Cardiovascular Effect of Dorsal Periaqueductal Gray During Lipopolysaccharide-induced Hypotension.

The mechanism of hypotension induced by endotoxin is not yet clear. However, it is often attributed to the direct effect of lipopolysaccharide (LPS) as a component of the outer wall of Gram-negative bacteria and other vascular mediators, including tumor necrosis factor (TNF) and nitric oxide (NO). One possibility is that the initial drop in LPS-induced arterial hypertension is mediated by a central mechanism. The ventral region of the transcranial gray matter is involved in lowering blood pressure, and the dorsal region is involved in increasing blood pressure. The dorsolateral region of the transcranial gray matter (dlPAG) also causes tachycardia, vasodilation in muscles, and tachypnea. dlPAG contains cells that produce NO and serotonin (5HT) and 5HT1 and 5HT2 receptors, which may play a role in hypotension due to stimulation of this region. LPS (1 mg/kg or higher IV) typically elicits a biphasic hypotensive response in rats. The first stage of this response begins immediately after LPS injection. The second phase begins about 1 hour after LPS injection. Thus, endotoxic hypertension begins through a central mechanism and further suggests that hypotension may play a critical role in developing fatal hypotension, representing the second stage of septic shock. Although dlPAG is an important site for regulating cardiovascular responses, its role in hypotension induced by LPS has not been investigated. We investigated the role of this nucleus in cardiovascular changes after LPS injection.