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ANOVA revealed no statistical changes after CGRP (P = 0.12) or placebo infusion (P = 0.41).
All of them received mechanical ventilation (p = 0.1) and catecholamine infusion (p = 0.001).
Similarly, the bone formation marker, bone-specific alkaline phosphatase, decreased continuously until 72 h after the ACTH infusion (P < 0.001).
Plasma concentrations of 13,14-dihydro-15-keto-prostaglandin F2α increased during oxytocin infusion (P <.022 vs saline solution infusion).
AV-diff negatively correlated with FBF at the end of the insulin infusion (P [lt ].001) for all studies.
The VMCA decreased during the PGE2 infusion (P = 0.005) but there was no significant dilatation of the STA (P = 0.850).
Left ventricular contractility increased with norepinephrine infusion (p = 0.002), but was not affected by fluid loading (p = 0.903).
Blood gas exchange (PaO2 and PaCO2) improved significantly 3 h after the start of infusion (p < 0.05).
MABP had normalized at the end of the study period (80 min from start of infusion) (P = 0.49) (Table 3).
The biochemical bone resorption markers tartrate-resistant acid phosphatase 5b and hydroxyproline decreased following ACTH infusion (P < 0.001 and P = 0.003, respectively).
A significant reduction was found in TNF-α in the sera of rabbits with ATL-146e infusion (P <.01) as compared with ischemic control animals.
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