Glutaraldehyde treated bovine pericardium: changes in calcification due to vitamins and platelet inhibitors.
Cardiovascular calcification, the formation of calcium phosphate deposits in cardiovascular tissue, is a common endstage phenomenon affecting a wide variety of bioprostheses. The purpose of the present paper is to study the possibility that some antiplatelet drugs (aspirin and persantine) and certain vitamins (vitamin C, vitamin B6, and vitamin E) and their combinations might prevent the mineralization of glutaraldehyde treated bovine pericardium (GABP) by modifying the pericardial surface. In this experimental protocol, we used Golomb and Wagner's (1991) in vitro model for studying GABP calcification and a diffusion cell with 2 compartments for evaluating the diffusion of calcium across the GABP. The results showed that a combination of aspirin and vitamins (0.5 mg% aspirin, 1.5 mg% vitamin C, 4 mg% vitamin B6, and 2 mg% vitamin E) in a metastable calcium phosphate solution not only reduced the transport of calcium ions through GABP, but along with the combinations of 0.5 mg% aspirin and 5 mg% persantine also produced significant reductions in GABP calcification. The exact mechanism of these changes in the calcification of GABP are still unknown. From these in vitro findings, it appears that a combined vitamin therapy with low doses of aspirin may be beneficial for platelet suppression and thereby prevent thrombosis. In addition, the vitamins may modify calcium transport and interfere with the adsorption at the surface, thus reducing GABP calcification. However, an important question that remains unanswered is whether this inhibitory effect would continue if the antiplatelet drugs and vitamins were discontinued. For the answer, more in vivo studies are needed to develop applications.
Vasudev
S C
SC
Division of Biosurface Technology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Poojapura, India.
Chandy
T
T
Sharma
C P
CP
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D001705:Bioprosthesis; D002114:Calcinosis / Q000188:drug therapy* / Q000378:metabolism; D002118:Calcium / Q000037:antagonists & inhibitors / Q000378:metabolism*; D002130:Calcium Phosphates / Q000494:pharmacology; D002417:Cattle; D004176:Dipyridamole / Q000494:pharmacology; D004338:Drug Combinations; D005404:Fixatives; D005976:Glutaral; D008855:Microscopy, Electron, Scanning; D010496:Pericardium / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D011736:Pyridoxine / Q000494:pharmacology; D014810:Vitamin E / Q000494:pharmacology; D014815:Vitamins / Q000494:pharmacology*
D002130:Calcium Phosphates; D004338:Drug Combinations; D005404:Fixatives; D010975:Platelet Aggregation Inhibitors; D014815:Vitamins; C485828:alpha-tricalcium phosphate; C485830:tetracalcium phosphate; D014810:Vitamin E; D004176:Dipyridamole; C485838:calcium phosphate, monobasic, anhydrous; C020243:calcium phosphate; D011736:Pyridoxine; C485829:calcium phosphate, dibasic, anhydrous; D001205:Ascorbic Acid; D001241:Aspirin; D002118:Calcium; D005976:Glutaral