial pressure to 106+/-3 (SEM) mm Hg (control=79+/-1). This was accompanied by a progressive increase in left ventricular end-diastolic pressure to 22+/-2 mm Hg (control=3+/-1), plasma renin activity to 21+/-5 ng of angiotensin/hour per ml (control=5+/-1), plasma aldosterone concentration to 99+/-23 pg/ml (control=14+/-4), and plasma sodium concentration to 142+/-1 mEq/liter (control=136+/-1). Urinary excretion of sodium decreased to 3.9+/-0.7 mEq/day and marked fluid retention occurred. We also found that these changes were accompanied by a decrease in hematocrit to 24+/-2% (control=40+/-1), formation of 36+/-9 ml of fluid in the thoracic cavity, 33+/-9 ml of ascites, pulmonary congestion and edema, hepatic congestion, and enlargement and hypertrophy of both the left and right ventricles. All rabbits died of ventricular failure at a time that was partly related to the degree of aortic constriction and that ranged from 2 to 12 days. The model we have established is chronic, highly reproducible, easy to produce, and inexpensive, and resembles the clinical syndrome of right and left congestive heart failure in man. Furthermore, the studies provide evidence for an important role of the renin-angiotensin-aldosterone system in the fluid retention that leads to pulmonary and systemic venous congestion after suprarenal aortic constriction.
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PMID:The renin-angiotensin-aldosterone system in rabbits with congestive heart failure produced by aortic constriction. 83 74

Antithrombogenicity of pneumatic ventricular assist devices (VAD) for postoperative ventricular failure was evaluated macroscopically and microscopically in relation to VAD flow, coagulation parameters, and other potentially thrombogenic factors. A total of 12 sack type pumps were used in nine cases after operations for ischemic heart diseases (4 cases), valvular diseases (3 cases), and congenital anomalies (2 cases). Durations of pumping of each device ranged from 18 hours to 37 days (mean, 10.9 days). The clinical protocol for antithrombogenicity of the device indicates maintenance of ACT around 150 sec and keeping VAD flow more than 2.0 L/min. In our clinical series, however, heparin was given only in most cases to maintain activated clotting times (ACT) at 120-140 sec for the first three postoperative days. Minute ringlike thrombi were noted at connectors of cannula in two pumps after low flow (1.5 L/min) pumping for 5 days or after frequent on/off studies for weaning. A small thrombus (2 X 2 mm) and fine granular thrombi were noted on actuating bladders in two pumps that were used with frequent on/off studies or in a patient with severe sepsis during VAD pumping. Other VAD pumps were macroscopically free of thrombus. SEM analyses on surfaces of actuating bladders demonstrated mild to moderate platelet adhesions, which were correlated with platelet count, but not with other coagulation parameters including platelet agglutination and pumping duration. In cases with leucocytosis during VAD uses, leucocyte adhesion was noted as well without correlation to the coagulation parameters.
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PMID:Antithrombogenicity of ventricular assist devices for postoperative myocardial dysfunction. 319 22

Isolated cat right ventricular papillary muscles were used to study the effects of antibodies with high affinity for ouabain and acetyl strophanthidin on myocardium exposed to these cardioactive steroids. Antibodies with average intrinsic affinity constants for ouabain and acetyl strophanthidin of the order of 10(8) M(-1) were raised in rabbits challenged by repeated injection of a conjugate of ouabain covalently linked to a poly D,L-alanyl derivative of human serum albumin. Effects were assessed in terms of time-course and extent of inotropy reversal, influence of experimentally induced ventricular failure, digitalis-antibody concentration relations, influence of digitalis-antibody complex on response to additionally added digitalis, and relation of antibody effects on digitalis-induced automaticity and contracture to reversal of inotropy. Specific antibody (but not control antibody) in 1.1-1.5-fold molar excess over cardioactive steroid concentrations blocked positive inotropic effects of ouabain and acetyl strophanthidin, and gradually reversed established contractile effects of these agents with a mean time for half-reversal of ouabain-induced inotropy of 124+/-6 (SEM) min and 37+/-3 min for half-reversal of acetyl strophanthidin-induced inotropy. Papillary muscles from cats with right ventricular failure induced by chronic pulmonary artery constriction responded similarly. Both normal and failing muscles returned to but not below levels of contractility existing before cardioactive steroid exposure, and time for half-reversal of inotropy by antibody was significantly shorter than time for half-reversal after removal of ouabain or acetyl strophanthidin by muscle bath washout alone. Presence of ouabain- or acetyl strophanthidin-antibody complex did not alter the myocardial contractile response to subsequently added cardioactive steroids. Spontaneous automaticity occurring as a toxic response to ouabain or acetyl strophanthidin in eight muscles was rapidly reversed by specific antibody at a time when positive inotropic effects were still fully manifest. Early contracture was also reversed by specific antibody. These studies provide further support for the concept that cardiac glycoside-specific antibodies are capable of reversing established cellular effects of cardioactive steroids.
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PMID:Reversal of ouabain and acetyl strophanthidin effects in normal and failing cardiac muscle by specific antibody. 459 13