Are fatty-acid oxidation and calcium homeostasis involved in the rescue of bupivacaine-induced cardiotoxicity by lipid emulsion in rats?
Fatty-acid oxidation is required for successful rescue of bupivacaine-induced cardiotoxicity by lipid emulsion. This rescue action is associated with inhibition of mitochondrial permeability transition pore opening.
Although salt pressor sensitivity was demonstrated in the subjects, there was no accompanying increase but rather a decrease in fasting insulin levels, suggesting that in the short term, salt sensitivity and hyperinsulinaemia are not linked in raising blood pressure in this sample of rural Zimbabwean subjects.