Réactions cardio-vasculaires du rat à I'hypercapnie ventilatoire

Abstract

1. Two populations of albino rats : normal and treated by phentolamine, or normal and vagotomized, have inhaled normoxic or hyperoxic mixtures with 3, 15 or 30% CO2 during 5 min. 2. Bradycardia is proportional to CO2 concentration, from 3% CO2. It is not suppressed by vagotomy. 3. Systemic arterial pressures, both systolic and diastolic, are decreased by 14% CO2. This hypotension is long lasting. At 30% CO2, immediate hypotension is followed by progressive recovery. After phentolamine, the return to normal is abolished. 4. Bradycardia is caused by CO2 or acidosis acting directly on the pace-maker cells. Variations of the systemic blood pressure are explained by an interference between a direct vasodilatation and a vasoconstriction due to sympathetic centres stimulation by CO2.

Influences on the cardiovascular response to graded levels of systemic hypoxia of the accompanying hypocapnia in the rat.

“…the renal vasodilatation is facilitated by inhibitory influences upon renal sympathetic activity. Taken together, the suggestions that the fall in Pa, c02 may exert a vasoconstrictor influence upon skeletal muscle, but a vasodilator effect on the kidney, are consistent with previous observations that the effects of a rise in Pa co2 in the rat depend upon the balance between vasodilator and vasoconstrictor influences (Lagneaux & Remacle, 1981;Hargreaves & Marshall, 1986).…”

“…This would be in accord with our previous evidence that the tachyeardia observed in hypocapnic hypoxia is largely due to increased sympathetic activity (Marshall & Metcalfe, 1988 b). However, another possibility is that tachycardia produced by the direct influence of a fall in Pa co2 upon the cardiac pacemaker plays a part, given the fact that the opposite effect predominates in the rat when Pa c°2 is raised (Lagneaux & Remacle, 1981;Hargreaves & Marshall, 1986). In summary, the present study suggests that the hypocapnia that accompanies the hyperventilatory response to systemic hypoxia substantially attenuates the hyperventilation by reducing the stimulation of peripheral and central chemoreceptors.…”

“…On the other hand, given that a rise in Pa co2can induce bradycardia and peripheral vasodilatation by local effects upon the heart and peripheral tissues (e.g. Lagneaux & Remacle, 1981;Marshall, 1986) it is reasonable to suppose that a fall in Pa c2 could produce opposite local effects. In addition, attenuation of both peripheral and central chemoreceptor activity would reduce central inspiratory drive, which in turn would be expected to facilitate cardiac vagal activity and to inhibit sympathetic activity to heart and vasculature, thus tending to reduce heart rate and produce vasodilatation (Spyer, 1981).…”

“…This implies that in the dog the predominating influence of the hypocapnia is to induce tachyeardia and mesenteric and renal vasodilatation. In previous studies on the rat, systemic hypercapnia induced by adding CO2 (3-10% C02) to the inspirate induced bradycardia, attributable to a predominance of the local myocardial depressant effect of CO2, while the peripheral vascular effect depended on the severity of hypercapnia: net vasoconstriction in mild hypercapnia attributable to increased sympathetic activity, and vasodilatation in more severe hypercapnia due to the local effects of CO2 (Lagneaux & Remacle, 1981;Hargreaves & Marshall, 1986). From this it could be predicted that in the rat, the hypocapnia that accompanies hypoxia would tend to induce tachycardia, but the peripheral vascular effects might be vasoconstrictor or vasodilator.…”

Analysis of cardiovascular responses evoked following changes in peripheral chemoreceptor activity in the rat.

“…Since, when the vagi were intact but ventilation held constant, the response evoked by chemoreceptor stimulation was reversed to bradycardia, it may be concluded that influences other than lung stretch receptors but which are secondary to hyperventilation can induce tachycardia, although the primary cardiac response is bradycardia as in other species (see Daly, 1984). Given that a rise in Pa co2 induces bradycardia in the rat, apparently by a direct action on the heart (Lagneaux & Remacle, 1981;Hargreaves & Marshall, 1986), those secondary influences could have included the direct effect of a fall in PaC002 resulting from hyperventilation, and possibly a reflex initiated by atrial stretch receptor stimulation caused by a respiratory-dependent increase in venous return (see Daly, 1984). The fact that the baseline level of heart rate was not always reduced by guanethidine may indicate that this drug was not fully effective in blocking cardiac sympathetic activity; however, the observation that after guanethidine when the vagi were intact, chemoreceptor stimulation evoked bradycardia, supports the idea that the primary response was vagally mediated and suggests that effects secondary to hyperventilation were predominantly mediated by sympathetic fibres.…”