EFFECTS OF GRADED HEMORRHAGE ON SHORT-TERM VARIABILITY OF BLOOD-PRESSURE IN CONSCIOUS RATS

A controlled graded bleeding was performed in conscious rats with 15 m in intervals between two withdrawals, in order to induce a 25% blood l oss without hypotension. Heart rate (HR) was unaffected as well. The s pectral profiles of systolic blood pressure (SEP) analyzed on 51.2 s s egments exhibited increases in the high frequency (HF, respiratory) co mponent. This increase paralleled the blood loss with a rise ranging f rom 20% for a I mL/kg hemorrhage to 90% for a II mL/kg removal. These changes were associated with increases in the mid-frequency (MF, Mayer waves) component of SEP variability. These latter rises were between 30 and 40% of the control value. Breathing frequency (BF) and blood ga ses were unaltered following hemorrhage. A shift of fluid occurred dur ing the 3 h session as reflected by the significant hemodilution. Rats were also bled after pretreatment with prazosin (1 mg/kg) or with an association of prazosin (1 mg/kg) and losartan (10 mg/kg). These treat ments increased HR. A marked fall in SEP occurred with the double bloc kade. Hemorrhage determined a relative bradycardia together with the S EP decrease (reversible shock) after prazosin and losartan treatment. Prazosin determined opposite changes in MF (-33%) and HF (+58%) SEP co mponents. A further decrease in the MF SEP component was observed foll owing the double blockade. Spectral profiles following hemorrhage were unchanged compared to the prehemorrhage blocked levels. Therefore gra ded nonhypotensive, ie, normotensive hemorrhage in rats, was associate d with progressive increases in the respiratory SEP variations, estima ted from the SEP spectrum. This sensitive index could reflect the low preload state due to hypovolemia. The hemorrhage-induced MF SEP compon ent increase could reflect an increased sympathetic vasomotor drive, p revented with prazosin, as a reflex adjustment to hypovolemia. Renin a ctivation could also contribute to the genesis of MF waves and its rol e in maintaining BP following hemorrhage was examplified with alpha(1) -adrenoceptor blockade.