Carotid, Not Aortic, Chemoreceptors Mediate the Fetal Cardiovascular Response to Acute Hypoxemia in Lambs

Abstract

ABSTRACI'. The fetal cardiovascular response to acute hypoxemia consists of a decrease in heart rate, a variable change in mean arterial pressure, and an increase in peripheral vascular resistance. This response is mediated by the arterial chemoreceptors. To determine whether chemoreceptors in the carotid artery or in the aorta mediate the fetal cardiovascular response to acute hypoxemia, we studied the response to acute hypoxemia in fetal lambs at 125 to 130 d of gestation after selective carotid (six fetuses) or aortic (five fetuses) denervation. One to 3 d after insertion of catheters, hypoxemia was induced by inflating a balloon occluder around the ewe's hypogastric artery or by giving the ewe 95% Nz and 5% 0 2 to breathe. The chemoreflex response was measured as decrease in heart rate per decrease in H b O2 saturation. To validate our results, we also studied the response to chemical stimulation of the chemoreceptors by injection of sodium cyanide into the inferior vena cava. We found that carotid denervation abolished the heart rate and peripheral vascular resistance responses to hypoxemia but that aortic denervation did not. Responses after injection of sodium cyanide were similar.to those seen during acute hypoxemia. We conclude that the carotid chemoreceptors, and not the aortic chemoreceptors, mediate the fetal cardiovascular response to acute hypoxemia. (Pediatr Res 34: [51][52][53][54][55] 1993) Abbreviations AHRIASa02, decrease in heart rate to decrease in oxygen saturation AHRIABP, decrease in heart rate to increase in mean arterial pressure NaCN, sodium cyanideThe fetal cardiovascular response to acute hypoxemia consists of a decrease in heart rate, a variable change in mean arterial pressure, an increase in peripheral vascular resistance, and a redistribution of blood flow (1-3). The changes in heart rate are mediated by arterial chemoreceptors located in the common carotid artery and aortic arch (4-6). Changes in arterial pressure, peripheral vascular resistance, and blood flow redistribution are mediated in part by chemoreceptors, but also by local mechanisms (3). However, whether the carotid or the aortic chemore- Based on studies in fetal lambs, Dawes et al. (7) suggested that the aortic chemoreceptors mediate the response to acute hypoxemia. They also suggested that the carotid chemoreceptors are inactive in the fetal physiologic range (8), although carotid-nerve activity has been recorded in fetal lambs (9). However, all of these experiments were performed in acutely exteriorized fetal lambs, whereas the ewe was given chloralose anesthesia. The effects of exteriorization and anesthesia may have influenced the results.The aim of this study was to determine whether chemoreceptors located in the carotid artery or in the aorta mediate the fetal cardiovascular response to acute hypoxemia. To avoid any effects of exteriorization and anesthesia, we studied the response to hypoxemia in six carotid-and five aortic-chemoreceptor-denervated fetal lambs chronically instrumented in urero at 125 to 13...

Mild chronic hypoxia modifies the fetal sheep neural and cardiovascular responses to repeated umbilical cord occlusion

“…During the first minute of occlusion the expected bradycardic response was present in both groups and no differences in the magnitude of the fall in heart rate were observed. This initial bradycardia is thought to represent a chemoreceptor response that is vagally mediated (Bartelds et al, 1993). Consistent with our data, in chronically hypoxic high altitude-exposed fetal sheep with a comparable reduction in fetal arterial pO 2 and without acidosis, the bradycardic response to umbilical cord occlusion was shown not to be affected (Imamura et al, 2004).…”

“…The mechanism of this late fall is less clear. Among the possible mechanisms are recruitment of other peripheral chemoreceptor input (Bartelds et al, 1993), a synergistic effect of severe hypercarbia on carotid chemoreceptors (Blanco et al, 1984), a direct effect of ischemia on cardiac pacemaker cells (Gryshchenko et al, 2002), and an activation of the cardioinhibitory Bezold-Jarisch reflex (Aviado and Guevara, 2001;Dawes and Comroe, Jr., 1954). This latter reflex originates from the stimulation of both mechanically and chemically sensitive receptors in the ventricle which can be elicited by coronary ischemia and asphyxia (Thoren, 1972).…”

The role of carotid chemoreceptors in the effects of hypoxia on renal blood flow in the late gestation sheep fetus

“…However, it seems likely that chemo-rather than baroreceptors mediate the rapid RBF responses and bradycardia during hypoxia, since the rise in MAP was slow in the CSD group and did not reach significance in the intact group. Previous studies have demonstrated that the initial bradycardia during hypoxia is a carotid rather than an aortic chemoreflex response (Bartelds et al 1993;Giussani et al 1993). In accordance with these findings we have shown a striking effect of CSD on bradycardia, as well as on the initial fall in RBF, during hypoxia.…”

Pathophysiology, Management, and Outcomes of Fetal Hemodynamic Instability During Prenatal Cardiac Intervention

“…There is abundant evidence that fetal hypoxia causes bradycardia, primarily through a carotid chemoreceptor reflex (15)(16)(17). Accordingly, carotid arterial hypoxia may contribute to PCI-related FHI.…”