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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Chemosensitive cardiopulmonary afferents and the haemodynamic response to simulated haemorrhage in conscious rabbits.

1. We set out to test whether the signal from the heart that initiates the decompensatory phase of acute central hypovolaemia in conscious rabbits is conveyed by chemosensitive afferents. 2. Haemorrhage was simulated by inflating an inferior vena caval cuff so that cardiac output fell at a constant rate of 8% of its baseline level per min. After sham or vehicle treatments the haemodynamic response had two phases. In the first, sympathoexcitatory, phase systemic vascular conductance fell in proportion to cardiac output so that mean arterial pressure fell by only 13 mmHg. When cardiac output had fallen by approximately 50% a second, sympathoinhibitory, phase supervened. There was an abrupt rise of systemic vascular conductance and an abrupt fall of mean arterial pressure, to approximately 40 mmHg. 3. The sympathoinhibitory phase was prevented by injection of the delta-opioid antagonist ICI 174864 (100-300 nmol) or the mu-opioid agonist H-Tyr-D-Ala-Gly-MePhe-NH(CH2)2OH (DAMGO) (100-300 pmol) into the fourth cerebral ventricle. 4. 5-HT3 receptors on myocardial or pulmonary afferents were excited by injection of ascending doses of phenylbiguanide (6.25-400 micrograms) into the left or right atrium respectively. Neuronal-type nicotinic cholinoceptors in the epicardium were excited by injecting ascending doses of nicotine bitartrate (6.25-400 micrograms) into the pericardial sac. Each of these treatment regimens caused a reproducible, dose-dependent, fall in mean arterial pressure. Intravenous injection of the 5-HT3 antagonist MDL 72222 (1.0 mg kg-1) markedly attenuated the responses to phenylbiguanide.(ABSTRACT TRUNCATED AT 250 WORDS)[1]


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