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 min intervals between two withdrawals, in order to induce a 25% blood loss without hypotension. Heart rate (HR) was unaffected as well. The spectral profiles of systolic blood pressure (SEP) analyzed on 51.2 s segments exhibited increases in the high frequency (HF, respiratory) component. This increase paralleled the blood loss with a rise ranging from 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 gases were unaltered following hemorrhage. A shift of fluid occurred during 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 treatments increased HR. A marked fall in SEP occurred with the double blockade. Hemorrhage determined a relative bradycardia together with the SEP decrease (reversible shock) after prazosin and losartan treatment. Prazosin determined opposite changes in MF (-33%) and HF (+58%) SEP components. A further decrease in the MF SEP component was observed following the double blockade. Spectral profiles following hemorrhage were unchanged compared to the prehemorrhage blocked levels. Therefore graded nonhypotensive, ie, normotensive hemorrhage in rats, was associated with progressive increases in the respiratory SEP variations, estimated from the SEP spectrum. This sensitive index could reflect the low preload state due to hypovolemia. The hemorrhage-induced MF SEP component increase could reflect an increased sympathetic vasomotor drive, prevented with prazosin, as a reflex adjustment to hypovolemia. Renin activation could also contribute to the genesis of MF waves and its role in maintaining BP following hemorrhage was examplified with alpha(1)-adrenoceptor blockade.