Since many critical conditions treated in intensive care units and operating rooms involve an imbalance between oxygen supply and oxygen demand, which may lead to a general breakdown of homeostasis, it is crucially important to develop a method for the early and reliable detection of these conditions. In addition, these pathophysiological conditions often involve the activation of the sympathetic system; hence, we tested the effect of epinephrine injection on these two organs. The results indicated that, following the injection of increasing doses of epinephrine, the brain showed an increase of tissue blood flow (TBF) in a dose-dependent manner, with no damage to its mitochondrial function and energetic state, while TBF in the small intestine decreased and NADH increased. The increase in cerebral blood supply under various concentrations of epinephrine reflects the ability of the central protection mechanism to preserve the blood supply to the brain, while “less vital” organs, like the small intestine, undergo vasoconstriction due to the predominates of alpha-stimulation. The effects of deep anesthesia induced by pentobarbitone caused the deterioration of cerebral blood flow (CBF), while intestinal blood flow (IBF) remained stable. The high sensitivity of CBF to pentobarbitone injection primarily indicates that this vasopressor agent has a central mechanism of activity. The activation of the sympathetic system by the injection of epinephrine under deep anesthesia demonstrated larger changes in CBF and metabolic state than those measured under mild anesthesia, due to the ability of deep anesthesia to reduce the level of Mean Arterial Pressure (MAP) and induce the elevation of vasodilator metabolites, such as adenosine (one of the mediators for the autoregulation of cerebral blood flow). In contrast, in the small intestine, there were no differences between the responses of TBF and NADH to epinephrine under different levels of anesthesia due to its low metabolic activity (relatively to the brain). The undershot of blood pressure during the recovery from the epinephrine injection episode was larger under deep anesthesia than that observed under mild anesthesia. This may be explained by the inhibitory effect of barbiturates on nitric oxide synthase activity (NOS). Our results showed that the blood supply to the brain is more affected by the level of NO in the body than IBF. In addition, NO is strongly involved in the pathogenesis of sepsis, yielding massive cardiovascular alterations. It appears that in the early stages of sepsis, the microcirculatory function is responsible for the maintenance of systemic circulation by redistributing the blood flow to the vital organs, while the blood flow in the “less vital” organs decreases.

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Effects of Vasoactive Mediators and Anesthesia on Brain and Small Intestine

  • Avraham Mayevsky,
  • Efrat Barbiro-Michaely,
  • Michael Tolmasov,
  • Mira M. Mandelbaum-Livnat

摘要

Since many critical conditions treated in intensive care units and operating rooms involve an imbalance between oxygen supply and oxygen demand, which may lead to a general breakdown of homeostasis, it is crucially important to develop a method for the early and reliable detection of these conditions. In addition, these pathophysiological conditions often involve the activation of the sympathetic system; hence, we tested the effect of epinephrine injection on these two organs. The results indicated that, following the injection of increasing doses of epinephrine, the brain showed an increase of tissue blood flow (TBF) in a dose-dependent manner, with no damage to its mitochondrial function and energetic state, while TBF in the small intestine decreased and NADH increased. The increase in cerebral blood supply under various concentrations of epinephrine reflects the ability of the central protection mechanism to preserve the blood supply to the brain, while “less vital” organs, like the small intestine, undergo vasoconstriction due to the predominates of alpha-stimulation. The effects of deep anesthesia induced by pentobarbitone caused the deterioration of cerebral blood flow (CBF), while intestinal blood flow (IBF) remained stable. The high sensitivity of CBF to pentobarbitone injection primarily indicates that this vasopressor agent has a central mechanism of activity. The activation of the sympathetic system by the injection of epinephrine under deep anesthesia demonstrated larger changes in CBF and metabolic state than those measured under mild anesthesia, due to the ability of deep anesthesia to reduce the level of Mean Arterial Pressure (MAP) and induce the elevation of vasodilator metabolites, such as adenosine (one of the mediators for the autoregulation of cerebral blood flow). In contrast, in the small intestine, there were no differences between the responses of TBF and NADH to epinephrine under different levels of anesthesia due to its low metabolic activity (relatively to the brain). The undershot of blood pressure during the recovery from the epinephrine injection episode was larger under deep anesthesia than that observed under mild anesthesia. This may be explained by the inhibitory effect of barbiturates on nitric oxide synthase activity (NOS). Our results showed that the blood supply to the brain is more affected by the level of NO in the body than IBF. In addition, NO is strongly involved in the pathogenesis of sepsis, yielding massive cardiovascular alterations. It appears that in the early stages of sepsis, the microcirculatory function is responsible for the maintenance of systemic circulation by redistributing the blood flow to the vital organs, while the blood flow in the “less vital” organs decreases.