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.
ABSTRACT
The contractility of airway smooth muscle (ASM) plays an important role in pathophysiology of several bronchial disorders. Increased contraction of ASM during asthma and respiratory viral infection has been attributed to the release of mediators acting through different receptors. In the present study, influence of influenza type A virus (H1N1) infection has been examined on ASM responsiveness to various bronchoactive agents e.g. adenosine, histamine, 5-hydroxytryptamine (5-HT) and isoproterenol in an organ bath set up for isolated tissue preparation. The contractile effect of adenosine, histamine and 5-HT was enhanced, however, relaxant response of isoproterenol was attenuated with the duration following viral exposure. The most prominent response was observed 48 to 72 hr after infection and tissues from multiple exposure to virus infected animals showed the maximum contractile response. Results demonstrated the deleterious effect of viral infection on ASM function and the findings will be helpful in understanding the mechanism of influenza virus induced bronchoconstriction.
Subject(s)
Orthomyxoviridae Infections/physiopathology , Respiratory Muscles/physiopathology , Adenosine/pharmacology , Animals , Female , Guinea Pigs , Histamine/pharmacology , In Vitro Techniques , Isoproterenol/pharmacology , Male , Muscle Contraction/drug effects , Respiratory Muscles/drug effects , Serotonin/pharmacology , Trachea/drug effects , Trachea/physiopathologyABSTRACT
The present study was undertaken to examine the endothelium modulated effects of polypharmaceutical drug lipotab and its individual ingredients in isolated aortic rings of rat. Endothelium intact and denuded aortic rings were precontracted with phenylephrine 10(-6) M and drugs were added in cumulative manner in concentration ranging from 1 to 50 microg/ml. The results demonstrated an endothelium-dependent vasorelaxant effect of lipotab and its individual ingredients, with the exception of nicotinic acid. The dose dependent relaxant response of nicotinic acid was not altered significantly in the endothelium-denuded rings, suggesting a direct effect of the drug on the vascular smooth muscle. Vasorelaxant effect of lipotab and its individual constituents suggests the therapeutic potential of these compounds in certain cardiovascular diseases.
