Calcium entry blockade prevents leakage of macromolecules induced by ischemia-reperfusion in skeletal muscle
| Autor: | Walter N. Durán, J Paul, A Y Bekker |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
Male
medicine.medical_specialty Physiology Macromolecular Substances Ischemia chemistry.chemical_element Rats Inbred WF Calcium Pharmacology Permeability Thromboxane A2 chemistry.chemical_compound medicine Animals Muscles Skeletal muscle Dextrans medicine.disease Calcium Channel Blockers Fluoresceins Surgery Rats Thromboxane B2 medicine.anatomical_structure chemistry Cremaster muscle Reperfusion Verapamil Eicosanoids Cardiology and Cardiovascular Medicine Fluorescein-5-isothiocyanate medicine.drug Blood vessel |
| Zdroj: | Circulation research. 66(6) |
| ISSN: | 0009-7330 |
| Popis: | Calcium kinetics and its intracellular mobilization are important in all biological processes. We used verapamil to examine the effect of calcium entry blockade on microvascular transport of macromolecules in ischemia-reperfusion injury. The rat cremaster muscle was splayed, placed in a Lucite intravital chamber, and suffused with bicarbonate buffer. The clearance of fluorescein isothiocyanate-conjugated dextran (FITC-dextran 150) was measured as an index of microvascular transport. After determination of baseline data (clearance of FITC-dextran 150, 3.0 +/- 0.5 microliters/5 min/g), the muscle was made ischemic for 2 hours by clamping its vascular pedicle and subsequently was reperfused for 2 hours. Ischemia-reperfusion produced a marked increase in FITC-dextran clearance. After a peak of 12 +/- 2-fold increase observed in the first 15 minutes into reperfusion, FITC-dextran 150 clearance decreased in magnitude and stabilized at about sixfold above baseline. Verapamil did not change the baseline clearance values. Importantly, verapamil inhibited the ischemia-induced increase in clearance and maintained the values at or near the baseline levels. We simultaneously determined the rate of release of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) into the suffusate. Verapamil decreased the baseline values of 6-keto-PGF1 alpha and increased those of TXB2. Verapamil inhibited the ischemia-reperfusion-induced increase in 6-keto-PGF1 alpha but did not alter the effect of ischemia-reperfusion on TXB2. Our main results demonstrate the effectiveness of verapamil in preventing microvascular alterations leading to increased leakage of macromolecules. |
| Databáze: | OpenAIRE |
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