C Ca ar rd di io ov va as sc cu ul la ar r c ch ha an ng ge es s d du ur ri in ng g a ac cu ut te e e ep pi is so od di ic c r re ep pe et ti it ti iv ve e h hy yp po ox xi ic c a an nd d h hy yp pe er rc ca ap pn ni ic c b br re ea at th hi in ng g i in n r ra at ts s The aim of this study was to investigate the acute haemodynamic changes observed during the repetitive inhalation of various gas mixtures in rats for HO alone and HO + HC, and to analyse the effects of vigilance and of the stress of gas administration.We studied 6 unanaesthetized Wistar rats chronically instrumented with an aortic catheter. Nitrogen, nitrogen + CO 2 mixtures and compressed air were randomly administered in a Plexiglass chamber for 10 s and then flushed by compressed air for 20 s. Two cycles were repeated every min for 10 to 12 min. The inhaled gas fractions (FI,O 2 , FI,CO 2 ) were monitored by O 2 and CO 2 analysers. Blood pressure (BP) was measured by a P23XL transducer. The blood gases were analysed by a 1306 IL meter.In control experiments, with compressed air alone, there were no significant acute changes in heart rate (HR) and BP. During HO there were no changes in HR or BP at FI,O 2 values from 0.05-0.14, whilst at FI,O 2 values from 0-0.05 systolic blood pressure (SBP) rose significantly (+25.3±25.7 (SD) mmHg) and HR decreased (-93.8±124.1 bpm). During HOHC, SBP rose (+35.1±26.4 mmHg) and HR decreased (-139.3±75.7 bpm), significantly more than in HO alone. SBP was linearly correlated with Pa,O 2 during HO (r=0.53) and also during HOHC (r=0.44) and was not directly related to Pa,CO 2 which has, nevertheless, an additive effect to HO. SBP rose with each challenge significantly more when the rats were awake than when asleep (behavioural sleep).We conclude that in this acute repetitive inhalation model, the rise in SBP is not related to gas stress or to Pa,CO 2 but to a decrease in Pa,O 2 and is enhanced by wakefulness.

Acute intermittent repetitive hypoxia simulating sleep apnoea syndrome is responsible for acute rises in blood pressure (BP). In the rat, the BP rises are enhanced by added hypercapnia. To investigate the role of the autonomic nervous system (ANS) in acute hypertension during repetitive hypoxia alone, FiO2 (inspiratory fractional concentration of oxygen) 2 to 5%, or combined with hypercapnia FiCO2 (inspiratory fractional concentration of carbon dioxide) 2 to 5%, we used autonomic blockade by atropine (1 mg kg-1) + propranolol (1 mg kg-1)-phentolamine (1 mg kg-1). Seven Wistar male rats were chronically instrumented with two aortic and venous catheters. Repetitive administration of N2 and N2 + CO2 for 10s followed by 20s compressed air was repeated for 4-5 min before (control) and after autonomic blockade. After autonomic blockade there was no significant difference in mean blood pressure (MBP) during severe hypoxia (SHO) (14.9 +/- 0.5 mmHg) compared to control (10.5 +/- 0.9 mmHg), while MBP was significantly decreased in severe hypoxia + hypercapnia (SHOHC) (14.1 +/- 0.4 mmHg) compared to control (26.8 +/- 0.3 mmHg) (p < 0.001). We conclude that the acute BP rise observed during hypoxic breathing is not due to the activation of ANS, but when hypercapnia is added to the hypoxic stimulus about half of pressor response is caused by ANS.