The development of corticosteroid binding globulin-like activity in fetal sheep blood.

Parturition in sheep is initiated by the fetus and is preceded by a rise in fetal cortisol and corticosteroid-binding globulin (CBG) late in gestation. In this study plasma cortisol and CBG concentrations were measured in fetal and maternal circulation from 40 days gestation to early post-partum. The fetal cortisol profile was shown to be triphasic in nature; being high in both the first and last trimester but low in the middle period of gestation. In the last trimester, total cortisol increased steadily, reaching it's highest level just prior to parturition (145 days gestation), before falling to maternal levels over the first 10 days post-partum. The changes seen in CBG concentrations throughout gestation and post-partum mirrored the triphasic nature seen in cortisol levels. CBG was significantly higher at 40, 56 and 140 days gestation than at mid-gestation (77 and 90 days). However, at 145 days gestation there was a significant fall in CBG levels. CBG levels were higher at 1 day post-partum when compared to 145 days gestation, the former rapidly falling to maternal levels over the subsequent 9 days. The maximum binding capacity at 40, 56, 70 and 90 days gestation exceeds the total serum cortisol concentration. However at 140 and 145 days gestation and 1 day post-partum the total serum cortisol exceeds the Bmax. The highest cortisol:Bmax ratio is seen at 145 days gestation due to the fall of CBG binding capacity at this time.(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial infarction in the guinea pig: cellular electrophysiology

The cellular electrophysiology of left ventricular preparations from guinea pig hearts was studied 1 hour, 24 hours, and 4-6 weeks after myocardial infarction produced by 6-8 single ties of the distal left coronary artery system or after sham operation. Microelectrode recordings were used to monitor cells from the endocardial surface of each preparation in tissue bath. All coronary ligated preparations displayed accelerated spontaneous activity compared to normal and sham operated preparations. Single and multiple premature ventricular depolarizations occurred frequently in coronary ligated and rarely in normal and sham operated preparations. Premature stimuli delivered to areas overlying and bordering the area of infarction, induced short bursts of self-terminating rapid repetitive ventricular activity in 4 of 8 (50%) acute (1-hour), 5 of 9 (55%) subacute (24-hour), and 14 of 20 (70%) healed (4-6-week) infarcted preparations. Such activity could not be induced in normal and sham operated preparations. The preparations with healed infarction were unique in that they demonstrated runs of self-terminating repetitive ventricular activity which occurred spontaneously or was inducible with premature stimulation. Recordings from multiple sites in acute, subacute, and healed preparations revealed a variety of transmembrane action potential abnormalities (i.e., reduced action potential amplitude and resting potential, decreased and increased action potential duration, and depressed maximum rates of phase 0 depolarization) in cells overlying and bordering areas of infarction. Only Purkinje fiber action potentials were recorded over the healed infarcts. These data demonstrate that a spectrum of electrophysiological alterations occur in response to ischemic injury and persist after healing of the injury in this new model of myocardial infarction utilizing the guinea pig.