SUMMARY It has been speculated that free amino acids digested from proteins in bird eggs are transported to the circulation for the nourishment of the embryo. In the present study, we found that early chicken embryo protein in the serum might be utilized efficiently as a nutrient. Proteins injected into the blood of embryonic day 3 (E3) embryos were partially degraded and rapidly cleared. The rapid clearance of the injected proteins might be the result of efficient pinocytosis by blood cells, which then efficiently digested the intracellular proteins. An evaluation of the fluorescence intensity of injected fluorescein isothiocyanate-labeled bovine serum albumin (FITC-BSA) indicated that about half was taken up by the blood cells 80 min after injection. About 4 h after injection, most of the FITC-BSA was digested and the products were released into the serum, which implies that circulating blood cells may serve as a digestive system in early chick embryos. However, the endocytic activity of blood cells decreased after E5, and BSA may reside in the circulation with a longer half-life after E5. These results imply that blood cells would serve as a digestive system only in early embryos. In summary, the mechanism revealed here gives the early embryo the ability to make use of protein as a nutrient without prior digestion outside the embryo.

SUMMARY Hypothermic incubation reduces the ability of the late-stage chicken embryo to mount endothermic heat production. This study investigates whether blood O 2 transport is similarly limited by cooler incubation temperatures. Two populations of chicken embryos were incubated at 38°C and 35°C. At Hamilton–Hamburger (HH) developmental stage 41–42, hypothermic incubation had no significant effect on hematocrit(∼26%) or [Hb] (7 g%). However, in the final stages of incubation (stage 43–44), hypothermic incubation reduced hematocrit from ∼31% at 38°C to ∼27.5% at 35°C. Hypothermic incubation similarly caused a reduced [Hb] from 8.5 g% (38°C) to 6.25 g% (35°C), indicating a reduction in blood O 2 -carrying capacity in embryos. Incubation temperature had a strong effect on blood–O 2 affinity in late development (stage 43–44), with P 50 at 38°C falling significantly from ∼6 kPa in 38°C embyros to ∼4 kPa in 35°C embryos. P O 2 values in chorioallantoic arterial blood at HH 41–42 were 4.3 kPa at pH 7.46 (38°C) and 3.4 kPa at pH 7.39 (35°C). In chorioallantoic venous blood these values were 9.1 kPa at pH 7.34 (38°C) and 8.1 kPa at pH 7.42 (35°C). With further development to HH 43–44, chorioallantoic arterial blood oxygenation fell to 2.4 kPa at pH 7.54 (38°C) and 2.8 kPa at pH 7.52 (35°C). Similarly, P O 2 in chorioallantoic venous blood fell slightly to 7.7 kPa at pH 7.42 (38°C) and 7.4 kPa at pH 7.48 (35°C). Collectively, these data reveal that beyond HH 41–42, 35°C embryos experience retarded hematological development, and the findings that support the observed delayed metabolic response to acute temperature changes.

SUMMARY Chronic exposure to a low incubation temperature clearly slows the development of poikilothemic chicken embryos (or any other poikilotherms), but little is known about the more subtle developmental effects of temperature,especially on physiological regulatory systems. Consequently, two populations of chicken embryos were incubated at 38°C and 35°C. When compared at the same development stage, incubation temperature had no significant impact on embryonic survival or growth. Moreover, the relative timing of major developmental landmarks (e.g. internal pipping), expressed as a percentage of development, was unaffected by temperature. The ability to maintain the rate of oxygen consumption( V̇ O 2 ) during an acute drop in ambient temperature ( T a ) improved from Hamburger–Hamilton (HH) stages 39–40 to 43–44 in the 38°C but not the 35°C populations. Late stage (HH43–44) embryos incubated at 38°C could maintain V̇ O 2 (approximately 27–33 μl g –1 min –1 )during an acute drop in T a to approximately 30°C. However, at the same stage 35°C embryos acutely measured at 38°C were unable to similarly maintain their V̇ O 2 , which fell as soon as T a reached 36°C. Thus, while hypothermic incubation does not affect gross development (other than would be predicted from a simple effect of Q 10 ), there is a significant delay in the relative timing of the onset of thermoregulatory ability induced by hypothermic incubation.