Systematic evaluation of nitric oxide, tetrahydrobiopterin, and anandamide levels in a porcine model of endotoxemia

Abstract

Our data suggest that the BH4 values were significantly increased in several organs, especially in the liver during endotoxic shock. Impaired cardiac output and decreased blood pressure appeared in the early phase of porcine endotoxemia. Longer-term observation of these parameters after LPS treatment should be performed as the next step in future studies.

The effect of obeticholic acid on hepatic blood flow in isolated, perfused porcine liver: Correction of oxygen‐nutrient mismatch might be a putative mechanism of action in NASH

“…It accounts for at least 80 per cent of total hepatic blood flow without myogenic elements to control the flow. The HA contains well oxygenated blood from the heart and lungs 7–9 . It has myogenic elements that can modulate flow and subsequent oxygen delivery.…”

“…The HA contains well oxygenated blood from the heart and lungs. [7][8][9] It has myogenic elements that can modulate flow and subsequent oxygen delivery. However, it accounts for only 20 per cent of hepatic blood flow.…”

Measurement of Tetrahydrobiopterin in Animal Tissue Samples by HPLC with Electrochemical Detection—Protocol Optimization and Pitfalls

“…We successfully detected BH4 in the brain, heart and kidney of control and LPS treated rats in the concentration range more similar to previously published data (Table 2). LPS-induced sepsis is known to increase nitric oxide and BH4 levels via inflammatory pathways via induction of iNOS [19][20][21][22]. Chromatogram peaks of BH4 in the brains were detectable in control and LPS-treated rats (Figure 7A).…”

“…Since BH 4 bioavailability is tightly linked to regulation of eNOS activity, the levels of BH 4 have a strong impact on vascular function, cardiovascular health and the adhesion/infiltration of immune cells [15][16][17][18]. On the other hand, induction of BH 4 synthesis is a hallmark of severe inflammatory conditions, as observed in the setting of endotoxemia (e.g., by lipopolysaccharide [LPS]) and septic shock [19][20][21]. A similar increase in BH 4 synthesis and nitric oxide formation was observed in a more moderate model of cardiovascular inflammation, mice with angiotensin-IIinduced arterial hypertension [18].…”