No abstract

In rat hindlimbs perfused with [1-14C]pyruvate and 5 mM-dichloroacetate, the calculated apparent rate of pyruvate decarboxylation was decreased with increasing perfusate pyruvate concentrations. However, in the absence of dichloroacetate the apparent rate of decarboxylation increased under these conditions. Dichloroacetate enhanced [1-14C]pyruvate uptake, but decreased the specific radioactivity of effluent lactate. Glycogen metabolism remained unaffected. The results were not consistent with a common pyruvate pool, but provide evidence for the compartmentation of pyruvate metabolism.

No abstract

Melting points measured with the capillary method were 150.5 degree C, 150.5 degree C and 224.0 degree C for hydrochlorides of (+)-bupranolol, (-)-bupranolol and (+/-)-bupranolol, respectively. The large difference in melting points of 73.5 degree C prompted us to determine possible contaminations of (+)-bupranolol with traces of (-)-bupranolol using differential scanning calorimetry. We detected as little as 0.001% (-)-bupranolol in a standard mixture of (+)-bupranolol and (-)-bupranolol. A batch of (+)-bupranolol not measurably contaminated with (-)-bupranolol (optically purity greater than 99.999%) was used in pharmacological and biochemical assays. The affinities of (-)-bupranolol and (+)-bupranolol were determined functionally by the blockade of isoprenaline stimulation of spontaneously beating rat right atria and electrically driven kitten papillary muscles; and directly by inhibition of binding of 3H-(-)-propranolol to kitten ventricle membrane particles. In all 3 systems the enantiomeric (-)/(+) affinity ratio was 50--120 for bupranolol. These experiments prove that (+)-bupranolol itself binds to the beta-adrenoceptors of mammalian myocardium.