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)

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

Amrinone was given to 14 patients with congestive heart failure as an intravenous bolus (1 mg/sec) at doses ranging from 0.5 to 3.5 mg/kg. Simultaneous determinations of cardiac index were made by thermodilution and of amrinone plasma concentration by high-performance liquid chromatography. A relationship between improvement in cardiac index and increasing plasma concentrations of amrinone was demonstrated for 13 of the 14 patients. The percentage increase in cardiac index correlated with amrinone plasma concentration (r = 0.81; p less than 0.001). Amrinone was given to four patients as an intravenous bolus dose of 1.5 mg/kg followed by a constant infusion of 10 micrograms/kg/min for 10 hr; simultaneous determinations of cardiac index and circulating levels of amrinone indicated that both declined after the initial rise. The plasma concentration of amrinone remained relatively constant during the infusion at about 1.7 micrograms/ml. In all cases, despite the relatively constant plasma levels there was a decline in cardiac index after about 4 to 5 hr of infusion, although the cardiac index remained above the baseline; during the constant infusion the cardiac index rose again and was maintained at a reasonably constant level for the last 3 hr. Seven patients received oral doses of amrinone of about 3 mg/kg, and simultaneous determinations of cardiac index and plasma concentration showed a relationship between amrinone level and rise in cardiac index (p less than 0.05). In 16 patients after amrinone orally sufficient blood samples were taken to estimate the apparent first-order terminal elimination t 1/2. The t 1/2 as estimated by log-linear regression ranged from about 3 to 15 hr; mean +/- SEM value was 8.3 (+/- 1.1) hr.
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PMID:Relationship between amrinone plasma concentration and cardiac index. 722 3

Amrinone has been shown to have therapeutic effects on bupivacaine-induced cardiovascular toxicity, but its exact effects on the heart are not well understood. This study evaluated the regional myocardial effect of amrinone on bupivacaine-induced cardiovascular toxicity in in situ beating hearts in 10 dogs using a selective coronary perfusion and sonomicrometry. In the control group, bupivacaine was administered into the left anterior descending coronary artery (LAD) for 15 min at four steps: baseline, step 1, step 2 and step 3, (calculated LAD plasma concentrations; 0, 5, 5 and 10 mu g center dot ml-1, respectively). In the amrinone group, amrinone (5 mu g center dot ml-1) was simultaneously infused at steps 2 and 3 in addition to bupivacaine infusions. Regional myocardial function of the LAD supplied area was evaluated by analysis of the left ventricular pressure-segment length loop. In the control group, systolic shortening decreased from the baseline (10.5 +/- 1.3%, mean +/- SEM) to step 3 (0.1 +/- 1.3%), and post-systolic shortening increased from the baseline (18.0 +/- 3.7%) to step 3 (52.3 +/- 5.5%) dose-dependently. In contrast, with amrinone infusion at steps 2 and 3, both variables returned to near baseline values. These results indicate that amrinone reverses bupivacaine-induced regional myocardial dysfunction.
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PMID:Amrinone reverses bupivacaine-induced regional myocardial dysfunction. 890 59