Mechanisms of acute cardiovascular response to periodic apneas in sedated pigs

This study was designed to evaluate the importance of sympathoadrenal activ ation in the acute cardiovascular response to apneas and the role of hypoxe mia in this response. In addition, we evaluated the contribution of the vag us nerve to apnea responses after chemical sympathectomy. In six pigs prein strumented with an electromagnetic flow probe and five nonpreinstrumented p igs, effects of periodic nonobstructive apneas were tested under the follow ing six conditions: room air breathing, 100% O-2 supplementation, both repe ated after administration of hexamethonium (Hex), and both repeated again a fter bilateral vagotomy in addition to Hex. With room air apneas, during th e apnea cycle, there were increases in mean arterial pressure (MAP; from ba seline of 108 +/- 4 to 124 +/- 6 Ton; P < 0.01), plasma norepinephrine (fro m 681 +/- 99 to 1,825 +/- 578 pg/ml, P < 0.05), and epinephrine (from 191 /- 67 to 1,245 +/- 685 pg/ml, P < 0.05) but decreases in cardiac output (CO ; from 3.3 +/- 0.6 to 2.4 +/- 0.3 l/min, P < 0.01) and cervical sympathetic nerve activity. With O-2 supplementation relative to baseline, apneas were associated with small increases in MAP (from 112 +/-: 4 to 118 +/- 3 Torr, P < 0.01) and norepinephrine (from 675 +/-. 97 to 861 +/-: 170 pg/ml, P < 0.05). After Hex, apneas with room air were associated with Small increases in MAP (from 103 +/- 6 to 109 +/- 6 Torr, P < 0.05) and epinephrine (from 136 +/- 45 to 666 +/-: 467 pg/ml, P < 0.05) and decreases in CO (from 3.6 /- 0.4 to 3.2 +/- 0.5 l/min, P < 0.05). After Hex, apneas with O-2 suppleme ntation were associated with decreased MAP (from 107 +/- 5 to 100 +/- 5 Tor r, P < 0.05) and no other changes. After vagotomy + Hex, with room air and O-2 supplementation, apneas were associated with decreased MAP (from 98 +/- 6 to 76 +/- 7 and from 103 +/- 7 to 95 +/- 6 Torr, respectively, both P < 0.01) but increased CO [from 2.7 +/- 0.3 to 3.2 +/- 0.4 l/min (P < 0.05) an d from 2.4 +/- 0.2 to 2.7 +/- 0.2 l/min (P < 0.01), respectively]. We concl ude that sympathoadrenal activation is the major presser mechanism during a pneas. Cervical sympathetic nerve activity does not reflect overall sympath oadrenal activity during apneas. Hypoxemia is an important but not the sole trigger factor for sympathoadrenal activation. There is an important vagal ly mediated reflex that contributes to the presser response to apneas.