Disease relevance of lomerizine

• These results suggest that calcium influx into neurons participates in the pathogenesis of DND, and also that KB-2796 might prevent both morphological and functional cell damage in CA1 neurons induced by transient ischemia [1].
• This study demonstrates that although MK-801 or KB-2796 does not prevent paraplegia due to spinal cord ischemia in the rabbit, both drugs can influence the rate of recovery after ischemic injury [2].
• The protective effect of KB-2796 exceeds the effect of calcium blockers previously used in experimental spinal cord ischemia [3].
• These results suggest that the protective effect of KB-2796 in cerebral hypoxia and ischemia is due in part to a mechanism independent of its effects as a cerebral vasodilator [4].
• KB-2796 showed an apparent protective potency against complete ischemia induced by decapitation, normobaric hypoxia and KCN-induced death in mice [4].

High impact information on lomerizine

• Effects of a new calcium channel blocker, KB-2796, on protein synthesis of the CA1 pyramidal cell and delayed neuronal death following transient forebrain ischemia [1].
• The effects of a new calcium channel blocker, 1-[bis(4-fluorophenyl)methyl]-4-(2,3,4-trimethoxybenzyl)-piperazine dihydrochloride (KB-2796), on delayed neuronal death (DND) in the hippocampus were examined in gerbils in comparison with those of pentobarbital and flunarizine [1].
• Comparative effects of the N-methyl-D-aspartate antagonist MK-801 and the calcium channel blocker KB-2796 on neurologic and metabolic recovery after spinal cord ischemia [2].
• All metabolic parameters determined (ATP, energy charge, and lactate) completely recovered at 4 days following 20 min of ischemia when NMDA receptor antagonist MK-801 (1 mg/kg given i.v.) or calcium channel blocker KB-2796 (50 mg/kg given i.p.) was administered either prior to or after ischemia [2].
• The relaxation induced by verapamil and KB-2796, in contrast, was greater in basilar than in other arteries, the magnitude of relaxation being in the order of basilar > coronary > renal and mesenteric arteries [5].

Biological context of lomerizine

• KB-2796 inhibited [3H]NTD binding in a dose-dependent manner with an IC50 value of 86 nM [6].
• Intravenous infusion of KB-2796 (10, 30, and 100 micrograms/kg/min) decreased mean blood pressure (MBP) and renal vascular resistance (RVR) in a dose-dependent manner, but did not change renal blood flow (RBF) [7].
• 1. The effects of KB-2796, a new diphenylpiperazine calcium antagonist, on the mitochondrial dysfunction and energy metabolism deficits were examined in the ischemic rat brain [8].
• Effects of a new Ca2+ antagonist, KB-2796, on the regional cerebral blood flow and somatosensory evoked potentials in the ischemic brain in cats [9].

Anatomical context of lomerizine

• Calcium antagonism by KB-2796, a new diphenylpiperazine analogue, in dog vascular smooth muscle [10].
• KB-2796, however, significantly increased the dissociation rate constant of [3H]NTD from radiolabeled membranes [6].
• In the 45Ca influx study, KB-2796 also effectively inhibited KCl-induced 45Ca influx in mesenteric arteries, with an IC50 value of 0.14 microM [10].
• When KB-2796 was infused into the renal artery at lower doses of 3 and 10 micrograms/kg/min, UF and urinary excretion of electrolytes increased without a significant change in RBF and GFR [7].
• The effect of KB-2796, a new diphenylpiperazine calcium antagonist, on [3H]nitrendipine ([3H]NTD) binding was investigated in synaptosomal membranes prepared from the guinea pig cerebral cortex [6].

Associations of lomerizine with other chemical compounds

• Intrarenal infusion of KB-2796 at 30 micrograms/kg/min and nicardipine at 0.3 microgram/kg/min produced a significant increase in GFR, RBF, UF, urinary excretion of electrolytes, and renin secretion rate [7].
• According to the hypothesis that calcium antagonists can potentiate the analgesic effect of opioids, we designed a study to investigate the effects of KB-2796, a new calcium channel blocker, on the antinociception of fentanyl at the level of the spinal cord in rats [11].

Gene context of lomerizine

• 2. KB-2796 (30 mg/kg, p.o.), administered 60 min prior to decapitation, improved the reduced respiratory activity of mitochondria obtained from rat brain 5 min after decapitative ischemia [8].

Analytical, diagnostic and therapeutic context of lomerizine

• KB-2796 (50 mg/kg, p.o.) significantly prolonged survival time in gerbils with bilateral carotid ligation [4].
• The effects of KB-2796 and BAY K 8644 on fentanyl-induced analgesia in rats [12].
• The metabolites of 1-[bis(4-fluorophenyl)methyl]-4-(2,3,4-trimethoxybenzyl)piperazine dihydrochloride (KB-2796) in the bile, urine and feces in rats were investigated after oral administration of [methine-14C], [benzyl-14C] and unlabelled KB-2796 [13].

References