{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T08:47:09Z","timestamp":1791190029387,"version":"4.1.0"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2001,3,20]]},"abstract":"\n Background<\/jats:italic>\n \u2014Altered excitation-contraction (E-C) coupling in canine pacing-induced heart failure involves decreased sarcoplasmic reticulum (SR) Ca uptake and enhanced Na\/Ca exchange, which could be expected to decrease SR Ca content (Ca\n SR<\/jats:sub>\n ) and may explain the reduced intracellular Ca (Ca\n i<\/jats:sub>\n ) transient. Studies in other failure models have suggested that the intrinsic coupling between L-type Ca current (\n I<\/jats:italic>\n Ca,L<\/jats:sub>\n ) and SR Ca release is reduced without a change in SR Ca load. The present study investigates whether Ca\n SR<\/jats:sub>\n and\/or coupling is altered in midmyocardial myocytes from failing canine hearts (F).\n <\/jats:p>\n \n Methods and Results<\/jats:italic>\n \u2014Myocytes were indo-1\u2013loaded via patch pipette (37\u00b0C), and Ca\n i<\/jats:sub>\n transients were elicited with voltage-clamp steps applied at various frequencies.\n I<\/jats:italic>\n Ca,L<\/jats:sub>\n density was not significantly decreased in F, but steady-state Ca\n i<\/jats:sub>\n transients were reduced to 20% to 40% of normal myocytes (N). Ca\n SR<\/jats:sub>\n , measured by integrating Na\/Ca exchange currents during caffeine-induced release, was profoundly decreased in F, to 15% to 25% of N. When Ca\n SR<\/jats:sub>\n was normalized in F by preloading in 5 mmol\/L external Ca before a test pulse at 2 mmol\/L Ca, a normal-amplitude Ca\n i<\/jats:sub>\n transient was elicited. E-C coupling gain was dependent on Ca\n SR<\/jats:sub>\n but was affected similarly in both groups, indicating that intrinsic coupling is unaltered in F.\n <\/jats:p>\n \n Conclusions<\/jats:italic>\n \u2014A decrease in Ca\n SR<\/jats:sub>\n is sufficient to explain the diminished Ca\n i<\/jats:sub>\n transients in F, without a change in the effectiveness of coupling. Therefore, therapeutic approaches that increase Ca\n SR<\/jats:sub>\n may be able to fully correct the Ca handling deficit in heart failure.\n <\/jats:p>","DOI":"10.1161\/01.cir.103.11.1577","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:09:32Z","timestamp":1339459772000},"page":"1577-1584","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":192,"title":["Decreased Sarcoplasmic Reticulum Calcium Content Is Responsible for Defective Excitation-Contraction Coupling in Canine Heart Failure"],"prefix":"10.1161","volume":"103","author":[{"given":"Ion A.","family":"Hobai","sequence":"first","affiliation":[{"name":"From the Institute of Molecular Cardiobiology, Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"O\u2019Rourke","sequence":"additional","affiliation":[{"name":"From the Institute of Molecular Cardiobiology, Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1978.tb41979.x"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1994.sp020037"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(92)81615-6"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.8235594"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.7754383"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.276.5313.800"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.84.4.424"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.85.3.1311223"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.1997.0626"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.85.1.38"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.84.5.562"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.78.2.262"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050496"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)83641-4"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(95)80318-8"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584965"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.87.8.690"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1995.sp020836"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-3495(00)76596-9"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1991.sp018528"},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.1997.385bb.x"},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.84.5.571"},{"key":"e_1_3_2_23_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0008-6363(99)00200-X"},{"key":"e_1_3_2_24_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.90.3.7522133"},{"key":"e_1_3_2_25_2","first-page":"H2425","volume":"272","year":"1997","unstructured":"Delbridge LM, Satoh H, Yuan W, et al. 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