In a previous paper we reported that in pigs and dogs hindlimb compression causes large blood pressure increases which appear to be neurogenic. The present studies explore the utility of this non-invasive pressor model by (a) determining the duration of the blood pressure increase, and (b) by providing definitive evidence that the pressor response is neurogenic.
All studies were done in chloralose-anaesthetized mongrel dogs. Prolonged experiments were performed in five experimental and four control dogs. Pressor responses could be elicited over a period of 9 h. The blood pressure increase during the 9th h was +30 ± (s.e.m.) 6/32 ± 5 mmHg (P < 0.001 by paired t-test). The blood pressure in control animals did not change.
Short-term hormonal and haemodynamic responses were analysed in 10 dogs. After 20 min hindlimb compression, mean blood pressure was elevated by 41.2 ± 8.0 mmHg (P < 0.001), plasma norepinephrine increased by 717 ± 133 pg/ml (P < 0.01) and plasma renin rose by 3.4 ± 1.0 ng/ml/h (P < 0.05). The pressure elevation was due to a 37% increase in total vascular resistance (P < 0.01).
Spinal anaesthesia at L4-L5 level in nine dogs caused a 70% reduction of blood pressure increase during lower body compression (P < 0.001) and totally abolished plasma renin and norepinephrine increases.
The infrarenal aorta and lower vena cava were occluded in eight dogs. After the ligation, there was a small rise in mean blood pressure (13.1 ± 3.7 mmHg, P < 0.01). Compression of the hindlimbs with already ligated vessels caused an additional 35.1 ± 6.4 mmHg increase in mean arterial pressure (P < 0.001). This increase was abolished after deflation of the suit. Pressor responses to compression of extremities, which were excluded from the circulation, showed that the reflex originates from the area of compression and is not due to a distant effect of some blood-borne factor.
Availability of a non-invasive method to elicit reproducible neurogenic blood pressure increases may provide a useful new tool to study target organ responses to transient neurogenic pressor episodes.
Journal of Hypertension 2:411-417, 1984