Blood pressure elevation during hindquarter compression in dogs is neurogenic

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 determining the duration of the blood pressure increase, and 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 less than 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 less than 0.001), plasma norepinephrine increased by 717 +/- 133 pg/ml (P less than 0.01) and plasma renin rose by 3.4 +/- 1.0 ng/ml/h (P less than 0.05). The pressure elevation was due to a 37% increase in total vascular resistance (P less than 0.01). Spinal anaesthesia at L4-L5 level in nine dogs caused a 70% reduction of blood pressure increase during lower body compression (P less than 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 less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)