Abstract
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~s) rose from 92 in the baseline to 125 (p <0.01) during arithmetic and to 124 (p <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. All these observations support the concept that systemic and pulmonary vasculatures become oversensitive to neural activation and that the two vascular beds are exposed to the same type of dysregulation in systemic hypertension.
| Original language | English |
|---|---|
| Pages (from-to) | 995-1002 |
| Number of pages | 8 |
| Journal | Dimensions of Critical Care Nursing |
| Volume | 7 |
| Issue number | 6 |
| Publication status | Published - 1985 |
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Keywords
- Arithmetic
- Blood gases cold vasoconstriction
ASJC Scopus subject areas
- Critical Care
- Emergency
Cite this
Pulmonary vascular overreactivity in systemic hypertension : A pathophysiological link between the greater and the lesser circulation. / Fiorentini, Cesare; Barbier, Paolo; Galli, Claudia; Loaldi, Alessandro; Tamborini, Gloria; Tosi, Elena; Guazzi, Maurizio D.
In: Dimensions of Critical Care Nursing, Vol. 7, No. 6, 1985, p. 995-1002.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Pulmonary vascular overreactivity in systemic hypertension
T2 - A pathophysiological link between the greater and the lesser circulation
AU - Fiorentini, Cesare
AU - Barbier, Paolo
AU - Galli, Claudia
AU - Loaldi, Alessandro
AU - Tamborini, Gloria
AU - Tosi, Elena
AU - Guazzi, Maurizio D.
PY - 1985
Y1 - 1985
N2 - 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~s) rose from 92 in the baseline to 125 (p <0.01) during arithmetic and to 124 (p <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. All these observations support the concept that systemic and pulmonary vasculatures become oversensitive to neural activation and that the two vascular beds are exposed to the same type of dysregulation in systemic hypertension.
AB - 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~s) rose from 92 in the baseline to 125 (p <0.01) during arithmetic and to 124 (p <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. All these observations support the concept that systemic and pulmonary vasculatures become oversensitive to neural activation and that the two vascular beds are exposed to the same type of dysregulation in systemic hypertension.
KW - Arithmetic
KW - Blood gases cold vasoconstriction
UR - http://www.scopus.com/inward/record.url?scp=84929970598&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84929970598&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:84929970598
VL - 7
SP - 995
EP - 1002
JO - Dimensions of Critical Care Nursing
JF - Dimensions of Critical Care Nursing
SN - 0730-4625
IS - 6
ER -