Effects of endothelial cell injury on pulmonary vascular reactivity.
Using the thiocarbamide model of acute lung injury in rats, we found that alpha-naphthylthiourea (ANTU) caused lung endothelial cell injury, as evidenced by increased permeability edema and decreased angiotensin I conversion. These effects were associated with enhanced pulmonary vascular reactivity. Recurrent ANTU lung injury caused pulmonary hypertension. The water-soluble thiocarbamide thiourea caused cultured vascular endothelial cells to release neutrophil chemoattractant activity. We speculate that endothelial cell injury may modulate the function of vascular smooth muscle and blood leukocytes.
D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D004727:Endothelium; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D008168:Lung / Q000098:blood supply*; D008171:Lung Diseases / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D009504:Neutrophils / Q000502:physiology; D011654:Pulmonary Edema / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D013890:Thiourea / Q000031:analogs & derivatives
D000804:Angiotensin II; D013890:Thiourea; C005277:alpha-naphthyl thiourea