Metabolic syndrome and the hepatorenal reflex.

Insufficient hepatic O in animal and human studies has been shown to elicit a hepatorenal reflex in response to increased hepatic adenosine, resulting in the stimulation of renal as well as muscle sympathetic nerve activity and activating the renin angiotensin system. Low hepatic ATP, hyperuricemia, and hepatic lipid accumulation reported in metabolic syndrome (MetS) patients may reflect insufficient hepatic O delivery, potentially accounting for the sympathetic overdrive associated with MetS. This theoretical concept is supported by experimental results in animals fed a high fructose diet to induce MetS.

Metabolic syndrome and the hepatorenal reflex.

Insufficient hepatic O2 in animal and human studies has been shown to elicit a hepatorenal reflex in response to increased hepatic adenosine, resulting in stimulation of renal as well as muscle sympathetic nerve activity and activating the renin angiotensin system. Low hepatic ATP, hyperuricemia, and hepatic lipid accumulation reported in metabolic syndrome (MetS) patients may reflect insufficient hepatic O2 delivery, potentially accounting for the sympathetic overdrive associated with MetS. This theoretical concept is supported by experimental results in animals fed a high fructose diet to induce MetS.

Dose-dependent hemodynamic and metabolic effects of vasoactive medications in normotensive, anesthetized neonatal piglets.

The developmentally regulated hemodynamic effects of vasoactive medications have not been well characterized. We used traditional and near-infrared spectroscopy monitoring technologies and investigated the changes in heart rate, blood pressure, common carotid artery (CCA) blood flow (BF), cerebral, renal, intestinal, and muscle regional tissue O2 saturation, and acid-base and electrolyte status in response to escalating doses of vasoactive medications in normotensive anesthetized neonatal piglets. We used regional tissue O2 saturation and CCA BF as surrogates of organ and systemic BF, respectively, and controlled minute ventilation and oxygenation.

Near-infrared spectroscopy monitoring of cerebral oxygen during assisted ventilation.

Background: Changes in the arterial partial pressure of CO(2) (PaCO(2)) has a direct though transient effect on the cerebral vasculature and cerebral circulation. Decreased PaCO(2) levels lead to vasoconstriction and can result in dangerously low levels of cerebral perfusion that resolve in 4-6 h. It is currently believed that perfusion abnormalities contribute to intraventricular hemorrhage (IVH) and periventricular leukomalacia (PVL) in the neonate.

Cerebral and somatic venous oximetry in adults and infants.

Background: The development in the last decade of noninvasive, near infrared spectroscopy (NIRS) analysis of tissue hemoglobin saturation in vivo has provided a new and dramatic tool for the management of hemodynamics, allowing early detection and correction of imbalances in oxygen delivery to the brain and vital organs.

Description: The theory and validation of NIRS and its clinical use are reviewed. Studies are cited documenting tissue penetration and response to various physiologic and pharmacologic mechanisms resulting in changes in oxygen delivery and blood flow to the organs and brain as reflected in the regional hemoglobin oxygen saturation (rSO(2)).