An in vitro study of histamine on the pulmonary artery of the Wistar–Kyoto and spontaneously hypertensive rats

Contribution of glibenclamide-sensitive, ATP-dependent K+ channel activation to acetophenone analogues-mediated in vitro pulmonary artery relaxation of rat

“…The Animal Experimentation Ethics Committee of The Chinese University of Hong Kong (HKSAR, PR of China) approved experiments performed in this study (approval no: 00/017/MIS). Experimental procedures involved in isometric tension measurement of isolated pulmonary artery (1 mm in length, 1st intra-lobar branch, O.D.¨800 Am) (Lau et al, 2003) (gassed with 16% O 2 /6% CO 2 balanced with N 2 , pO 2 100 mmHg) (MacLean et al, 1996) (resting tension: 2.0 T 0.1 mN, corresponded to a transmural pressure of¨15 mmHg) have been described previously (Doggrell et al, 1999;Thomas and Wanstall, 2003). Fat and connective tissues were carefully removed under the dissecting microscope.…”

Histamine-mediated increases in cytosolic [Ca2+] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

“…Histamine, a molecule synthesized and released mainly from mast cells in the adventitial layer of pulmonary vessels (e.g., during inflammatory response), is a vasoactive substance with dual effects on the pulmonary vasculature. Histamine can elicit vasoconstriction or vasodilation depending on the cell type (e.g., smooth muscle cells or endothelial cells) on which it is acting and on the receptor subtypes (e.g., H 1 , H 2 , H 3 , or H 4 ) activated (1,11,28,30,31,50).Histamine exerts a vasocontrictive effect, presumably via activation of H 1 receptors, but also exerts a vasodilatory effect on pulmonary arterial muscle preparations (9, 39). Whereas the dual effects of histamine on vessel caliber of human pulmonary arteries have been known for some time, the Ca 2ϩ signals that underlie stimulation of PASMC and PAEC with histamine have not been extensively examined.…”

“…Histamine, a molecule synthesized and released mainly from mast cells in the adventitial layer of pulmonary vessels (e.g., during inflammatory response), is a vasoactive substance with dual effects on the pulmonary vasculature. Histamine can elicit vasoconstriction or vasodilation depending on the cell type (e.g., smooth muscle cells or endothelial cells) on which it is acting and on the receptor subtypes (e.g., H 1 , H 2 , H 3 , or H 4 ) activated (1,11,28,30,31,50).…”

Refractory Persistent Pulmonary Hypertension of the Newborn Responsive Only to Neuromuscular Blockade

“…Some explanations may be raised: firstly this could be related to improved and more effective ventilation due to a better wall compliance and a fully synchronize infant's breathing (decreased struggling) but our patient was comfortable under a fentanyl continuous perfusion and on HFO. The neuromuscular blocker could trigger a release of histamine, which in two studies [9,10], has been recognised as a pulmonary vasodilator acting on H2-receptors in pulmonary vasculature in dogs and rats; however our patient did not present any signs of systemic vasodilatation, and pancuronium is known to usually have an overall hypertensive effect. Respiratory paralysis may reduce oxygen consumption by eliminating the work of breathing and may also reduce peak transthoracic pressure decreasing risk of barotrauma, but our patient was ventilated on HFO and was already apneic prior to curare.…”