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...

The influence of hypercarbia, combined hypercarbia and hypoxemia, and hypocarbia on cerebral blood flow of preterm infants with a gestational age of less than 34 weeks was investigated by measuring peak systolic flow velocity (PSFV), end diastolic flow velocity (EDFV), pulsatility index (PI) and area under the velocity curve (AUVC) ofthe anterior cerebral artery (ACA) using transcutaneous Doppler technique. Mild and moderate hypocarbia did not change cerebral blood flow velocity. During severe hypercarbia (PaC0 2 6.7 kPa) significantly lower PI-values were detected, mainly caused by an increase of EDFV, indicating a decreased cerebrovascular resistance and increased cerebral blood flow. A highly significant decrease in PI-values during combined severe hypercarbia and hypoxemia (Pa0 2 < 6.0 kPa) was found suggesting that hypoxemia superimposed on hypercarbia strengthens the increase of cerebral blood flow. While the increase of EDFV is thought to be due to carbon dioxide-induced vasodilation ofcerebral arterioles, we assume that the accompanied increase of PSFV during combined hypercarbia and hypoxemia is caused by an increase in cardiac output due to hypoxemia which can alter the blood flow velocity wave form ofthe ACA.

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Indomethacin lowers neonatal cerebral perfusion immediately after intravenous administration. It is important to elucidate whether this reduction is mediated by inhibition of production of prostaglandins, especially prostacyclin, which plays an important role in the autoregulation of the neonatal cerebral vascular bed. We studied changes in cerebral blood flow by serial measurements of temporal mean flow velocity in the anterior cerebral artery (TMFY-ACA), relative cerebral vascular resistance (R-cer), and prostaglandins (measured as changes in thiobarbituric acid reactive substances concentration; TBARS) after a therapeutic dose of 0.1 mg/kg indomethacin administered intravenously for noninvasive closure of patent ductus arteriosus. TMFV-ACA decreased and R-cer increased immediately after the indomethacin administration with a sustained recovery to preindomethacin values. The TBARS concentrations, however, did not change during the study period. We conclude that the present study suggests that a therapeutic dose of 0.1 mg/kg of indomethacin has no impact on prostaglandin metabolism.