Int J Angiol 1995; 4(4): 212-217
DOI: 10.1007/BF02042923
Original Articles

© Georg Thieme Verlag KG Stuttgart · New York

The effect of isradipine in acute altitude hypoxia on cerebral, renal, and splanchnic blood flow evaluated by Doppler measurements

Michel Court-Payen1 , Aram Ter Minassian2 , Niels Vidiendal Olsen3 , Inge -Lis Kanstrup4 , Claude Dubray5 , Jean -Paul Richalet6
  • 1Department of Ultrasound, Herlev Hospital, University of Copenhagen, Herlev, Denmark
  • 2Department of Anesthesia, Henri Mondor Hospital, University of Paris, Paris, France
  • 3Department of Anesthesia, Herlev Hospital, University of Copenhagen, Herlev, Denmark
  • 4Department of Clinical Physiology, Herlev Hospital, University of Copenhagen, Herlev, Denmark
  • 5Centre de Recherche, Laboratoires Sandoz, France
  • 6Association pour la Recherche en Physiologie de l'Environnement, U.F.R. de Médecine, Bobigny, France
Presented at the 35th Annual World Congress, International College of Angiology, Copenhagen, Denmark, July 1993This study was supported by the Danish Society of Diagnostic Ultrasound, Denmark; B & K Medical, France; Laboratoires Sandoz, France
Further Information

Publication History

Publication Date:
22 April 2011 (online)

Abstract

Recent studies have suggested that calcium antagonists may have a beneficial effect on high altitude pulmonary edema, but the effect on regional blood flow distribution is unknown. This study by transcranial and duplex Doppler evaluated the effect of the calcium antagonist isradipine on cerebral, renal, and splanchnic blood flows in acute altitude hypoxia. Twelve healthy subjects were investigated at sea level and repeatedly after 3–56 hours at high altitude (4350 m). Before the ascent, the subjects were randomized to treatment with isradipine 5 mg/day (n = 6) or placebo (n = 6). We measured flow velocities in middle cerebral arteries; flow rates in internal carotid arteries, portal vein, and right renal artery; and resistance indices in middle cerebral, internal carotid, renal, superior mesenteric, and hepatic arteries. Hypoxia increased middle cerebral artery flow velocity by 30% (placebo, p < 0.05) and 39% (isradipine, p < 0.01); increased internal carotid artery flow rate by 57% (placebo, p < 0.01) and 55% (isradipine, p < 0.05); and decreased middle cerebral and internal carotid artery resistance indices without differences between placebo and isradipine groups. Superior mesenteric artery resistance index was lower in hypoxia with isradipine compared with placebo (p < 0.05), suggesting a higher splanchnic blood flow. In conclusion, acute hypoxia induced an increase in cerebral blood flow. Besides decreasing superior mesenteric artery resistance index, prophylactic isradipine did not modulate the circulatory responses to acute hypoxia. The clinical significance of this increased splanchnic blood flow remains unclear.

    >