Acclimation to hypothermic incubation in developing chicken embryos (Gallus domesticus): I. Developmental effects and chronic and acute metabolic adjustments.

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 degrees C and 35 degrees 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 ((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 degrees C but not the 35 degrees C populations. Late stage (HH43-44) embryos incubated at 38 degrees C could maintain (O(2)) (approximately 27-33 micro l g(-1) min(-1)) during an acute drop in T(a) to approximately 30 degrees C. However, at the same stage 35 degrees C embryos acutely measured at 38 degrees C were unable to similarly maintain their (O(2)), which fell as soon as T(a) reached 36 degrees 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.

Acclimation to hypothermic incubation in developing chicken embryos (Gallus domesticus): II. Hematology and blood O2 transport.

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 degrees C and 35 degrees C. At Hamilton-Hamburger (HH) developmental stage 41-42, hypothermic incubation had no significant effect on hematocrit ( approximately 26%) or [Hb] (7 g%). However, in the final stages of incubation (stage 43-44), hypothermic incubation reduced hematocrit from approximately 31% at 38 degrees C to approximately 27.5% at 35 degrees C. Hypothermic incubation similarly caused a reduced [Hb] from 8.5 g% (38 degrees C) to 6.25 g% (35 degrees 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 degrees C falling significantly from approximately 6 kPa in 38 degrees C embryos to approximately 4 kPa in 35 degrees C embryos. P(O(2)) values in chorioallantoic arterial blood at HH 41-42 were 4.3 kPa at pH 7.46 (38 degrees C) and 3.4 kPa at pH 7.39 (35 degrees C). In chorioallantoic venous blood these values were 9.1 kPa at pH 7.34 (38 degrees C) and 8.1 kPa at pH 7.42 (35 degrees C). With further development to HH 43-44, chorioallantoic arterial blood oxygenation fell to 2.4 kPa at pH 7.54 (38 degrees C) and 2.8 kPa at pH 7.52 (35 degrees C). Similarly, P(O(2)) in chorioallantoic venous blood fell slightly to 7.7 kPa at pH 7.42 (38 degrees C) and 7.4 kPa at pH 7.48 (35 degrees C). Collectively, these data reveal that beyond HH 41-42, 35 degrees C embryos experience retarded hematological development, and the findings that support the observed delayed metabolic response to acute temperature changes.