Effects of Repetitive Airway Obstruction on O₂Saturation and Systemic and Pulmonary Arterial Pressure in Anesthetized Dogs

Abstract

We examined the effects of multiple repetitive airway obstruction (RAO) on arterial oxygen saturation (SaO2) and pulmonary and systemic arterial pressure in eight anesthetized spontaneously breathing dogs. SaO2 was monitored at the tongue with a pulse oximeter. RAO created by an electrical valve that was attached to a tracheal cannula was alternated with seven consecutive spontaneous breaths until the nadir SaO2 (nSaO2) became constant or decreased to less than 35%. Tracheal occlusion durations of 15, 30, 45 and 60 s were chosen arbitrarily. In each animal nSaO2 decreased with every trial number in an exponential fashion, and the rate of nSaO2 fall was greater for the longer occlusion duration. In each animal the increases in pulmonary arterial pressure (PAP) and systemic arterial pressure (SAP) were inversely related to the nSaO2 values, and the relationship between nSaO2 and PAP or SAP was identical for all occlusion durations. Moreover, when the animals breathed pure oxygen and SaO2 did not decrease, there were no significant increases in the PAP and SAP at similar levels of pleural pressure (Ppl). In another six dogs, the effects of RAO on PAP and SAP were compared with those of intermittent hypoxic exposure without apnea, which was achieved by the inhalation of hypoxic gas (4 to 6% O2, 5% CO2 in N2) instead of RAO, to examine the effects of interruption of ventilation. The relationships between nSaO2 and both pressures did not differ significantly from those during RAO.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular changes during acute episodic repetitive hypoxic and hypercapnic breathing in rats

“…On the other hand, increasing Pa,CO 2 by 1.4 kPa in anaesthetised dogs increased arterial pressure only by about 5 mmHg [13] when blood pressure increased more than 20 mmHg during the obstructive period in sleep apnoea [1]. These results [3,5,7] conflict with previous data [1,[8][9][10] and our finding showing the predominant role of hypoxaemia over hypercapnia in acute changes in SBP, DBP and HR. In our study, increases in SBP were higher with HOHC (+35.1±26.4 mmHg) than with HO (+25.3±25.7 mmHg) and HR decreased more with HOHC, (severe, -139.3±75.7 bpm; mild, -28.5±52.0 bpm) than HO (severe, -93.8±124.1 bpm; mild, -3.1±67.8 bpm) ( fig.…”

“…In agreement with this finding, STOOHS and GUILLEMINAULT [8] demonstrated in five men with severe obstructive sleep apnoea, that mean blood pressure always increased during the obstructive period and that the changes in HR were correlated with the degree of hypoxaemia. In experimental models of repetitive airway obstruction in anaesthetised dogs, IWASE et al [9] showed that the main factor in the increase in systemic arterial pressure during repetitive airway obstruction was hypoxaemia and that hypercapnia and acidosis had no significant effects. Increases in apnoeic and postapnoeic blood pressure correlate with the degree of hypoxia during apnoea [1].…”

Slow and fast changes in transmural pulmonary artery pressure in obstructive sleep apnoea

“…The factors which have been proposed for the pathogenesis of Ppa changes in OSA are: changes in cardiac output [3,5], the mechanical influences of intrathoracic pressure swings [6,7], and hypoxia [1,4,5,8].…”

“…In fact, Ppa during sleep increases more during room air breathing than during oxygen administration [5]; Ppa values during OSA are usually inversely correlated with arterial oxygen tension (PaO 2 ) or oxyhaemoglobin saturation (SaO 2 ) values [1,4]; and Ppa at apnoea termination increases as SaO 2 decreases during repetitive airway occlusion trials in dogs [8]. However, when oxygen was administered to blunt SaO 2 oscillations during OSA occurring in non rapid eye movement sleep (NREM) sleep, no significant effect was found on transmural Ppa oscillations within apnoeas [9].…”

“…The studies published, so far, concerning the effect of hypoxia on Ppa in OSA have been limited to the highest nocturnal Ppa value [5], the highest value after occlusion [8], or the values recorded only in NREM sleep, when the range of SaO 2 oscillation is limited [9]. In our previous study [9], we hypothesized that although hypoxia may determine, if any, only a minor increase in Ppa within each apnoea, it could cause a sustained increase in Ppa in consecutive apnoeas, since the time course of the response of the pulmonary vessels to hypoxia may be slower than the SaO 2 swings occurring in each apnoea episode.…”