CARDIOVASCULAR-RESPONSES TO HEAT-STRESS IN LATE-GESTATION FETAL SHEEP

Citation
Dw. Walker et al., CARDIOVASCULAR-RESPONSES TO HEAT-STRESS IN LATE-GESTATION FETAL SHEEP, Experimental physiology, 80(5), 1995, pp. 755-766
Citations number
29
Categorie Soggetti
Physiology
Journal title
ISSN journal
09580670
Volume
80
Issue
5
Year of publication
1995
Pages
755 - 766
Database
ISI
SICI code
0958-0670(1995)80:5<755:CTHILF>2.0.ZU;2-8
Abstract
Heat stress during pregnancy in sheep is associated with respiratory a lkalosis in both the mother and fetus, and, if prolonged, fetal growth is retarded. In seven pregnant sheep at 130-137 days gestation we use d 15 mu m diameter radioactive microspheres to determine the effect of raising the environmental temperature from 20 to 43 degrees C for 8 h on uteroplacental blood flows and the distribution of cardiac output in the ewe and fetus. Fetal cardiac output increased slightly from 47 . 0 +/- 3 . 2 (mean +/- S.E.M.) to 54 . 0 +/- 3 . 6 ml min(-1) (100 g tissue)(-1), fetal arterial pressure and heart rate were unchanged, an d total vascular conductance in the fetus increased significantly from 12397 +/- 1111 to 14732 +/- 1569 ml min(-1) kg(-1) mmHg(-1) (P < 0 . 01). Tissue blood flows (in ml min(-1) (100 g)(-1)) increased signific antly (P < 0 . 05) in the fetal body (e.g. nasal mucosa, torso and for eleg skin, adrenal, thyroid and thymus glands, brown and omental fats, heart, urinary bladder and carcass) and the fetal brain (e.g. cerebel lum, cerebral grey matter, cervical spinal cord and pituitary gland). These regional vasodilatations occurred despite a significant fall (P < 0 . 01) in fetal arterial O-2 saturation (55 . 2 +/- 1 . 8 vs. 38 . 6 +/- 2 . 4%), P-O2 (18 . 1 +/- 0 . 7 vs. 13 . 5 +/- 0 . 8 mmHg) P-CO2 (51 . 0 +/- 1 . 8 vs. 36 . 1 +/- 2 . 3 mmHg); under normothermic cond itions hypoxia is associated with peripheral vasoconstriction. Because hypocapnia would also be expected to cause cerebral vasoconstriction it is suggested that during hyperthermia, hypoxia- and hypocapnia-indu ced vasoconstrictions are reduced by the release of vasodilator substa nces, or a decrease of sympathoadrenal effector responses. Blood flow to the fetal and maternal sides of the placenta did not change during the heat stress, suggesting that perfusion-dependent transfer of heat from fetus to mother across the placenta does not increase under hyper thermic conditions.