Lappuse 1 no 142 rezultātiem
Neurogenic pulmonary edema is an acute life-threatening complication of central nervous system injury. We introduce a hypothesis that early i.v. administration of high-dose atropine can prevent neurogenic pulmonary edema development on the basis of the prevention of baroreflex-induced bradycardia,
This study was undertaken to evaluate the role of vagal nerves in the development of neurogenic pulmonary edema. We injected fibrinogen and thrombin into the cisterna magna of rats, a model of neurogenic pulmonary edema. When the vagal nerves were left intact, pulmonary edema occurred
Electroconvulsive therapy (ECT) was scheduled for a 61-yr-old woman with major depression who had been taking a beta-blocker for hypertension. She underwent the first ECT under thiamylal anesthesia uneventfully. The second ECT was performed under propofol anesthesia on the next day. Immediately
Although pulmonary vascular engorgement has often been hypothesized to decrease airway caliber, leading to airway obstruction in asthma, direct evidence for this hypothesis is lacking. In the present study, we used high-resolution computed tomography to directly measure the changes in the caliber
Changes in pulmonary endothelium permeability and in microvascular hemodynamics induced by parathion (Pth) and paraoxon (Pox), its active metabolite, were investigated in isolated, perfused rabbit lungs. Blood-free perfusate was recirculated through isolated and ventilated lungs in an isogravimetric
Neurogenic pulmonary edema (NPE), which is induced by acute spinal cord compression (SCC) under the mild (1.5 %) isoflurane anesthesia, is highly dependent on baroreflex-mediated bradycardia because a deeper (3 %) isoflurane anesthesia or atropine pretreatment completely abolished bradycardia
Three consecutive patients participated in a prospective evaluation of pseudophakic cystoid macular edema. The duration of the macular edema ranged from 6 to 8 months. On the initial visit, the best corrected acuity with spectacles was determined and a potential acuity meter reading was obtained;
Three classes of drugs were found, after their i.p. administration, to inhibit Paf-acether-induced edema of the rat's paw. These were beta-adrenergic agonists (isoproterenol, salbutamol), alpha-adrenergic antagonists (prazosin, ergotamine, yohimbine, phenoxybenzamine), and calcium entry blockers
The intratracheal injection of one moderate dose of adrenalin in rabbits whose vagi are divided produces a marked pulmonary edema in a large percentage of cases. The same dose in normal animals causes only slight effects. Artificial respiration greatly reduces the production of pulmonary edema in
Acute lung injury has been reported in man and animals with intracranial disorders, head trauma or cerebral compression. Early studies in our laboratory demonstrated that pulmonary hemorrhagic edema (PHE) of acute and fulminating type occurred accompanying severe hypertension and bradycardia
We evaluated the efficacy of aerosolized acetylcholinesterase (AChE) reactivator oxime MMB-4 in combination with the anticholinergic atropine sulfate for protection against respiratory toxicity and lung injury following microinstillation inhalation exposure to nerve agent soman (GD) in guinea pigs.
FR113680 is a newly developed tripeptide substance P (SP) receptor antagonist. The effects of FR113680 on airway constriction and airway edema induced by neurokinins were investigated in guinea-pigs. In in vitro experiments, FR113680 inhibited the contraction of isolated guinea-pig trachea induced