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R Ohlendorf

Publications and source records attributed to R Ohlendorf.

7 recordsLinked to original sources
PubMed1988

Identification of trimethyllead in urine by high-performance liquid chromatography with column switching and chemical reaction detection and by liquid chromatography-mass spectrometry.

Incorporated tetraalkyllead compounds are metabolized in the liver and the highly toxic trialkyllead species are excreted via the urine. The procedure for the determination of these metabolites in urine consists of solid-phase enrichment, reversed-phase pre-column high-performance liquid chromatography (HPLC) and chemical reaction detection. As urine is a very complex matrix, it must be questioned whether the retention time alone is a sufficient criterion for the identification of the analytes. For the trimethyllead ion the validity of the results was examined by selectivity checks of the chemical reaction detector, by the application of different stationary and mobile phases in single and dual pre-column HPLC systems and by the use of thermospray LC-mass spectrometry as an independent method. The results demonstrated that the recommended method is accurate for the determination of trimethyllead in urine samples.

Chromatography, High Pressure Liquid↗
PubMed1981

Prostacyclin prevents ischemia-induced increase of lactate and cyclic AMP in ischemic myocardium.

The effect of prostacyclin (PGI2, 0.5 nmol . kg-1 . min-1,i.v.) on myocardial metabolism was studied in cats subjected to 5 h of myocardial ischemia (MI) and compared to vehicle-treated MI cats. MI was followed by a 52% decrease in ATP and a concomitant increase (2-3 fold) in lactate and lactate/pyruvate ratio in the severely ischemic area. PGI2 prevented this increase in lactate with an unchanged ATP and lactate/pyruvate ratio. Moreover, PGI2 abolished the ischemia-induced in myocardial cAMP. It is concluded, the PGI2 exerts its beneficial actions on ischemic myocardium partly via cAMP-linked mechanisms.

Animals↗
PubMed1981

Beneficial effects of a new carbacyclin derivative, ZK 36 374, in acute myocardial ischemia.

The potential therapeutic value of the chemically stable carbacyclin analog ZK 36 374 was studied in acute myocardial ischemia (MI). In anesthetized cats, the left anterior descending coronary artery was ligated and 30 min later an i.v. infusion of ZK 36 374 (0.18 microgram/kg X min) on vehicle was initiated and continued for 4.5 hr. ZK 36 374 reduced the ST-segment elevation at 2 to 5 hr (P less than .01) when compared to vehicle-treated MI cats. ZK 36 374 completely prevented the loss of CK specific activities and the decrease in percentage of bound cathepsin D in the infarcted area of the myocardium (P less than .01), but had no influences on any of these parameters in shamoperated animals. In addition, ZK 36 374 reversed the MI-induced decrease in circulating platelet count toward the preinfarction levels, probably by dispersion of circulating platelet aggregates. ZK 36 374 prevented the ischemia-induced loss of myocardial catecholamines from adrenergic nerve terminals. ZK 36 374, at 0.18 microgram/kg X min, exerted a maximum antiplatelet effect, whereas a significant decrease in arterial blood pressure was seen at 1.79 microgram/kg X min (-30-40%). This indicates a considerable dissociation between antiplatelet and blood pressure-lowering activities of ZK 36 374 in this model. The data demonstrate a significant protective effect of ZK 36 374 in acute MI that might be associated with its platelet-stabilizing, antiadrenergic and myocardial cytoprotective activities.

Animals↗
PubMedDate not supplied

Dissociation of antiplatelet effects from myocardial cytoprotective activity during acute myocardial ischemia in cats by a new carbacyclin derivative (ZK 36 375).

We studied the potential therapeutic value of the chemically stable carbacyclin analogue ZK 36 375 during acute myocardial ischemia and compared the cardiovascular and anti- and disaggregatory effects of the compound in vitro and ex vivo. In anesthetized cats the left anterior descending coronary artery was ligated, and 30 min later an intravenous infusion of ZK 36 375 (3.6 micrograms/kg X min) or vehicle was initiated and continued for 4.5 h. ZK 36 375 reduced the ST-segment elevation at 2-5 h (p less than 0.01) when compared to vehicle-treated cats. ZK 36 375 significantly inhibited both the loss of creatine phosphokinase--specific activity and the decrease in the percentage of bound cathepsin D in the infarcted area of the myocardium (p less than 0.05). ZK 36 375 did not reverse ischemia-induced formation of platelet aggregates in vivo and was found ex vivo to be two to three orders of magnitude less active in preventing platelet aggregation, redispersing platelet aggregates, and relaxing bovine coronary arteries than prostacyclin (PGI2) or its (5E) stereoisomer ZK 36 374. It is concluded that ZK 36 375 has a significant cardioprotective activity in acute myocardial ischemia of the cat that can be dissociated from antiplatelet effects in vivo.

Animals↗