{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T06:40:54Z","timestamp":1790318454993,"version":"4.1.0"},"reference-count":0,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1991,8]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND<\/jats:title>\n            <jats:p>Ischemia-induced electrophysiological changes are more prominent in epicardial cells than in endocardial cells. Epicardial action potentials shorten more than endocardial action potentials during ischemia. Since the L-type Ca2+ current plays an important role in the maintenance of action potential duration, we hypothesized that the Ca2+ current is affected more in epicardial cells than in endocardial cells during ischemia.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS AND RESULTS<\/jats:title>\n            <jats:p>To test this hypothesis, we examined the effect of metabolic inhibition, a major component of ischemia, on action potentials and the Ca2+ current in single cells isolated from the endocardial and epicardial layers of the feline left ventricle. The membrane voltage and current were measured by using the whole-cell mode of the patch-clamp technique. During control periods, action potentials recorded from epicardial myocytes had lower amplitude, a prominent notch between phases 1 and 2, and shorter action potential duration compared with those recorded from endocardial myocytes. However, the amplitude and current-voltage relation of the Ca2+ current were similar in endocardial and epicardial cells at test potentials of -30 to 60 mV elicited from a holding potential of -40 mV. The time course of inactivation of the Ca2+ current also was identical in the two cell types. After 15 minutes of superfusion with glucose-free Tyrode's solution containing 1 mM CN-, action potential duration was reduced by 13 +\/- 7% in endocardial cells and by 80 +\/- 9% in epicardial cells (p less than 0.01). The peak Ca2+ current was reduced by 21 +\/- 9% in endocardial cells and by 37 +\/- 6% in epicardial cells (p less than 0.01).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS<\/jats:title>\n            <jats:p>We conclude that enhanced depression of the Ca2+ current may account in part for the greater action potential shortening in epicardial cells during ischemia and metabolic inhibition.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/01.cir.84.2.768","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:01:09Z","timestamp":1339459269000},"page":"768-777","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":23,"title":["Differences in the effect of metabolic inhibition on action potentials and calcium currents in endocardial and epicardial cells."],"prefix":"10.1161","volume":"84","author":[{"given":"S","family":"Kimura","sequence":"first","affiliation":[{"name":"Department of Medicine (Cardiology), University of Miami School of Medicine, FL 33101."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A L","family":"Bassett","sequence":"additional","affiliation":[{"name":"Department of Medicine (Cardiology), University of Miami School of Medicine, FL 33101."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T","family":"Furukawa","sequence":"additional","affiliation":[{"name":"Department of Medicine (Cardiology), University of Miami School of Medicine, FL 33101."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N","family":"Furukawa","sequence":"additional","affiliation":[{"name":"Department of Medicine (Cardiology), University of Miami School of Medicine, FL 33101."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R J","family":"Myerburg","sequence":"additional","affiliation":[{"name":"Department of Medicine (Cardiology), University of Miami School of Medicine, FL 33101."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","container-title":["Circulation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/pdf\/10.1161\/01.CIR.84.2.768","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T15:52:16Z","timestamp":1715529136000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.CIR.84.2.768"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1991,8]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1991,8]]}},"alternative-id":["10.1161\/01.CIR.84.2.768"],"URL":"https:\/\/doi.org\/10.1161\/01.cir.84.2.768","relation":{},"ISSN":["0009-7322","1524-4539"],"issn-type":[{"value":"0009-7322","type":"print"},{"value":"1524-4539","type":"electronic"}],"subject":[],"published":{"date-parts":[[1991,8]]},"assertion":[{"value":"1991-08-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}