{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,13]],"date-time":"2025-10-13T19:53:53Z","timestamp":1760385233722},"reference-count":27,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"21","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2000,11,21]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            \u2014Ischemia is characterized by an increase in intracellular calcium and occurrence of diastolic dysfunction. We investigated whether the myocyte calcium level is an important direct determinant of ischemic diastolic dysfunction.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods and Results<\/jats:italic>\n            \u2014We exposed isolated, perfused isovolumic (balloon in left ventricle) rat and rabbit hearts to low-flow ischemia and increased extracellular calcium (from 1.5 to 16 mmol\/L) for brief periods. Intracellular calcium was measured by aequorin. Low-flow ischemia resulted in a 270% increase (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05) in diastolic intracellular calcium, a 50% (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05) calcium transient amplitude decrease, and a 52% (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05) slowing of calcium transient decline. Diastolic pressure increased by 6\u00b12 mm Hg (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05), and rate of systolic pressure decay decreased by 65% (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). Experimentally increasing extracellular calcium doubled both intracellular diastolic calcium and calcium transient amplitude, concomitant with a developed pressure increase; however, there was no increase in ischemic diastolic pressure, slowing of the calcium transient decay, or further slowing of systolic pressure decay. Similarly, after 45 minutes of low-flow ischemia, after diastolic pressure had increased from 8.5\u00b10.6 to 19.7\u00b13.5 mm Hg (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001), intracoronary high-molar calcium chloride infusion increased systolic pressure from 36\u00b14 to 63\u00b111 mm Hg (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001), indicating an increase in intracellular calcium, but it decreased diastolic pressure from 19.7\u00b13.5 to 17.5\u00b13.7 mm Hg (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01). Conversely, EGTA infusion decreased systolic pressure, indicating a decrease in intracellular calcium, but did not decrease diastolic pressure.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            \u2014When calcium availability was experimentally altered during ischemia, there was no alteration in left ventricular diastolic pressure, suggesting that ischemic diastolic dysfunction is not directly mediated by a calcium activated tension.\n          <\/jats:p>","DOI":"10.1161\/01.cir.102.21.2643","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:42:29Z","timestamp":1339461749000},"page":"2643-2649","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":24,"title":["Lack of Direct Role for Calcium in Ischemic Diastolic Dysfunction in Isolated Hearts"],"prefix":"10.1161","volume":"102","author":[{"given":"Franz R.","family":"Eberli","sequence":"first","affiliation":[{"name":"From the Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, Mass (F.R.E., M.A.F., N.V., C.S.A.); Medizinische Universita\u0308tsklinik, Wu\u0308rzburg, Germany (H.S., S.N.); and Harvard Medical School, Boston, Mass (J.P.M.). Drs Eberli and Stro\u0308mer contributed equally to this article."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hinrik","family":"Stro\u0308mer","sequence":"additional","affiliation":[{"name":"From the Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, Mass (F.R.E., M.A.F., N.V., C.S.A.); Medizinische Universita\u0308tsklinik, Wu\u0308rzburg, Germany (H.S., S.N.); and Harvard Medical School, Boston, Mass (J.P.M.). Drs Eberli and Stro\u0308mer contributed equally to this article."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Margaret A.","family":"Ferrell","sequence":"additional","affiliation":[{"name":"From the Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, Mass (F.R.E., M.A.F., N.V., C.S.A.); Medizinische Universita\u0308tsklinik, Wu\u0308rzburg, Germany (H.S., S.N.); and Harvard Medical School, Boston, Mass (J.P.M.). Drs Eberli and Stro\u0308mer contributed equally to this article."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Niraj","family":"Varma","sequence":"additional","affiliation":[{"name":"From the Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, Mass (F.R.E., M.A.F., N.V., C.S.A.); Medizinische Universita\u0308tsklinik, Wu\u0308rzburg, Germany (H.S., S.N.); and Harvard Medical School, Boston, Mass (J.P.M.). Drs Eberli and Stro\u0308mer contributed equally to this article."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James P.","family":"Morgan","sequence":"additional","affiliation":[{"name":"From the Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, Mass (F.R.E., M.A.F., N.V., C.S.A.); Medizinische Universita\u0308tsklinik, Wu\u0308rzburg, Germany (H.S., S.N.); and Harvard Medical School, Boston, Mass (J.P.M.). Drs Eberli and Stro\u0308mer contributed equally to this article."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefan","family":"Neubauer","sequence":"additional","affiliation":[{"name":"From the Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, Mass (F.R.E., M.A.F., N.V., C.S.A.); Medizinische Universita\u0308tsklinik, Wu\u0308rzburg, Germany (H.S., S.N.); and Harvard Medical School, Boston, Mass (J.P.M.). Drs Eberli and Stro\u0308mer contributed equally to this article."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carl S.","family":"Apstein","sequence":"additional","affiliation":[{"name":"From the Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, Mass (F.R.E., M.A.F., N.V., C.S.A.); Medizinische Universita\u0308tsklinik, Wu\u0308rzburg, Germany (H.S., S.N.); and Harvard Medical School, Boston, Mass (J.P.M.). Drs Eberli and Stro\u0308mer contributed equally to this article."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2828(87)80551-5"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9149(77)80212-9"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.74.5.8156639"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119220"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.68.2.1991351"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.65.4.2791218"},{"key":"e_1_3_2_7_2","first-page":"H100","volume":"268","year":"1995","unstructured":"Meissner A, Morgan JP. Contractile dysfunction and abnormal Ca2+ modulation during postischemic reperfusion in rat heart. 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