Open AccessIN VIVO FLUORESCENCE MICROSCOPY OF KIDNEY SUBCAPSULAR BLOOD FLOW IN MICE EFFECTS OF CYCLOSPORINE, (NVA)-CYCLOSPORINE, AND ISRADIPINE, A NEW CALCIUM ANTAGONIST
Author(s) -
P. Rooth,
Ingemar Dawidson,
Norm Clothier,
Kenneth R. Diller
Publication year - 1988
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/00007890-198810000-00020
Subject(s) - isradipine , antagonist , nephrotoxicity , pharmacology , microcirculation , kidney , calcium , renal blood flow , perfusion , renal circulation , in vivo , blood flow , vasoconstriction , chemistry , medicine , endocrinology , biology , receptor , microbiology and biotechnology
The subcapsular kidney microcirculation in mice was observed through a fluorescence microscope, recorded on videotape, and examined for response to infusions of cyclosporine A (CsA) and cyclosporine G (CsG). Coded video recordings were evaluated by a semiquantitative method. CsA infusion (1.6 +/- 0.4 mg/kg/min) induced a nearly complete inhibition of the subcapsular blood flow. At lower infusion rates (0.46 +/- 0.2 mg/kg/min), the blood flow inhibition was less pronounced. CsG infusions at corresponding rates induced significantly less inhibition. Pretreatment with a new calcium antagonist, isradipine (18-20 micrograms/kg bwt), completely prevented the CsA-induced impairment of subcapsular microcirculation. The calcium antagonist, however, did not improve blood flow when administered after induction of inhibition by CsA (16.8 +/- 2.5 mg/kg), emphasizing the importance of pretreatment. This study suggests hypoperfusion due to vasoconstriction as an important pathophysiologic mechanism for CsA-induced nephrotoxicity. CsG, when given at corresponding rates, induced less inhibition of the blood flow. Pretreatment with a calcium antagonist, isradipine, completely prevented a CsA-induced inhibition of blood flow, suggesting a potential value in the prevention of CsA-induced nephrotoxicity.