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Biomedical subjects

C Hollmann

Publications and source records attributed to C Hollmann.

35 records · Page 2Linked to original sources
PubMed1994

Chronic exposure to cyclosporine affects endothelial and smooth muscle reactivity in the rat aorta.

Chronic exposure to cyclosporine affects vascular reactivity. Experiments were designed to characterize the endothelium-dependent and endothelium-independent vascular reactivity of rats exposed to oral cyclosporin A (CyA). Two subsets of rats (n = 6) were treated with CyA (20 mg/kg/day) and olive oil (cyclosporine vehicle), respectively, for a period of 8 weeks. Aortic rings (4-5 mm) were suspended for isometric force measurement in organ chambers containing Krebs Ringer solution (37 degrees C, 95% O2, 5% CO2). The maximal endothelium-dependent relaxation to cumulative doses of acetylcholine was significantly decreased in the CyA-treated aortic rings compared to olive oil-treated ones (data expressed as percent of initial contraction; CyA, 50% +/- 3% versus olive oil, 37% +/- 7%; p < 0.05). However, endothelium-dependent relaxations to histamine and adenosine diphosphate and endothelium-independent relaxation to sodium nitroprusside were not affected in both groups. An endothelium-dependent contraction to serotonin and aggregating platelets were observed in the CyA group, but not in the control group. The endothelium-independent contraction to norepinephrine was enhanced in the CyA group (CyA ED50, log -7.66 +/- 0.18 mol/L versus olive oil ED50, log -7.01 +/- 0.11 mol/L; p < 0.01). These experiments suggest that chronic exposure to cyclosporine A could contribute to augmenting vascular tone by (1) decreased release of endothelial relaxing factor mediated by muscarinic receptors, (2) increased production of endothelium-related constricting factor mediated by serotoninergic receptors, and (3) greater vascular smooth muscle sensitivity to circulating catecholamine.

Acetylcholine↗
PubMed1994

A preliminary study of the usefulness of the Behavior Assessment Systems for Children in the evaluation of mental health needs in a Head Start population.

122 parents and 18 teachers rated Head Start children on the preschool version of the Behavioral Assessment System for Children. Parents tended to rate their children as having greater problem scores than did their teacher, but both ratings, when compared to general norms, were within normal limits. Low to moderate correlations were found for the same scales on Parent and Teacher forms. Teachers rated children in the center program as having fewer problems than their home-based peers, while parents evaluated center children as having better adaptive behavior than children in the home-based program. Boys had more clinical problems than girls, while girls were rated as showing more adaptive behavior than boys. The usefulness and need for further research on this assessment are mentioned.

Attention Deficit Disorder with Hyperactivity↗
PubMed1993

Effects of pressure and duration of hyperkalemic infusions on endothelial function.

Infusions of crystalloid hyperkalemic cardioplegic solutions (CHCSs) are known to impair endothelium-dependent coronary relaxation. This impairment might also be influenced by high perfusion pressure and duration of CHCS infusion. To verify this hypothesis, we designed experiments to study the influence of pressure and duration of CHCS infusion as modulating factors in CHCS-related endothelial impairment. Isolated hearts of Sprague-Dawley rats were studied in a Langendorff apparatus for coronary endothelial function. Hearts (n = 6) were exposed to four different CHCSs containing 12, 24, 40, or 100 mmol/L of potassium chloride (KCl). Endothelial and smooth muscle functions were respectively tested by infusion of 5-hydroxytryptamine (1 x 10(-6) mol/L) and sodium nitroprusside (1 x 10(-5) mol/L) before and after CHCS perfusion. In group I (n = 24), 37 degrees C CHCSs were perfused at 80 cm H2O of pressure for 30 minutes. In group II (n = 24), the same CHCSs were perfused at 160 cm H2O for 30 minutes. In group III (n = 18), CHCSs containing 24, 40, and 100 mmol/L of KCl were infused at 160 cm H2O for 10 minutes. In all groups, response to sodium nitroprusside was unaltered by CHCS infusion, indicating that smooth muscle function was preserved. However, in group II, 5-hydroxytryptamine-induced vasodilation was significantly impaired in hearts perfused with CHCS containing 24 mmol/L of KCl or more, suggesting endothelial damage. This study demonstrates that, in addition to KCl concentration, pressure and duration of infusion are two major determinants in CHCS-mediated endothelial damage.

Animals↗
PubMed1993

Effects of University of Wisconsin solution on endothelium-dependent coronary artery relaxation in the rat.

University of Wisconsin (UW) solution has been reported to enhance myocardial preservation in heart transplantation. To evaluate the effects of UW solution on coronary artery endothelial function, we designed experiments to compare UW solution with a standard crystalloid hyperkalemic cardioplegic solution (CHCS). Isolated rat hearts were studied in a modified Langendorff apparatus for coronary endothelial function. Groups 1 and 2 were perfused with 4 degrees C CHCS (24 mmol/L of KCl) and UW solution, respectively, for 10 minutes at a pressure of 80 cm H2O, whereas group 3 underwent warm ischemia for 10 minutes. Groups 4 and 5 were perfused with and stored for 4 hours in cold (4 degrees C) CHCS and UW solution, respectively. Group 6 underwent 4 hours of topical cooling (4 degrees C) without any cardioplegic perfusion. All groups had 6 hearts each. Endothelium-dependent relaxation and endothelium-independent relaxation of the coronary arteries were tested by infusing 5-hydroxytryptamine (5HT) (10(-6) mol/L) and sodium nitroprusside (10(-5) mol/L), respectively, before and after perfusion with and storage in one of the two cardioplegic solutions. The coronary vasodilatation induced by 5HT and sodium nitroprusside was not altered in hearts perfused with (group 1) or perfused with and stored in CHCS (group 4). Coronary flow increase after 5HT infusion was significantly decreased in hearts perfused with (group 2) (before, 35% +/- 10%; after, 13% +/- 10%; p < 0.01) or perfused with and stored in UW solution (group 5) (before, 34% +/- 5%; after, -5% +/- 12%), indicating severe endothelial dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1993

The role of preservation solutions in coronary endothelial damage during cold storage.

The effects of cold storage and type of preservation solution on coronary endothelial function are not well understood. Experiments were designed to evaluate coronary endothelial-dependent relaxation after a 4-hr cold (4 degrees C) storage in different preservation solutions. Isolated rat hearts were studied in the Langendorff apparatus for coronary endothelial function. After 30 min of stabilization, hearts were arrested with a 10-min perfusion of 4 degrees C crystalloid hyperkalemic cardioplegic solution (CHCS) containing 24 mmol/L of KCl and stored for 4 hr in the following preservation solutions: CHCS, Krebs-Ringer's solution (KR), 0.9% NaCl (NS), and University of Wisconsin solution (UW). A fifth group was perfused and stored in UW solution. Endothelial-dependent and independent coronary artery vasorelaxation were tested, respectively, by infusing 5-hydroxytryptamine (5-HT) (1 x 10(-6) mol/L) and sodium nitroprusside (SNP) (1 x 10(-5) mol/L) before and 30 min after the storage period. In hearts stored in CHCS and KR, the coronary artery flow increase to 5-HT and SNP infusion were not significantly affected. However, in hearts preserved with NS and UW solutions, 5-HT coronary response was significantly decreased, indicating endothelial dysfunction. In addition to these findings, coronary flow increase to SNP infusion was decreased in the group perfused and stored with UW, suggesting smooth muscle damage. These experiments suggest that 4-hr cold storage in NS or UW impairs endothelial-dependent coronary relaxation in the isolated rat heart model.

Adenosine↗
PubMed1993

[Effect of different solutions of preservatives on the endothelial function of coronary arteries in rats].

The effects of cold storage and type of preservation solution on coronary endothelial function are not well established. Experiments were designed to evaluate coronary endothelial-dependent relaxation after a 4-hour cold (4 degrees C) storage in different preservation solutions. Rat hearts, mounted in the Langendorff apparatus, were arrested with a 10-minute perfusion of 4 degrees C crystalloid hyperkaliemic cardioplegic solution (CHCS) (KCl 24 mEq/l) and stored for 4 hours in the following preservation solutions: CHCS (n = 6), Krebs-Ringer solution (KR) (n = 6), 0.9% NaCl (NS) (n = 6) and the University of Wisconsin solution (UW) (n = 6). A fifth group (n = 6) was perfused and stored in UW solution. Endothelium-dependent and independent coronary artery vasorelaxations were respectively tested by infusing 5-hydroxytryptamine (5-HT) (10(-6) mol/l) and sodium nitroprusside (SNP) (10(-5) mol/l) before and after the storage period. In hearts stored with CHCS or KR, coronary artery flow increase to 5-HT and SNP infusions were not significantly affected. However, in hearts preserved with NS or UW solutions, 5-HT coronary response was significantly decreased, indicating endothelial dysfunction. In addition to these findings, coronary flow increase to SNP infusion was decreased in the group perfused and stored with UW, suggesting smooth muscle dysfunction. These experiments suggest that 4-hour cold storage in NS or UW impairs endothelial-dependent coronary relaxation in the isolated rat heart model.

Adenosine↗
PubMed1991

Beneficial effects of volatile anesthetics on decrease in coronary flow and myocardial contractility induced by oxygen-derived free radicals in isolated rabbit hearts.

Oxygen-derived free radicals have been implicated in reperfusion injury whereas volatile anesthetics have been shown to enhance myocardial recovery during reperfusion. To explore the mechanism by which these agents improve myocardial recovery, we measured the effect of volatile anesthetics on the free radical-induced reduction in left ventricular pressure (LVP), coronary flow, and endothelium-dependent dilation induced by acetylcholine (Ach). Isolated rabbit hearts were perfused in a Langendorff apparatus. Isovolumetric LVP and coronary flow were measured throughout the study. Oxygen-derived free radicals were produced by the electrolysis (direct current of 0.6 mA) of the perfusate. The following volatile anesthetics were used: halothane 0.5 or 1.0%, isoflurane 0.7 or 1.4%, and enflurane 1.0 or 2.0%. Oxygen free radicals induced a significant decrease in systolic LVP and coronary flow. Pretreatment of the heart with enflurane 1.0 or 2.0%, halothane 1.0%, or isoflurane 0.7% attenuated the effect of the free radicals on both systolic LVP and coronary flow. Free radicals reduced the dilating response induced by 0.1 microM Ach with or without addition of volatile anesthetics. These data suggest that the volatile agents have beneficial effects on the free radical cell damage pathway and that this protection is not related to the preservation of endothelium-dependent dilation.

Anesthetics↗
PubMed1991

Electrophysiologic effects of bupivacaine in the isolated rabbit heart.

To assess the direct electrophysiologic effects of bupivacaine, we examined the spontaneous sinus rhythm and induced rapid and premature atrial and ventricular pacing in 11 isolated rabbit hearts perfused in the Langendorff apparatus with varying concentrations (designated by []) of bupivacaine (control, n = 2; 0.3 microgram/mL, n = 3; 1.5 micrograms/mL, n = 3; 3.0 micrograms/mL, n = 3). There was no change in sinus node automaticity or sinus node recovery time at any concentration and no evidence of abnormal automaticity. Depression of conduction was reflected by prolongation of the PR interval at the following concentrations: 1.5 micrograms/mL (65.0 ms before, 96.6 ms after) and 3.0 micrograms/mL (61.6 ms before, 103.3 ms after) and increase in atrial and ventricular pacing thresholds at 3.0 micrograms/mL (atrial: 0.86-8.6 mA, ventricular: 2.0-10.0 mA). No spontaneous tachyarrhythmias occurred; 2:1 spontaneous atrioventricular block (n = 1) and a decrease in maximal paced rate with 1:1 anterograde or retrograde atrioventricular conduction were noted at all concentrations of bupivacaine. Thus bupivacaine did not change automaticity but had a depressant effect on conduction at the atrial, ventricular, and atrioventricular levels, providing a basis for clinically occurring atrioventricular block and reentrant arrhythmias.

Action Potentials↗
PubMed1991

Isoproterenol corrects the effects of bupivacaine on the electrophysiologic properties of the isolated rabbit heart.

The purpose of this study was to test the hypothesis that isoproterenol could reverse bupivacaine toxicity. In eight isolated rabbit hearts an electrophysiologic evaluation was performed then repeated during infusion of bupivacaine (1 microgram/mL) alone and bupivacaine plus isoproterenol (1-2 micrograms/mL). Bupivacaine alone increased electrocardiographic intervals (P wave, QRS complex, PR, AV, and QTc interval) and refractory periods of the myocardium and atrioventricular junction as well as the Wenckebach cycle and pacing thresholds. The addition of isoproterenol corrected partially or completely all bupivacaine-induced abnormalities, and decreased sinus cycle length, suggesting a potential therapeutic value in the treatment of bupivacaine intoxication.

Action Potentials↗