{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T12:33:28Z","timestamp":1790944408719,"version":"4.1.0"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1995,12,15]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            Left ventricular relaxation rate in the failing heart depends more on the systolic load than in the normal heart. To elucidate the mechanisms for the enhanced load sensitivity of left ventricular relaxation in heart failure, we examined the relative contributions of changes in end-systolic volume and loading sequence to the left ventricular relaxation rate.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods and Results<\/jats:italic>\n            In seven conscious dogs, the time constant (T\n            <jats:sub>d<\/jats:sub>\n            ) of left ventricular pressure decay, end-systolic volume, systolic circumferential force, and time to peak force during caval occlusion were compared before and after development of tachycardia-induced heart failure. Rapid ventricular pacing decreased the slope of the end-systolic pressure-volume relation from 4.5 to 2.8 mm Hg\/mL (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01) and prolonged T\n            <jats:sub>d<\/jats:sub>\n            from 33 to 49 ms (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01). In normal conditions, caval occlusion reduced end-systolic force (\u2212580 g,\n            <jats:italic>P<\/jats:italic>\n            &lt;.01) and end-systolic volume (\u22127 mL,\n            <jats:italic>P<\/jats:italic>\n            &lt;.01) but did not change T\n            <jats:sub>d<\/jats:sub>\n            or time to peak force. In heart failure, however, caval occlusion shortened T\n            <jats:sub>d<\/jats:sub>\n            (\u221211 ms,\n            <jats:italic>P<\/jats:italic>\n            &lt;.01), with a concomitant decrease in the time to peak force (\u221230 ms,\n            <jats:italic>P<\/jats:italic>\n            &lt;.01), while end-systolic volume and force declined slightly. Consequently, for a comparable reduction in end-systolic force, T\n            <jats:sub>d<\/jats:sub>\n            decreased more in heart failure than in normal hearts, suggesting enhanced load sensitivity. Moreover, changes in T\n            <jats:sub>d<\/jats:sub>\n            correlated well with those in the time to peak force (\n            <jats:italic>r<\/jats:italic>\n            =.79,\n            <jats:italic>P<\/jats:italic>\n            &lt;.01) but not with those in end-systolic volume.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            Loading sequence rather than elastic recoil seems to play the predominant role in the enhanced load sensitivity of left ventricular relaxation in heart failure.\n          <\/jats:p>","DOI":"10.1161\/01.cir.92.12.3560","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:34:42Z","timestamp":1339461282000},"page":"3560-3567","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":37,"title":["Loading Sequence Plays an Important Role in Enhanced Load Sensitivity of Left Ventricular Relaxation in Conscious Dogs With Tachycardia-Induced Cardiomyopathy"],"prefix":"10.1161","volume":"92","author":[{"given":"Shinji","family":"Ishizaka","sequence":"first","affiliation":[{"name":"From the Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hidetsugu","family":"Asanoi","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Osamu","family":"Wada","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomoki","family":"Kameyama","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroshi","family":"Inoue","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI115787"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajplegacy.1969.216.5.1084"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.69.1.6227428"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1983.244.3.H417"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.85.6.1350521"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.62.6.3383365"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1985.249.4.H747"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.68.1.1984870"},{"key":"e_1_3_2_9_2","first-page":"H805","volume":"261","year":"1991","unstructured":"Gillebert TC, Lew WYW. 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