Effects of prenatal maternal TRH stimulation on the postnatal ability of neonatal piglets to cope with a cold challenge.

The effect of administering thyrotropin-releasing hormone (TRH) before farrowing on the ability of their newborn piglets to withstand a cold challenge was studied. Sows received intravenous infusions of TRH (5 microg kg(-1); TRH group) or physiological saline (0.9% NaCl; control group) from day 105 of gestation until farrowing. The plasma concentrations of thyroxine and triiodothyronine increased in sows treated with TRH. There were no differences in thyroxine and triiodothyronine between pigs born to sows in the TRH group and those of the control group. The rectal temperature of piglets born to TRH-treated sows decreased less than that of piglets born to controls as a consequence of a 1-hour cold challenge. Piglets born to sows in the TRH group had higher body weights at birth, and by day 28 they were an average 600 g heavier than those born to sows in the control group. Summarizing, prenatal maternal treatment with TRH appears to increase piglets' resistance to cold as well as to have beneficial effects on birth and weaning weights.

Three openings of the blood-brain barrier produced by forebrain ischemia in the rat.

A sensitive radiotracer method was used to explore the time course and regional pattern of blood-brain barrier (BBB) opening that occurs in a rat forebrain ischemia model that mimics temporary cardiac arrest. Immediately following 10 min of ischemia, transfer constants (Ki) for blood to brain permeation of [3H]sucrose were augmented severalfold, indicating widespread BBB opening. After 6 h, a delayed intensification of opening was evident in striatum and hippocampus, regions known to undergo selective, delayed neuronal death. There was generalized BBB recovery by 24 h except in experiments that involved prolonged ischemia (25 min) or concomitant brain hyperthermia (41 degrees C, 10 min). These protocols evoked a third opening; a marked upward increment in Ki and % H2O developed in neocortex between 6 and 24 h post-ischemia. Pharmacological or other manipulations of these temporal and regional patterns of altered transfer constants may aid understanding of the interplay between microvascular damage, edema, and neuronal death following brain ischemia.