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Biomedical subjects

A Buchwald

Publications and source records attributed to A Buchwald.

46 records · Page 3Linked to original sources
PubMed1988

Antiinflammatory agent BW 755 C in ischemic reperfused porcine hearts.

The effect of the antiinflammatory compound BW 755 C on myocardial infarctions was evaluated in regionally ischemic reperfused hearts of 35 pigs. The left anterior descending coronary artery was occluded distally in 23 anesthetized pigs for 45 min and was reperfused for 24 h. The BW 755 C (10 mg/kg) was intravenously injected prior to ischemia in seven pigs (group A). A second dose of BW 755 C (5 mg/kg) was given after 4 h of reperfusion. Group B consisted of eight animals. They were treated with BW 755 C immediately before (10 mg/kg i.v.) and after 4 h of reperfusion (5 mg/kg). Another eight pigs served as controls. At the end of the experiments, infarct size was determined as the ratio of the infarcted myocardium (tetrazolium stain) over the risk region (fluorescent dye). Leukocyte infiltration of the risk region was histologically quantitated in one slice of each experiment. In a second set of experiments recovery of regional myocardial function of the risk region was determined by sonomicrometry during 2 weeks of reperfusion. The BW 755 C (10 mg/kg) was injected intravenously in six pigs before ischemia and at a dose of 5 mg/kg after 4 h of reperfusion. Six pigs served as controls. Hemodynamic parameters and total leukocyte blood count did not differ between the groups. Treatment protocol of group A reduced the infarct size from 72 +/- 13% (control group) to 50.9 +/- 12% (p less than 0.005). Infarct size of group B (65 +/- 16%) did not differ from control experiments. Leukocyte infiltration of the risk region was only attenuated in group A (p = 0.01) compared with the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1988

[Coronary fistula of the right ventricular outflow tract as a complication of combined transaortic-trans-right ventricular myectomy in hypertrophic obstructive cardiomyopathy].

We report on a patient who showed a fistula between the first septal branch of the left anterior descending coronary artery and the right ventricular outflow tract, as a complication of combined trans-aortic right ventricular myectomy for treatment of hypertrophic obstructive cardiomyopathy (HOCM).

Aorta, Thoracic↗
PubMed1987

Influence of mioflazine on canine coronary blood flow and on adenine nucleotide and nucleoside content under normal and ischemic conditions.

Intravenous injection of mioflazine, a nucleoside transport antagonist, caused maximal coronary vasodilation in canine hearts. This was completely reversed by intravenous injection of the enzyme adenosine deaminase. Coronary vasodilation was induced again by the adenosine deaminase inhibitor EHNA [Erythro-9(2-hydroxy-3-nonyl)adenine]; however, without previous injection of mioflazine, EHNA did not produce coronary vasodilation. Mioflazine-induced coronary vasodilation was antagonized by theophylline, but it was not associated with increased plasma levels of adenosine. Under the influence of mioflazine, ischemic myocardium contained adenosine and inosine at a ratio of 65:30, which is the reverse of the control ratio. Total nucleoside content following mioflazine showed reduced nucleoside losses as compared with control. A significant amount of the accumulated adenosine is extracellular since it was accessible to exogenous adenosine deaminase. Reperfusion of ischemic myocardium did not result in increased rates of adenosine phosphorylation, another indicator of its extracellular accumulation. The data are best explained by assuming release of adenosine by mioflazine in addition to its known effect of inhibiting nucleoside transport. The adenosine release occurs most probably into the interstitial space where it occupies smooth muscle adenosine receptors. The existence of nonsymmetric transport (uptake is more inhibited than release) is postulated for the myocyte, as well as for the endothelial cell plasma membrane.

Adenine Nucleotides↗
PubMedDate not supplied

Antiproliferative effects of a c-myc antisense oligonucleotide on human arterial smooth muscle cells.

The effects of a c-myc antisense phosphorothioate DNA oligonucleotide were assessed on the proliferation rate of human arterial smooth muscle cells (HSMCs). Compared to a control oligonucleotide the antisense oligonucleotide suppressed the proliferation of HSMCs in a concentration-dependent manner without a major cytotoxic effect. Outgrowth of HSMCs from media explants was significantly inhibited as well. Induction of c-myc expression by serum stimulation of cells was blunted by the antisense oligonucleotide, as shown by immunoblotting. These results demonstrate that c-myc expression is an essential factor for proliferation of HSMCs after growth stimulation, and they show the potential of antisense technology for modulating gene expression of HSMCs in vitro.

Base Sequence↗
PubMedDate not supplied

Intracoronary superoxide dismutase for the treatment of "reperfusion injury", A blind randomized placebo-controlled trial in ischemic, reperfused porcine hearts.

The effect of recombinant human superoxide dismutase (rh-SOD) on infarct size was investigated in porcine hearts. The left anterior descending coronary artery was occluded in each of 24 anesthetized pigs for 45 min and reperfused for 24 h. The animals were randomly assigned to either rh-SOD (n = 12) or placebo treatment (n = 12). 2 min before reperfusion, an intracoronary (i.c.) infusion of rh-SOD (total dose: 2000 U/kg) or placebo was started which lasted for up to 45 min reperfusion. At the end of the experiment, the infarcted myocardium was assessed using a tetrazolium stain (NBT) and related to the risk region which was determined with a fluorescent dye. Two pigs of the SOD group and one of the control group died before the end of the experiments. Except for a lower calculated myocardial oxygen consumption and a lower dp/dtmax in the SOD group during ischemia, hemodynamic parameters of the two groups did not differ significantly. rh-SOD i.c. treatment during reperfusion did not reduce infarct size significantly. Infarct size amounted to 74 +/- 13% in the control group and to 66 +/- 19% in the treated group. The incidence of reperfusion arrhythmias was not affected by rh-SOD treatment. It is concluded that i.c. rh-SOD treatment at the beginning of reperfusion neither significantly reduces infarct size nor diminishes the incidence of reperfusion arrhythmias in this preparation.

Animals↗