Uday Yanamandra1, S P Singh2, Sushma Yanamandra3, Deepak Mulajkar4, R S Grewal5, Shashibala Singh6, M Z Ashraf7, Prasanna Reddy8, Velu Nair9. 1. Classified Specialist (Med) & Hematologist, Army Hospital (Research & Referral), Delhi Cantt 110010, India. 2. Associate Professor, Department of Physiology, Armed Forces Medical College, Pune, 411040, India. 3. Medical Officer, Max Hospital, Mohali, Punjab 160012, India. 4. Classified Specialist (Med) & Oncologist, Command Hospital (Southern Command), Pune, 411040, India. 5. MG (Med) Eastern Command Fort William, Kolkata, India. 6. DS & Director General, Life Sciences (LS), DRDO, Ministry of Defence, DRDO Bhavan, New Delhi 110011, India. 7. Former Scientist E &, Division Head, Genomics Division, DIPAS, DRDO, Timarpur, Delhi 110054, India. 8. Scientist F, DIPAS, DRDO, Timarpur, Delhi 110054, India. 9. Former Director General Medical Services (Army), Integrated Headquarters, Ministry of Defence, New Delhi 110001, India.
Abstract
BACKGROUND: Chronic intermittent hypoxia is known to induce systemic arterial hypertension whereas chronic hypoxia causes pulmonary arterial hypertension. High altitude (HA) induced systemic hypertension (HASH) in previously normotensive lowlanders following acclimatisation and prolonged stay at moderate HA is a commonly encountered medical problem. HASH has been attributed to increased sympathetic discharge. Endothelial dysfunction (ED) is implicated in hypertension in the plains hence this study was conducted in HA. This is relevant especially because of the established role of ED in the aetiopathogenesis of HA illnesses. Since hypoxia may induce ED, we aimed at studying the association of endothelial dysfunction with HASH in temporary residents at HA. METHODS: In this case-control single-centre study, we evaluated ED, by measuring endothelial molecular markers, soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (VCAM-1), vascular endothelial growth factor (VEGF) and endothelial selectin (E-Selectin) in 24 cases with HASH and 25 age, sex matched normotensive controls at moderate high altitude (11,500 ft). RESULTS: The levels of sICAM-1 (patients: 214.3 ± 34.2 μg/L, controls: 196.2 ± 28.5 μg/L; p = 0.049) and VCAM-1 (patients 766.1 ± 123.4 ng/mL, controls: 668.6 + 117.6 ng/mL; p = 0.007) were statistically higher in the patient group. However, VEGF and E-Selectin were not significantly different between the groups. sICAM-1 significantly correlated with levels of systolic and diastolic blood pressure (r = 0.401, p = 0.003 and 0.486, p = 0.000) respectively. CONCLUSION: HASH is associated with endothelial dysfunction in form of raised levels of sICAM-1 and VCAM-1.
BACKGROUND: Chronic intermittent hypoxia is known to induce systemic arterial hypertension whereas chronic hypoxia causes pulmonary arterial hypertension. High altitude (HA) induced systemic hypertension (HASH) in previously normotensive lowlanders following acclimatisation and prolonged stay at moderate HA is a commonly encountered medical problem. HASH has been attributed to increased sympathetic discharge. Endothelial dysfunction (ED) is implicated in hypertension in the plains hence this study was conducted in HA. This is relevant especially because of the established role of ED in the aetiopathogenesis of HA illnesses. Since hypoxia may induce ED, we aimed at studying the association of endothelial dysfunction with HASH in temporary residents at HA. METHODS: In this case-control single-centre study, we evaluated ED, by measuring endothelial molecular markers, soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (VCAM-1), vascular endothelial growth factor (VEGF) and endothelial selectin (E-Selectin) in 24 cases with HASH and 25 age, sex matched normotensive controls at moderate high altitude (11,500 ft). RESULTS: The levels of sICAM-1 (patients: 214.3 ± 34.2 μg/L, controls: 196.2 ± 28.5 μg/L; p = 0.049) and VCAM-1 (patients 766.1 ± 123.4 ng/mL, controls: 668.6 + 117.6 ng/mL; p = 0.007) were statistically higher in the patient group. However, VEGF and E-Selectin were not significantly different between the groups. sICAM-1 significantly correlated with levels of systolic and diastolic blood pressure (r = 0.401, p = 0.003 and 0.486, p = 0.000) respectively. CONCLUSION: HASH is associated with endothelial dysfunction in form of raised levels of sICAM-1 and VCAM-1.
Entities:
Keywords:
Endothelial dysfunction; High altitude; Systemic hypertension
Authors: V Pavlicek; H H Marti; S Grad; J S Gibbs; C Kol; R H Wenger; M Gassmann; J Kohl; F E Maly; O Oelz; E A Koller; C Schirlo Journal: Eur J Appl Physiol Date: 2000-04 Impact factor: 3.078
Authors: Aram V Chobanian; George L Bakris; Henry R Black; William C Cushman; Lee A Green; Joseph L Izzo; Daniel W Jones; Barry J Materson; Suzanne Oparil; Jackson T Wright; Edward J Roccella Journal: JAMA Date: 2003-05-14 Impact factor: 56.272