CONTRIBUTION OF HUMORAL SYSTEMS TO THE RECOVERY OF BLOOD-PRESSURE FOLLOWING SEVERE HEMORRHAGE

1 Profound haemorrhage activates a number of presser mechanisms, inclu ding the release of catecholamines, angiotensin II and arginine-vasopr essin, which contribute to the subsequent cardiovascular recovery. Usi ng specific single or combined blockade with prazosin, losartan and Ma nning compound (AVPX), the aim of this study was to evaluate the invol vement of the three presser systems in blood pressure recovery followi ng severe heamorrhage (20 mi kg(-1)). 2 Haemorrhage of conscious, unre strained rats resulted in a significant initial decrease in blood pres sure of approximately 60 mmHg, and heart rate of approximately 70 bpm. Then, blood pressure tended to return to the control level within 10 min. The total cardiovascular recovery corresponded to increments of 5 2 +/- 5 mmHg (81% of the acute fall) for systolic blood pressure, and of 92 +/- 22 bpm (124%) for heart rate at 60 min post-bleeding. Signif icant falls in haematocrit (-10.5 +/- 1.2%, P < 0.01), in plasma conce ntrations of proteins (-10.3 +/- 0.9 g l(-1), P < 0.01) and haemoglobi n (-2.58 +/- 0.72 g 100 ml(-1), P < 0.05) were observed at 60 min post -bleeding. 3 Pretreatment with one or two specific antagonists did not exaggerate the initial fall in blood pressure. The initial bradycardi a was weakened only by combined blockade with losartan and AVPX. 4 The blood pressure recovery from a haemorrhage was delayed by approximate ly 25 min by the inhibition of vasopressin activity. The systolic bloo d pressure recovery in control animals (81% of the acute fall) was blu nted by losartan (55% of the acute fall), prazosin (49%), combined los artan and AVPX (36%), prazosin and AVPX (36%), and also by prazosin pl us losartan (13%). The diastolic blood pressure recovery was blunted o nly in the groups where the activity of angiotensin II was inhibited b y losartan. 5 In conclusion, we have shown that neither catecholamines , angiotensin II nor vasopressin, although activated, individually com pensate the acute hypotensive response to haemorrhage. The contributio n of vasopressin to the blood pressure recovery post-bleeding is trans ient and is rapidly replaced by the presser activity of the catecholam ines and angiotensin II. The full systolic blood pressure recovery fro m severe haemorrhage requires the combined activity of these two press er systems, while the diastolic blood pressure recovery seems to be on ly dependent upon angiotensin II activity.