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Biomedical subjects

L Flohe

Publications and source records attributed to L Flohe.

6 recordsLinked to original sources
PubMed1986

Coronary thrombolysis by intravenous infusion of recombinant single chain urokinase-type plasminogen activator or recombinant urokinase in baboons: effect on regional blood flow, infarct size and hemostasis.

An occlusive thrombus was produced by thrombin-induced coagulation in the left anterior descending coronary artery of 18 open chest baboons. In six control animals, occlusive thrombosis persisting for 4 hours resulted in a large transmural infarct (66 +/- 4% of the perfusion area, mean +/- SEM). In six animals, single chain urokinase-type plasminogen activator, obtained by recombinant deoxyribonucleic acid (DNA) technology, was infused intravenously at a rate of 20 micrograms/kg per min for 60 minutes after approximately 45 minutes of coronary thrombosis. Persistent reperfusion occurred within 21 +/- 4 minutes (mean +/- SD). The mean duration of occlusion before reperfusion was 72 +/- 6 minutes. Recanalization resulted in a reduction of infarct size (42 +/- 4%, p less than 0.01 versus control animals). Myocardial blood flow in the perfusion area of the left anterior descending coronary artery was 107% of normal 2.5 hours after recanalization. The infusion of recombinant single chain urokinase-type plasminogen activator was not associated with systemic activation of the fibrinolytic system, fibrinogen breakdown or evident bleeding. In six baboons recombinant low molecular weight urokinase (molecular weight 33,000) was infused intravenously at a rate of 20 micrograms/kg per min for 60 minutes after approximately 45 minutes of coronary thrombosis. Persistent reperfusion occurred within 14 +/- 5 minutes (p less than 0.05 versus recombinant single chain urokinase-type plasminogen activator). The mean duration of occlusion was 69 +/- 14 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1984

Rabbit sural nerve responses to chronic treatment with thalidomide and supidimide.

Chronic treatment of rabbits with thalidomide (3-(N-phthalimido) glutarimide) produced progressive decrements in sural nerve conduction velocity (NCV) that were unassociated with qualitative or quantitative morphological changes of nervous tissue. Three groups of eight rabbits received 100 mg/kg/day thalidomide (group I), 200 mg/kg/day supidimide (a related drug) (group II), or a carboxymethylcellulose vehicle (group III) 5 days/week for 40 weeks. At 6 months of treatment, a noninvasive determination of the mean maximum sural NCV for group I was significantly reduced relative to the conduction velocities of groups II and III. Direct measurement of conduction velocity when treatment was terminated confirmed these findings and demonstrated similar conduction deficits in proximal and distal portions of the sural nerve in group I animals. At 6 months, rabbits in group II showed a significant reduction in mean conduction velocity, and, at the termination of treatment, they displayed mean values similar to that of group III and significantly greater than that of group I. Morphological findings were unremarkable in 20 regions of the central nervous system (CNS) and the peripheral nervous system (PNS) known to display changes early in toxic neuropathies. Morphometric estimation of unmyelinated and myelinated fibers in the sural nerve at the heel revealed no between-group differences in axon diameter, fiber diameter, g-ratio (the ratio of inside/outside diameters), or internodal length. In conclusion, chronic treatment with thalidomide produces selected decrements in sural nerve function that have an unknown relationship to the poorly reversible sensory neuropathy reported in humans receiving this drug.

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