{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T08:35:07Z","timestamp":1775205307809,"version":"3.50.1"},"reference-count":19,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[1993,8,1]],"date-time":"1993-08-01T00:00:00Z","timestamp":744163200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1993,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>With sleep apnea syndrome, mean cardiac output (CO) may fall. This implies a fall in venous return (VR) that is equal to the product of the pressure gradient for VR (GVR) \u2014 mean circulatory pressure (MCP) \u2014 right ventricular end-diastolic pressure and the conductance for VR (Gv). During airway obstruction there could also be shifts of blood volume between central and peripheral circulatory compartments. We studied these parameters in anesthetized closed-chest, spontaneously breathing dogs when hypoxia occurred (room air [RA] breathing) and when hypoxia was prevented (100% O2 breathing). Obstructive apneas were induced by completely occluding the endotracheal tube at end expiration for 1 min and allowing 1 min of spontaneous ventilation. During RA apneas, arterial PO2 decreased to 32.7 \u00b1 6.1 mm Hg (p &amp;lt; 0.01). Apnea reduced respiratory effort rate by 22.0 to 37.0% and was associated with inspiratory airway pressure swings in both RA and O2 of approximately \u221216.0 mm Hg. During apnea, on RA and O2 heart rate and mean arterial pressure decreased by 20 to 30 beats\/min and by 8 to 12 mm Hg, respectively. On RA, CO decreased by 7.0% (not significant). In contrast, on O2, CO increased by 21.0% (p &amp;lt; 0.01). With RA apneas, GVR and MCP increased by 55% (p &amp;lt; 0.05) and Gv decreased by 63% (p &amp;lt; 0.05). On O2, there were no changes in GVR or Gv, and changes in CO were predictable from the baseline VR curve. With O2 there was an increase in central blood volume by 21.0% (p &amp;lt; 0.01) during the apneic phase. We conclude that (1) changes in the VR curve with apneas were related to hypoxemia; and (2) changes in VR were not related to shifts in blood volume from peripheral to central circulations.<\/jats:p>","DOI":"10.1164\/ajrccm\/148.2.323","type":"journal-article","created":{"date-parts":[[2013,4,4]],"date-time":"2013-04-04T17:46:01Z","timestamp":1365097561000},"page":"323-329","source":"Crossref","is-referenced-by-count":19,"title":["Effects of Periodic Obstructive Apneas on Venous Return in Closed-chest Dogs"],"prefix":"10.1093","volume":"148","author":[{"given":"Ariel","family":"Tarasiuk","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Long Island Medical Center Campus, Albert Einstein College of Medicine, New Hyde Park, New York"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven M.","family":"Scharf","sequence":"additional","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Long Island Medical Center Campus, Albert Einstein College of Medicine, New Hyde Park, New York"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[1993,8,1]]},"reference":[{"key":"p_1","first-page":"1159","volume":"8","author":"Coccagna G","year":"1972","journal-title":"Bull Physiopath Respir"},{"key":"p_3","doi-asserted-by":"crossref","first-page":"609","DOI":"10.1152\/ajplegacy.1957.189.3.609","volume":"189","author":"Guyton AC","year":"1957","journal-title":"Am J Physiol"},{"key":"p_4","doi-asserted-by":"crossref","first-page":"261","DOI":"10.1152\/ajplegacy.1954.179.2.261","volume":"179","author":"Guyton AC","year":"1954","journal-title":"Am J Physiol"},{"key":"p_5","first-page":"1122","volume":"236","author":"Sylvester JT","year":"1979","journal-title":"Am J Physiol"},{"key":"p_6","doi-asserted-by":"publisher","DOI":"10.1378\/chest.89.3.331"},{"key":"p_7","doi-asserted-by":"crossref","first-page":"583","DOI":"10.1152\/jappl.1992.72.2.583","volume":"72","author":"Stoohs R","year":"1992","journal-title":"J Appl Physiol"},{"key":"p_8","doi-asserted-by":"crossref","first-page":"321","DOI":"10.1164\/ajrccm\/146.2.321","volume":"146","author":"Scharf SM","year":"1992","journal-title":"Am Rev Respir Dis"},{"key":"p_9","doi-asserted-by":"publisher","DOI":"10.1063\/1.344402"},{"key":"p_10","doi-asserted-by":"publisher","DOI":"10.1016\/0167-5273(81)90050-4"},{"key":"p_11","doi-asserted-by":"publisher","DOI":"10.1378\/chest.95.2.338"},{"key":"p_12","doi-asserted-by":"publisher","DOI":"10.1007\/BF02714137"},{"key":"p_13","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.61.3.463"},{"key":"p_14","doi-asserted-by":"crossref","first-page":"557","DOI":"10.1152\/jappl.1960.15.4.557","volume":"15","author":"Ting EY","year":"1960","journal-title":"J Appl Physiol"},{"key":"p_15","first-page":"137","author":"Motta J","year":"1978","journal-title":"New York: Alan R. 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