{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T09:39:35Z","timestamp":1785577175287,"version":"3.56.0"},"reference-count":29,"publisher":"American Veterinary Medical Association (AVMA)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["ajvr"],"published-print":{"date-parts":[[2000,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n\t\t\t\t<jats:p>\n\t\t\t\t\t<jats:bold>Objective<\/jats:bold>\u2014To determine whether an alteration in calcium\nregulation by skeletal muscle sarcoplasmic reticulum,\nsimilar to known defects that cause malignant\nhyperthermia (MH), could be identified in membrane\nvesicles isolated from the muscles of Thoroughbreds\nwith recurrent exertional rhabdomyolysis (RER).<\/jats:p>\n\t\t\t\t<jats:p>\n\t\t\t\t\t<jats:bold>Sample Population<\/jats:bold>\u2014Muscle biopsy specimens\nfrom 6 Thoroughbreds with RER and 6 healthy (control)\nhorses.<\/jats:p>\n\t\t\t\t<jats:p>\n\t\t\t\t\t<jats:bold>Procedures<\/jats:bold>\u2014RER was diagnosed on the basis of a history\nof &gt; 3 episodes of exertional rhabdomyolysis confirmed\nby increases in serum creatine kinase (CK) activity.\nSkeletal muscle membrane vesicles, prepared by\ndifferential centrifugation of muscle tissue\nhomogenates obtained from the horses, were characterized\nfor sarcoplasmic reticulum (SR) activities, including\nthe Ca<jats:sup>2+<\/jats:sup> release rate for the ryanodine receptor-Ca<jats:sup>2+<\/jats:sup>\nrelease channel, [<jats:sup>3<\/jats:sup>H]ryanodine binding activities, and\nrate of SR Ca<jats:sup>2+<\/jats:sup>-ATPase activity and its activation by Ca<jats:sup>2+<\/jats:sup>.<\/jats:p>\n\t\t\t\t<jats:p>\n\t\t\t\t\t<jats:bold>Results<\/jats:bold>\u2014Time course of SR Ca<jats:sup>2+<\/jats:sup>-induced Ca<jats:sup>2+<\/jats:sup>\nrelease and [<jats:sup>3<\/jats:sup>H]ryanodine binding to the ryanodine\nreceptor after incubation with varying concentrations\nof ryanodine, caffeine, and ionized calcium did not differ\nbetween muscle membranes obtained from control\nand RER horses. Furthermore, the maximal rate\nof SR Ca<jats:sup>2+<\/jats:sup>-ATPase activity and its affinity for Ca<jats:sup>2+<\/jats:sup> did\nnot differ between muscle membranes from control\nhorses and horses with RER.<\/jats:p>\n\t\t\t\t<jats:p>\n\t\t\t\t\t<jats:bold>Conclusions and Clinical Relevance<\/jats:bold>\u2014Despite clinical\nand physiologic similarities between RER and MH,\nwe concluded that RER in Thoroughbreds does not\nresemble the SR ryanodine receptor defect responsible\nfor MH and may represent a novel defect in muscle\nexcitation-contraction coupling, calcium regulation,\nor contractility. 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