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)

Approximately 20% of patients who receive left ventricular assist devices (LVADs) for refractory cardiac failure after open heart surgery have had complications of right ventricular failure. To evaluate this problem in the diseased heart we simulated an LVAD in the operating room by bypassing and unloading the left ventricle with the heart-lung machine before routine open heart surgery. Right ventricular function was assessed in 12 patients with preoperative left ventricular ejection fractions of less than 0.55 (poor left ventricular function) (mean +/- SEM 0.40 +/- 0.03) and 10 patients with ejection fractions greater than 0.55 (normal left ventricular function) (0.63 +/- 0.02). Measurements before and during left ventricular bypass in the normal left ventricular function group revealed no change in cardiac output (from 5.7 +/- 0.6 to 5.8 +/- 0.4 liters/min), with a decrease in right ventricular end-diastolic pressure (from 8 +/- 2 to 6 +/- 1 mm Hg). However, in the poor left ventricular function group, cardiac output was increased significantly during left ventricular bypass from 4.5 +/- 0.2 to 5.3 +/- 0.4 liters/min and right ventricular end-diastolic pressure was decreased significantly from 13 +/- 2 to 8 +/- 2 mm Hg. During bypass there were significant reductions in mean pulmonary arterial pressure from 17 +/- 3 to 10 +/- 2 mm Hg in the normal left ventricular function group and from 27 +/- 3 to 12 +/- 2 mm Hg in the poor left ventricular function group. These measurements reflect passive changes in pulmonary pressures due to reductions in left ventricular filling pressure during left ventricular bypass.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Right ventricular function in an operating room model of mechanical left ventricular assistance and its effects in patients with depressed left ventricular function. 406 72

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

The effects of amrinone (5.3 X 10(-4) M) on isometric contraction and K+-induced contracture force of right ventricular muscle isolated from normal cats (n = 6) and cats in right ventricular failure (RVF, n = 6), 3-14 days after partial pulmonary artery ligation, were studied. Peak isometric contractile force (Po) and maximal rate of force development (dP/dt) of RVF muscles (1.38 +/- 0.21 g/mm2; means +/- SEM, and 11 +/- 1 g/s/mm2, respectively) were significantly lower than normal muscles (2.46 +/- 0.41 g/mm2, p less than 0.025, and 24 +/- 3 g/s/mm2, p less than 0.005, respectively). Duration of contraction (DC) was significantly longer in RVF muscles (442 +/- 32 ms) than in normal muscles (361 +/- 11 ms, p less than 0.025). Times to peak twitch force (TTP) and peak K+-induced contracture force (Pc) of RVF and normal muscles were not different. Amrinone increased Po and dP/dt significantly in normal muscles (+78 +/- 24%; means +/- SEM; p less than 0.01, and +53 +/- 17%, p less than 0.025, respectively), but not RVF muscles (+11 +/- 16% and +8 +/- 19%, respectively). TTP and DC of normal muscle were unchanged by amrinone, whereas TTP was unchanged while DC was shortened (-12 +/- 3%, p less than 0.025) in RVF muscle. Amrinone relaxed Pc similarly and significantly in normal (-28 +/- 7%, p less than 0.005) and RVF (-26 +/- 4%, p less than 0.025) muscles. These results suggest that part of amrinone's salutary action in the failing heart occurs through modification of myocardial relaxation.
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PMID:Amrinone relaxes potassium-induced contracture of failing right ventricular muscle of cats. 618 12

Right ventricular failure during acute pressure overload has been attributed to ischemia which occurs when maximal coronary vasodilation is achieved so that further increases in myocardial blood flow cannot occur. To test the hypothesis that coronary vasodilator reserve is exhausted during acute right ventricular pressure overload, right and left ventricular myocardial blood flow was measured in 14 awake dogs during progressive pulmonary artery occlusion; coronary vasodilator reserve was tested by infusion of adenosine (4 microM/kg per min) before and during pulmonary artery occlusion. Right ventricular myocardial blood flow rose from 0.77 +/- 0.09 ml/min per g (mean +/- SEM) during control conditions to 1.69 +/- 0.27 ml/min per g during moderate pulmonary artery occlusion (P less than 0.01). With further pulmonary artery occlusion to cause increased right ventricular end-diastolic pressure and decreased aortic pressure, a selective decrease in myocardial blood flow to the right ventricular subendocardium was observed, and the right ventricular subendocardial-to-subepicardial blood flow ratio fell from 1.36 +/- 0.14 to 0.77 +/- 0.06 (P less than 0.05). With restoration of mean aortic pressure to control levels, right ventricular systolic pressure increased, right ventricular end-diastolic pressure decreased, and the right ventricular subendocardial-to-subepicardial ratio increased to 1.36 +/- 0.18 (P less than 0.01). Adenosine infusion during pulmonary artery occlusion in five dogs caused an increase in mean right ventricular blood flow (1.11 +/- 0.10 to 2.25 +/- 0.30; P less than 0.05). This increase was most marked in the outer layers but, nevertheless, was also significant in the subendocardium. These data indicate that acute severe right ventricular pressure overload may be associated with right ventricular subendocardial hypoperfusion, even when coronary vasodilator reserve is not exhausted.
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PMID:Transmural right ventricular blood flow during acute pulmonary artery hypertension in the sedated dog. Evidence for subendocardial ischemia despite residual vasodilator reserve. 709 29

Pressure in the right ventricle (RV) as well as the right atrium (RA) and pulmonary artery (PA) were measured in 80 patients with catheter-tip micromanometers and evaluated to determine if the pressures are compatible with the concept of RV diastolic suction. In 40 patients with normal PA pressure, minimal RV diastolic pressure that occurred during early filling, was negative (-2 +/- 0.3 mm Hg) (mean +/- SEM). In 29 patients with PA hypertension, minimal RV diastolic pressure during expiration also was negative (-2 +/- 0.7 mm Hg). In 11 patients with right ventricular failure, however, minimal RV diastolic pressure was positive (9 +/- 2 mm Hg). These results indicate that the human right ventricle, in the absence of failure, has a negative early diastolic pressure, which may reflect RV diastolic suction.
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PMID:Can the human right ventricle create a negative diastolic pressure suggestive of suction? 728 4

Sildenafil is a selective inhibitor of phosphodiesterase type 5 (PDE-5). Its chronic administration has been shown to improve exercise capacity, World Health Organization functional class, and haemodynamics in patients with symptomatic pulmonary arterial hypertension (PAH). There is however, no data describing the clinical consequences of sudden cessation of sildenafil treatment. In this series, 9 patients with NYHA Class II-IV PAH who were stable on 2 months of sildenafil monotherapy, had their sildenafil ceased to accommodate a 2-week washout period, required for enrollment in research involving an endothelin receptor antagonist. Six minute walk distance (SMWD) and clinical assessments were performed before cessation of sildenafil, and again 2 weeks later. Over the course of this 2-week washout period, 6 of the 9 patients reported increased breathlessness and fatigue, 1 of these was hospitalized with worsening right heart failure. The SMWD fell in 6 patients, with falls of greater than 100 m recorded in 4 patients. This was accompanied by a worsening of NYHA Class from 2.5 +/- 0.2 to 3.1 +/- 0.1 (mean +/- SEM, p = 0.01). These data indicate that sudden cessation of sildenafil monotherapy, in patients with PAH, carries with it a significant and unpredictable risk of rapid clinical deterioration. We recommend that if sildenafil needs to be ceased, it would be more prudent to consider concurrent vasodilator therapy before the gradual cessation of sildenafil.
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PMID:Clinical deterioration after sildenafil cessation in patients with pulmonary hypertension. 1918 60