Hampl et al. (A-69) note that inhaled nitric oxide (NO) is a selective pulmonary vasodilator. They hypothesized

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Hampl et al. (A-69) note that inhaled nitric oxide (NO) is a selective pulmonary vasodilator. They hypothesized that a nebulized diethylenetriamine/NO (DETA/NO) would stay in the lower airways and continuously supply sufficient NO to achieve sustained vasodilation in chronic pulmonary hypertension. Experimental material consisted of adult, male, specific pathogen-free SpragueDawley rats randomly divided into four groups: untreated, pulmonary normotensive controls;

monocrotaline-injected (to induce hypertension) with no treatment (MCT); monocrotaline-injected treated with either a 5 mmol dose or a 50 mmol dose of DETA/NO. Nineteen days after inducing pulmonary hypertension in the two groups of rats, the researchers began the treatment procedure, which lasted for 4 days. They collected, among other data, the following measurements on cardiac output for the animals in the four groups:
MCT รพ DETA/NO Control MCT 5mmol 50mmol 71.8 42.8 72.5 47.1 66.1 53.2 62.9 86.6 67.6 56.1 58.9 56.0 66.4 56.5 69.3 Source: Data provided courtesy of Dr. Stephen L. Archer.

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