{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T02:38:05Z","timestamp":1772159885096,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"4","funder":[{"DOI":"10.13039\/100007048","name":"Mayo Foundation for Medical Education and Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007048","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100013232","name":"Norwegian Air Ambulance Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100013232","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2019,10,1]]},"abstract":"<jats:p> Rewarming the intact heart after a period of hypothermia is associated with reduced myocardial contractility, decreased Ca<jats:sup>2+<\/jats:sup> sensitivity, and increased cardiac troponin-I (cTnI) phosphorylation. We hypothesized that hypothermia\/rewarming (H\/R) induces left ventricular (LV) contractile dysfunction due to phosphorylation of cTnI at Ser<jats:sup>23\/24<\/jats:sup>. To test this hypothesis, the response of wild-type mice ( n = 7) to H\/R was compared with transgenic (TG) mice expressing slow skeletal TnI (TG-ssTnI; n = 7) that lacks the Ser<jats:sup>23\/24<\/jats:sup> phosphorylation sites. Hypothermia was induced by surface cooling and maintained at 23\u201325\u00b0C for 3 h. Subsequently, the animals were rewarmed to 37\u00b0C. LV systolic and diastolic function was assessed using a 1.4 F pressure-volume Millar catheter introduced via the right carotid artery. At baseline conditions, there were no significant differences in LV systolic function between wild-type and TG-ssTnI mice, whereas measurements of diastolic function [isovolumic relaxation constant (\u03c4) and end-diastolic pressure-volume relationship (EDPVR)] were significantly ( P &lt; 0.05) reduced in TG-ssTnI animals. Immediately after rewarming, significant differences between groups were found in cardiac output (CO; wild-type 6.6\u2009\u00b1\u20090.7 vs. TG-ssTnI 8.8\u2009\u00b1\u20090.7 mL\/min), stroke work (SW; wild-type 796\u2009\u00b1\u2009112 vs. TG-ssTnI 1208\u2009\u00b1\u200967 mmHg\/\u03bcL), and the preload recruited stroke work (PRSW; wild-type 38.3\u2009\u00b1\u20094.9 vs. TG-ssTnI 68.8\u2009\u00b1\u20098.2 mmHg). However, EDPVR and \u03c4 returned to control levels within 1 h in both groups. We conclude that H\/R-induced LV systolic dysfunction results from phosphorylation of cTnI at Ser<jats:sup>23\/24<\/jats:sup>. <\/jats:p><jats:p> NEW &amp; NOTEWORTHY Rewarming following a period of accidental hypothermia leads to a form of acute cardiac failure (rewarming shock), which is in part due to reduced sensitivity to Ca<jats:sup>2+<\/jats:sup> activation of myocardial contraction. The results of the present study support the hypothesis that rewarming shock is due to phosphorylation of cardiac troponin I. <\/jats:p>","DOI":"10.1152\/ajpheart.00101.2019","type":"journal-article","created":{"date-parts":[[2019,8,2]],"date-time":"2019-08-02T08:35:51Z","timestamp":1564734951000},"page":"H726-H731","source":"Crossref","is-referenced-by-count":16,"title":["Cardiac troponin-I phosphorylation underlies myocardial contractile dysfunction induced by hypothermia rewarming"],"prefix":"10.1152","volume":"317","author":[{"given":"Torkjel","family":"Tveita","sequence":"first","affiliation":[{"name":"Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota"},{"name":"Anesthesia and Critical Care Research Group, Institute of Clinical Medicine, The Arctic University of Norway, Troms\u00f8, Norway"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Grace M.","family":"Arteaga","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Young-Soo","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gary C.","family":"Sieck","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, Minnesota"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.13.6.909"},{"key":"B2","first-page":"22","volume":"2","author":"Connolly E","year":"2000","journal-title":"Crit Care Resusc"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.cryobiol.2014.09.007"},{"key":"B4","doi-asserted-by":"crossref","unstructured":"Edwards W. 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