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Biomedical subjects

V C Baum

Publications and source records attributed to V C Baum.

28 records · Page 2Linked to original sources
PubMed1993

Effect of calcium channel agonist (BAY K8644) on volatile anesthetic-mediated depression in neonatal rabbit papillary muscle.

Heart muscle is dependent on the entry of calcium from the extracellular fluid to support contraction, and neonatal hearts are particularly sensitive to reductions in transsarcolemmal entry of calcium. Accordingly, this study evaluated the ability of the calcium channel agonist BAY K8644 to prevent or reverse the myocardial depressant effects of halothane or isoflurane in right ventricular papillary muscles from neonatal rabbits. The ability of BAY K8644 to reverse reductions in force (F) and dF/dt (halothane and isoflurane) or prevent reduction (halothane) was studied. Halothane decreased F to 24 +/- 2% of baseline values (p = 0.001). The addition of BAY K8644 reversed F to only 54 +/- 3% of baseline (p = 0.001 vs. baseline and p = 0.002 vs. halothane alone). Isoflurane decreased F to 20 +/- 2% of baseline (p = 0.001) with a return to 45 +/- 4% of baseline with the addition of BAY K8644 (p = 0.0001 vs. baseline and p = 0.0025 vs. isoflurane alone). With BAY K8644 in the bath prior to the addition of halothane, halothane decreased F to 38 +/- 4% of baseline (p = 0.001). dF/dt mirrored changes in F in all studies. These data show that a calcium channel agonist is only partially effective in modulating volatile anesthetic-induced depression in neonatal rabbit ventricular papillary muscle.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Progesterone potentiation of bupivacaine arrhythmogenicity in pentobarbital-anesthetized rats and beating rat heart cell cultures.

The effects of progesterone treatment on bupivacaine arrhythmogenicity in beating rat heart myocyte cultures and on anesthetized rats were determined. After determining the bupivacaine AD50 (the concentration of bupivacaine that caused 50% of all beating rat heart myocyte cultures to become arrhythmic), we determined the effect of 1-hour progesterone HCl exposure on myocyte contractile rhythm. Each concentration of progesterone (6.25, 12.5, 25, and 50 micrograms/ml) caused a significant and concentration-dependent reduction in the AD50 for bupivacaine. Estradiol treatment also increased the arrhythmogenicity of bupivacaine in myocyte cultures, but was only one fourth as potent as progesterone. Neither progesterone nor estradiol effects on bupivacaine arrhythmogenicity were potentiated by epinephrine. Chronic progesterone pretreatment (5 mg/kg/day for 21 days) caused a significant increase in bupivacaine arrhythmogenicity in intact pentobarbital-anesthetized rats. There was a significant decrease in the time to onset of arrhythmia as compared with control nonprogesterone-treated rats (6.2 +/- 1.3 vs. 30.8 +/- 2.5 min, mean +/- SE). The results of this study indicate that progesterone can potentiate bupivacaine arrhythmogenicity both in vivo and in vitro. Potentiation of bupivacaine arrhythmia in myocyte cultures suggests that this effect is at least partly mediated at the myocyte level.

Anesthesia↗
PubMed1992

Will the calcium channel agonist BAY K8644 inhibit halothane-induced impairment of calcium current?

The inhaled anesthetics impair transsarcolemmal calcium entry (ICa) in myocardial cells, although the mechanism of this interaction is not known. This inhibition of calcium entry has been implicated in the myocardial depression of the volatile anesthetics. To further characterize this interaction and to evaluate whether a calcium channel agonist could attenuate or prevent the inhibition of calcium entry, the effect of the calcium channel agonist BAY K8644 on the impairment of ICa by halothane was evaluated in single guinea pig ventricular myocytes. Calcium currents were evoked by means of the whole-cell voltage-clamp technique. Baseline peak ICa was higher in the cells exposed to 5 microM BAY K8644 (311 vs 206 pA/cm2, P less than 0.04). On exposure to 1% halothane, peak ICa was impaired to an identical degree whether or not cells were exposed to BAY K8644 (78% and 79% of baseline value). This is consistent with the suggestion that the effects of these agents on ICa are nonspecific. However, the increase in ICa suggests that appropriate calcium channel agonists might serve to ameliorate the myocardial depressant effects of halothane.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Ketamine inhibits transsarcolemmal calcium entry in guinea pig myocardium: direct evidence by single cell voltage clamp.

To clarify the direct effect of ketamine on calcium entry into myocardium, we directly measured transsarcolemmal calcium entry into single enzymatically dissociated guinea pig myocardial cells by means of the whole cell voltage clamp. Cells were studied in the presence of 0, 10(-5) M, or 10(-4) M ketamine. Peak baseline calcium current was similar in all three groups (911 +/- 92 pA, 954 +/- 66 pA, and 962 +/- 54 pA, respectively). During exposure to ketamine, peak calcium current was unchanged in the no-ketamine control group (886 +/- 74 pA) but decreased in both the 10(-5) M group (723 +/- 38 pA) and the 10(-4) M group (798 +/- 62 pA) (P less than 0.002 vs no-ketamine cells for both groups). We conclude that ketamine has a direct inhibitory effect on transsarcolemmal calcium influx in guinea pig myocardial cells.

Animals↗
PubMed1991

Excitation-contraction coupling in neonatal myocardium: effects of halothane and isoflurane.

We evaluated the effects of halothane and isoflurane on force, action potential, and staircase, an indicator of sarcoplasmic reticulum function, in right ventricular papillary muscles from 4- to 8-day rabbits using a single sucrose gap myograph at a low baseline stimulating frequency of 12 min-1. The ED50 for depression of peak force was 0.25% for halothane and 0.54% for isoflurane. Both anesthetics were more depressant to neonatal myocardium than has been reported in adult myocardium. The ratio of ED50 in neonatal myocardium to that reported in adult myocardium was similar for both anesthetics (0.42 and 0.39). Both anesthetics decreased the height of the plateau phase of the action potential by an equivalent amount but neither affected action potential duration.

Action Potentials↗
PubMed1989

Cardiac myosin isoenzyme shifts in non-insulin treated spontaneously diabetic rats.

We evaluated myocardial myosin isoform distribution in a group of diabetic BB/W rats from which insulin was withheld for varying periods in order to evaluate the time course and extent of myosin isoform shifts in these animals. Prior studies of myosin isoform distribution in diabetic rats have utilized chemically induced diabetic rats or insulin-treated BB/W rats. Following a stabilization period on insulin therapy, insulin was withheld for 9-28 days during which the animals received supplemental parenteral bicarbonate and Ringer's lactate. Left ventricular myocardial myosin isoform distribution was determined by nondenaturing pyrophosphate gel electrophoresis. We found that the normal predominance of V1 isomyosin in these rats was shifted to V3 predominance by approximately two weeks after the cessation of insulin therapy. This was significantly sooner than was seen in another study which utilized insulin treated BB/W rats, and is similar to the time course seen with chemically induced diabetic rats. In addition, the normal V1 myosin isoform distribution observed during insulin therapy and the progressive shift to the V3 isoform distribution during increasing periods without insulin suggest that this shift can be prevented with insulin alone.

Animals↗
PubMed1980

Pulsus paradoxus in a patient with tricuspid atresia and hypoplastic right heart.

Increased inspiratory right ventricular filling with a consequent shift of the ventricular septum to the left, thereby decreasing left ventricular filling, has been suggested as a mechanism of pulsus paradoxus. We recently saw a patient with tricuspid atresia and hypoplastic right ventricle who developed pulsus paradoxus. His course may help clarify the contribution of this mechanism.

Cardiac Tamponade↗
PubMedDate not supplied

Abnormal cardiac function after exercise in insulin-dependent diabetic children and adolescents.

We evaluated the cardiac response to dynamic exercise in a group of otherwise healthy insulin-dependent older children and adolescents and in a nondiabetic control group by postexercise echocardiography. Both groups had similar left ventricular function at rest. After exercise we found abnormalities in the indicators of systolic function, fractional shortening (0.37 vs. 0.43) and rate-corrected velocity of circumferential fiber shortening (2.80 vs. 3.35 circumferences/s). In addition, we found an association of flattened interventricular septal motion with finger contractures in the diabetic subjects. Echocardiographic abnormalities in asymptomatic young diabetic adolescents can be elucidated by postexercise echocardiography. Postexercise echocardiography is a noninvasive procedure that can easily be done in the adolescent population and is useful for evaluating subclinical cardiomyopathy.

Adolescent↗