{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T13:44:04Z","timestamp":1773755044594,"version":"3.50.1"},"reference-count":28,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1997,8,1]]},"abstract":"<jats:p> Chen, Ling, and Steven M. Scharf. Comparative hemodynamic effects of periodic obstructive and simulated central apneas in sedated pigs. J. Appl. Physiol. 83(2): 485\u2013494, 1997.\u2014It has been speculated that because of increased left ventricular (LV) afterload, decreased intrathoracic pressure (ITP) is responsible for decreased cardiac output (CO) in obstructive sleep apnea. If this were true, then obstructive apnea (OA) should have a greater effect on CO than would central apnea (CA). To assess the importance of decreased ITP during OA, we studied seven preinstrumented sedated pigs with OA and simulated CA that were matched for blood gases and apnea periodicities (with 15- or 30-s apnea duration). Compared with OA, CA with 30-s apnea duration produced comparable decreases in heart rate (from baseline to end apnea: OA, 106.6 \u00b1 4.8 to 93.4 \u00b1 4.4 beats\/min, P &lt; 0.01; and CA, 111.1 \u00b1 6.2 to 94.0 \u00b1 5.2 beats\/min, P &lt; 0.01) and comparable increases in LV end-diastolic pressure and LV end-diastolic myocardial segment length but greater increases in mean arterial pressure (97.1 \u00b1 3.7 to 107.7 \u00b1 4.3 Torr, P &lt; 0.05; and 97.3 \u00b1 4.8 to 119.3 \u00b1 7.4 Torr, P &lt; 0.01) and systemic vascular resistance (2,577 \u00b1 224 to 3,346 \u00b1 400 dyn \u22c5 s \u22c5 cm<jats:sup>\u22125<\/jats:sup>, P &lt; 0.01; and 2,738 \u00b1 294 to 5,111 \u00b1 1,181 dyn \u22c5 s \u22c5 cm<jats:sup>\u22125<\/jats:sup>, P &lt; 0.01) and greater decreases in CO (3.18 \u00b1 0.31 to 2.74 \u00b1 0.26 l\/min, P &lt; 0.05; and 3.07 \u00b1 0.38 to 2.30 \u00b1 0.36 l\/min, P &lt; 0.01) and stroke volume (32.2 \u00b1 2.9 to 25.9 \u00b1 2.4 ml, P &lt; 0.05; and 31.5 \u00b1 1.9 to 19.8 \u00b1 3.1 ml, P &lt; 0.01). Only CA increased LV end-systolic myocardial segment length. Similar findings were observed with 15-s apnea duration. We conclude that CA produced greater depression of CO and greater changes of afterload-related LV dysfunction than did OA. Therefore, decreased ITP was not the dominant factor determining LV function with apneas. <\/jats:p>","DOI":"10.1152\/jappl.1997.83.2.485","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T18:39:11Z","timestamp":1513967951000},"page":"485-494","source":"Crossref","is-referenced-by-count":22,"title":["Comparative hemodynamic effects of periodic obstructive  and simulated central apneas in sedated pigs"],"prefix":"10.1152","volume":"83","author":[{"given":"Ling","family":"Chen","sequence":"first","affiliation":[{"name":"Pulmonary and Critical Care Division, Long Island Jewish Medical Center, Long Island Campus for the Albert Einstein College of Medicine, New Hyde Park, New York 11042"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven M.","family":"Scharf","sequence":"additional","affiliation":[{"name":"Pulmonary and Critical Care Division, Long Island Jewish Medical Center, Long Island Campus for the Albert Einstein College of Medicine, New Hyde Park, New York 11042"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(82)90072-8"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1183\/09031936.94.07040786"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0165-1838(89)90008-8"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1992.73.5.1743"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1994.77.4.1602"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1378\/chest.89.3.331"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1982.sp014208"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1991.00400030025005"},{"key":"B10","first-page":"283","volume":"21","author":"Lugaresi E.","year":"1984","journal-title":"Sleep and Breathing"},{"key":"B11","first-page":"1021","volume":"42","author":"McIntyre K.","year":"1989","journal-title":"Heart-Lung Interactions in Health and Disease"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1993.74.6.2969"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1996.80.3.773"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199304293281712"},{"key":"B15","first-page":"435","volume":"69","author":"Podszus T.","year":"1986","journal-title":"Eur. 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