In adults, cough sensitivity is influenced by gender and is heightened in those with non-productive cough. This study examined if cough sensitivity is (i) altered in children with asthma, recurrent cough, and cystic fibrosis and (ii) influenced by age, gender, or forced expiratory volume in one second (FEV 1 ).Cough sensitivity to capsaicin and spirometry were performed on 209 children grouped by the diagnosis of asthma, recurrent dry cough, cystic fibrosis, and controls.Cough sensitivity was increased in children with recurrent cough, and lower in children with cystic fibrosis when compared with children with asthma and controls. Age influenced cough sensitivity in the controls. In the asthmatics, FEV 1 (% predicted) correlated to cough sensitivity measures. There was no gender diVerence in cough sensitivity.It is concluded that cough sensitivity is diVerent among children with recurrent dry cough, asthma, and cystic fibrosis. In children, age, but not gender, influences cough sensitivity measures and when cough sensitivity is used in comparative studies, children should be matched for age and FEV 1 .

Increased resistance to portal flow and increased portal inflow due to mesenteric\ud vasodilatation represent the main factors causing portal hypertension in\ud cirrhosis. Endothelial cell dysfunction, defined as an imbalance between the\ud synthesis, release, and effect of endothelial mediators of vascular tone,\ud inflammation, thrombosis, and angiogenesis, plays a major role in the increase of\ud resistance in portal circulation, in the decrease in the mesenteric one, in the\ud development of collateral circulation. Reduced response to vasodilators in liver \ud sinusoids and increased response in the mesenteric arterioles, and, viceversa,\ud increased response to vasoconstrictors in the portal-sinusoidal circulation and\ud decreased response in the mesenteric arterioles are also relevant to the\ud pathophysiology of portal hypertension. Arachidonic acid (AA) metabolites through\ud the three pathways, cyclooxygenase (COX), lipoxygenase, and cytochrome P450\ud monooxygenase and epoxygenase, are involved in endothelial dysfunction of portal \ud hypertension. Increased thromboxane-A2 production by liver sinusoidal endothelial\ud cells (LSECs) via increased COX-1 activity/expression, increased leukotriens,\ud increased epoxyeicosatrienoic acids (EETs) (dilators of the peripheral arterial\ud circulation, but vasoconstrictors of the portal-sinusoidal circulation),\ud represent a major component in the increased portal resistance, in the decreased \ud portal response to vasodilators and in the hyper-response to vasoconstrictors.\ud Increased prostacyclin (PGI2) via COX-1 and COX-2 overexpression, and increased\ud EETs/heme-oxygenase-1/K channels/gap junctions (endothelial derived\ud hyperpolarizing factor system) play a major role in mesenteric vasodilatation,\ud hyporeactivity to vasoconstrictors, and hyper-response to vasodilators. EETs,\ud mediators of liver regeneration after hepatectomy and of angiogenesis, may play a\ud role in the development of regenerative nodules and collateral circulation,\ud through stimulation of vascular endothelial growth factor (VEGF) inside the liver\ud and in the portal circulation. Pharmacological manipulation of AA metabolites may\ud be beneficial for cirrhotic portal hypertension

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