{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,25]],"date-time":"2026-10-25T20:55:48Z","timestamp":1792961748552,"version":"4.5.0"},"reference-count":28,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[1997,6]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            Alcohol intake has been shown to worsen obstructive sleep apnea and increase nocturnal hypoxemia. The mechanisms of this action are unclear. Animal studies suggest that a reduction in chemoreflex sensitivity may be implicated. Using a double-blind, randomized, vehicle-controlled design, we tested the hypothesis that oral alcohol intake depresses chemoreflex sensitivity in humans. We examined the effects of oral alcohol intake (1.0 g\/kg body wt) on blood pressure, heart rate, heart rate variability, muscle sympathetic nerve activity, forearm vascular resistance, and minute ventilation in 16 normal male subjects. Peripheral and central chemoreflex sensitivity were measured in response to hypoxia (n=10) and hypercapnia (n=6), respectively. Plasma alcohol increased from 0 to 23.2\u00b11.5 mmol\/L (107\u00b17 mg\/dL) at 60 minutes and 20.2\u00b11 mmol\/L (93\u00b14 mg\/dL) at 85 minutes after alcohol intake (\n            <jats:italic>P<\/jats:italic>\n            &lt;.0001). Alcohol induced an increase in heart rate from 59\u00b12 to 66\u00b12 beats per minute (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01) and increased the ratio of low- to high-frequency variability of heart rate (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05). Although alcohol increased sympathetic nerve activity by up to 239\u00b122% of baseline values (\n            <jats:italic>P<\/jats:italic>\n            &lt;.01), forearm vascular resistance after alcohol was lower than that after vehicle (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05). Blood pressure did not increase compared with the vehicle session. Oxygen saturation during hypoxia after alcohol was 4\u00b11% lower than it was during hypoxia after vehicle (\n            <jats:italic>P<\/jats:italic>\n            &lt;.05) although arterial blood P\n            <jats:sc>o<\/jats:sc>\n            <jats:sub>2<\/jats:sub>\n            was unchanged. Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol. Alcohol does not alter chemoreflex responses to hypoxia or hypercapnia; thus, alterations in chemoreflex sensitivity are unlikely to explain the effects of alcohol on sleep apnea. Alcohol may reduce the affinity of hemoglobin for oxygen.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.29.6.1278","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"1278-1283","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":103,"title":["Effects of Alcohol on Sympathetic Activity, Hemodynamics, and Chemoreflex Sensitivity"],"prefix":"10.1161","volume":"29","author":[{"given":"Philippe","family":"van de Borne","sequence":"first","affiliation":[{"name":"From the Cardiovascular Division, Department of Internal Medicine, University of Iowa, Iowa City, and Centro Ricerche Cardiovascolari, CNR, Medicina Interna II, Ospedale \u201cL. Sacco,\u201d Universita di Milano (Italy) (N.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allyn L.","family":"Mark","sequence":"additional","affiliation":[{"name":"From the Cardiovascular Division, Department of Internal Medicine, University of Iowa, Iowa City, and Centro Ricerche Cardiovascolari, CNR, Medicina Interna II, Ospedale \u201cL. Sacco,\u201d Universita di Milano (Italy) (N.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicola","family":"Montano","sequence":"additional","affiliation":[{"name":"From the Cardiovascular Division, Department of Internal Medicine, University of Iowa, Iowa City, and Centro Ricerche Cardiovascolari, CNR, Medicina Interna II, Ospedale \u201cL. Sacco,\u201d Universita di Milano (Italy) (N.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Decio","family":"Mion","sequence":"additional","affiliation":[{"name":"From the Cardiovascular Division, Department of Internal Medicine, University of Iowa, Iowa City, and Centro Ricerche Cardiovascolari, CNR, Medicina Interna II, Ospedale \u201cL. Sacco,\u201d Universita di Milano (Italy) (N.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Virend K.","family":"Somers","sequence":"additional","affiliation":[{"name":"From the Cardiovascular Division, Department of Internal Medicine, University of Iowa, Iowa City, and Centro Ricerche Cardiovascolari, CNR, Medicina Interna II, Ospedale \u201cL. Sacco,\u201d Universita di Milano (Italy) (N.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(81)90124-8"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/sleep\/5.4.318"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp.45.4.353"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1164\/arrd.1984.130.2.153"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0025-7125(16)30987-7"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1164\/arrd.1984.130.2.156"},{"key":"e_1_3_2_7_2","first-page":"247","volume":"129","year":"1984","unstructured":"Krol RC, Knuth SL, Bartlett D Jr. Selective reduction of genioglossal muscle activity by alcohol in normal human subjects. 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