Hypertension, Vol 7, 995-1002, Copyright © 1985 by American Heart Association
C Fiorentini, P Barbier, C Galli, A Loaldi, G Tamborini, E Tosi and MD Guazzi
This study was undertaken to test whether the emphasized systemic
vasomotion during sympathetic activation in hypertension is shared by the
pulmonary circulation. To this end, 10 normotensive and 29 primary
hypertensive subjects were investigated during adrenergic stimulation by
mental arithmetic and cold pressor test. Both stimuli induced a systemic
pressor reaction in both groups, which was mediated through an increase in
cardiac output and a mild reduction in vascular resistance during
arithmetic and through a predominant rise in systemic vascular resistance
during cold. Each of these changes was emphasized in the hypertensive
population as compared with the normotensive one. Pressure in the pulmonary
artery remained unchanged during cold and was slightly raised (systolic)
during arithmetic in normotensive subjects. On the contrary, in
hypertensive subjects systolic and diastolic pulmonary pressures were
consistently augmented by both stimuli, and pulmonary arteriolar resistance
(dyn sec cm-5) rose from 92 in the baseline to 125 (p less than 0.01)
during arithmetic and to 124 (p less than 0.01) during the cold test. This
reaction is interpreted as reflecting a neurally mediated vasoconstriction
and not as the consequence of mechanical or chemical changes, since no
difference was observed in pulmonary wedge pressure, pleural pressure,
arterial blood gas levels, and pH between controls and hypertensive
subjects in the steady state and during either stressful stimulation.
Baseline pulmonary arteriolar resistance was also found to correlate
positively with systemic vascular resistance in the hypertensive group.
When pressure changes occurred, the time course was similar in the two
circuits; resistance increased to a proportionally similar degree in the
two districts during the cold stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Pulmonary vascular overreactivity in systemic hypertension. A pathophysiological link between the greater and the lesser circulation
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