Department of Pediatrics, University of Tennessee Health Science Center (UTHSC), Memphis, TN, USA.
Department of Physiology, University of Tennessee Health Science Center (UTHSC), Memphis, TN, USA.
Pediatr Res. 2018 Aug;84(2):290-295. doi: 10.1038/s41390-018-0061-5. Epub 2018 May 28.
Hypercapnia causes cerebral vasodilation and increased cerebral blood flow (CBF). During prolonged hypercapnia it is unknown whether cerebral vasodilation persists and whether cerebrovascular function is preserved. We investigated the effects of prolonged severe hypercapnia on pial arteriolar diameters (PAD) and cerebrovascular reactivity to vasodilators and vasoconstrictors.
Piglets were anesthetized, intubated and ventilated. Closed cranial windows were implanted to measure PAD. Changes in PAD were documented during hypercapnia (PaCO 75-80 mm Hg). Cerebrovascular reactivity was documented during normocapnia and at 30, 60, and 120 min of hypercapnia.
Cerebral vasodilation to hypercapnia was sustained over 120 min. Cerebrovascular responses to vasodilators and vasoconstrictors were preserved during hypercapnia. During hypercapnia, vasodilatory responses to second vasodilators were similar to normocapnia, while exposure to vasoconstrictors caused significant vasoconstriction.
Prolonged severe hypercapnia causes sustained vasodilation of pial arteriolar diameters indicative of hyperperfusion. During hypercapnia, cerebral vascular responses to vasodilators and vasoconstrictors were preserved, suggesting that cerebral vascular function remained intact. Of note, cerebral vessels during hypercapnia were capable of further dilation when exposed to additional cerebral vasodilators and, significant vasoconstriction when exposed to vasoconstrictors. Extrapolating these findings to infants, we suggest that severe hypercapnia should be avoided, because it could cause/increase cerebrovascular injury.
高碳酸血症可引起脑血管扩张和脑血流增加（CBF）。在长时间高碳酸血症期间，尚不清楚脑血管扩张是否持续存在，以及脑血管功能是否得到保留。我们研究了长时间严重高碳酸血症对软脑膜小动脉直径（PAD）和脑血管对血管扩张剂和血管收缩剂反应性的影响。
猪崽被麻醉、插管并通气。植入封闭的颅窗以测量 PAD。在高碳酸血症期间（PaCO 75-80mmHg）记录 PAD 的变化。在正常碳酸血症和高碳酸血症 30、60 和 120 分钟时记录脑血管反应性。
高碳酸血症期间脑血管扩张持续 120 分钟。高碳酸血症期间，血管扩张剂和血管收缩剂的脑血管反应性得以保留。在高碳酸血症期间，第二血管扩张剂的血管扩张反应与正常碳酸血症相似，而暴露于血管收缩剂会导致明显的血管收缩。
长时间严重高碳酸血症可导致软脑膜小动脉直径持续扩张，表明存在过度灌注。在高碳酸血症期间，脑血管对血管扩张剂和血管收缩剂的反应性得以保留，提示脑血管功能保持完整。值得注意的是，在高碳酸血症期间，当暴露于其他脑血管扩张剂时，脑血管能够进一步扩张，而当暴露于血管收缩剂时，则会发生明显的血管收缩。将这些发现外推至婴儿，我们建议应避免严重高碳酸血症，因为它可能导致/增加脑血管损伤。
