Trophic influences of human and rat amniotic fluid on neural tube-derived rat fetal cells.

Normal human (week 17-20) and rat (E16-17) amniotic fluids were used as culture media for primary cultures of rat fetal (E 16) cortical, mesencephalic and striatal cell dissociates, or astroglial subcultures from the same brain regions. Phase-bright and dark cells were identified under phase contrast microscopy and their cell processes were measured utilizing semi-automated procedures. Subcultured astroglia were immuno-reacted against glial fibrillary acidic protein and fibronectin.

Effect of long-term oral nisoldipine on infarct size and collateral development in pigs undergoing gradual occlusion of the left circumflex artery.

We examined the effects of nisoldipine on infarct size and collateral development in pigs, whose coronary circulation is similar to that of humans, using an experimental protocol reproducing as closely as possible the usual clinical setting. Fifteen pigs undergoing left circumflex Ameroid-occlusion were randomized into a control group (n = 8) and a group (n = 7) treated with oral nisoldipine 0.03 mg/kg every 6 h for 1 month starting on the second postoperative day.

The effect of the new calcium antagonist nisoldipine (BAY k-5552) on myocardial infarct size limitation in conscious dogs.

The effect of the new calcium antagonist nisoldipine (BAY k-5552) on myocardial infarct size was studied in four groups of conscious dogs undergoing acute left anterior descending coronary artery occlusion. Group I received placebo for 48 hours before and for 24 hours after occlusion; group II received placebo before and nisoldipine (0.3 mg/kg orally every 6 hours) after occlusion; group III received nisoldipine before and placebo after occlusion; and group IV received nisoldipine before and after occlusion.

Sensitivity of enzymatic release due to ischemia in the isolated rat heart.

The sensitivity of cardiac enzymes (GOT, a-HBDH, LDH, LDH-1, CPK and CPK-MB) was studied in the isolated rat heart subjected to 0 (non-ischemic), 20, 30 and 40 min of total global ischemia (0 ml/min) followed by reperfusion in which three consecutive perfusate samples were collected for enzymatic measurements. Cardiac function, estimated by peak tension (Tp), maximal rate of tension development (Tc) and relaxation (Tr) decreased to 0 with ischemia and recovered with reperfusion to 100% in the 20 min, 50% in the 30 min and 10% in the 40 min ischemic groups. In these three groups, enzymatic release, measured as the relative increment (RI) with respect to the control samples, gave significantly higher values than those of non-ischemic hearts (P less than 0.

Myocardial triglycerides increased by fasting. Effects of hypoxia on contractility and enzymatic release.

The effect of fasting on the mechanics of contraction was studied in the isolated perfused rat heart, in oxygenated and hypoxic conditions. Animals were subjected to 48 h of fasting, a condition which produces augmented endogenous triglycerides (TG). Normal and fasted rats were submitted to a 10-min period of hypoxia, which depressed peak tension (Tp), maximal rate of contraction (Tc), and relaxation (Tr); all three parameters recovered with reoxygenation.