Sepsis is a systemic inflammatory response representing the leading cause of death in critically ill patients,mostly due to multiple organ failure.The gastrointestinal tract plays a pivotal role in the pathogenesis of...Sepsis is a systemic inflammatory response representing the leading cause of death in critically ill patients,mostly due to multiple organ failure.The gastrointestinal tract plays a pivotal role in the pathogenesis of sepsisinduced multiple organ failure through intestinal barrier dysfunction,bacterial translocation and ileus.In this review we address the role of the gastrointestinal tract,the mediators,cell types and transduction pathways involved,based on experimental data obtained from models of inflammation-induced ileus and (preliminary) clinical data.The complex interplay within the gastrointestinal wall between mast cells,residential macrophages and glial cells on the one hand,and neurons and smooth muscle cells on the other hand,involves intracellular signaling pathways,Toll-like receptors and a plethora of neuroactive substances such as nitric oxide,prostaglandins,cytokines,chemokines,growth factors,tryptases and hormones.Multidirectional signaling between the different components in the gastrointestinal wall,the spinal cord and central nervous system impacts inflammation and its consequences.We propose that novel therapeutic strategies should target inflammation on the one hand and gastrointestinal motility,gas-trointestinal sensitivity and even pain signaling on the other hand,for instance by impeding afferent neuronal signaling,by activation of the vagal anti-inflammatory pathway or by the use of pharmacological agents such as ghrelin and ghrelin agonists or drugs interfering with the endocannabinoid system.展开更多
Objective To study the arrhythmia induced by stimulation of nicotine-sensitive neurons in cardiac ganglial plexuses. Methods When nicotine (100 μg ) was injected into canine right atrial ganglial plexus (RAGP) and ga...Objective To study the arrhythmia induced by stimulation of nicotine-sensitive neurons in cardiac ganglial plexuses. Methods When nicotine (100 μg ) was injected into canine right atrial ganglial plexus (RAGP) and ganglial plexus between aorta and pulmonary artery (A-PGP) in 33 anesthetized open-chest dog, electrocardiogram, atrial force and ventricular intramyocardial pressures (IMP) were recorded. The responses were also recorded following administration of atropine or propranolol and after heart acute decentralization. Results Ventricular arrhythmia (VA) was induced by injections of nicotine into A-PGP, but not by injections of nicotine into RAGP in 13 dogs. Atrioventricilar (A-V) block was induced by nicotine activating RAGP in 10 dogs, but not by nicotine activating A-PGP. Propranolol could reduce the frequency of VA elicited by stimulating A-PGP, atropine could reduce the frequency of A-V block elicited by stimulating RAGP. After acute decentralization, VA was still induced by activation of A-PGP in 9 dogs, but A-V block elicited by stimulating RAGP was decreased. Conclusion VA is induced by stimulating N receptor in cardiac nicotine-sensitive efferent sympathetic neurons of ventricular ganglial plexus (A-PGP), and then modifying β receptor of ventricles. A-V block is elicited by stimulating N receptor in atrial ganglial plexus (RAGP), then modifying M receptor of A-V node not only via efferent parasympathetic neurons, but also via afferent pathway.展开更多
A previous study by our research group showed that nerve growth factor is involved in the onset of asthma through regulating SH2-Bβ expression in the lung and visceral primary afferent neurons of asthmatic mice. This...A previous study by our research group showed that nerve growth factor is involved in the onset of asthma through regulating SH2-Bβ expression in the lung and visceral primary afferent neurons of asthmatic mice. This study sought to assess the expression level of interleukin-1β in primary afferent neurons in C7-T5 spinal ganglia, spinal cord and lung in asthmatic mice after blockage of SH2-Bβ. The levels of interleukin-1β protein in primary afferent neurons in the C7-T5 spinal ganglia and lung were decreased, and interleukin-1β mRNA expression also down-regulated in the spinal cord, medulla oblongata and lung tissue after blockage of SH2-Bβ. Our findings indicate that SH2-Bβ can upregulate the expression of interleukin-1β in C7-T5 spinal ganglia, spinal cord and lung of asthmatic mice.展开更多
AIM: To study a novel technique to record spinal and cortical evoked potentials (EPs) simultaneously in response to electrical stimulation in the human rectum. METHODS: Eight male and nine female healthy volunteers pa...AIM: To study a novel technique to record spinal and cortical evoked potentials (EPs) simultaneously in response to electrical stimulation in the human rectum. METHODS: Eight male and nine female healthy volunteers participated. Stimulating electrodes were attached to the rectal mucosa at 15 cm and 12 cm above the dentate line. Recording skin electrodes were positioned over vertebrae L4 through S2. The electrical stimulus was a square wave of 0.2 ms duration and the intensity of the stimulus varied between 0 and 100 mA. EP responses were recorded using a Nicolet Viking IV programmable signal conditioner.RESULTS: Simultaneous recording of cortical and spinal EPs was obtained in > 80% of the trials. The EP responses increased with the intensity of the electrical stimulation, were reproducible overtime, and were blocked by application of Lidocaine jelly at the site of stimulation. The morphology (N1/P1), mean ± SD for latency (spinal N1, 4.6 ± 0.4 ms; P1, 6.8 ± 0.5 ms; cortical N1, 136.1 ± 4.2 ms; P1, 233.6 ± 12.8 ms) and amplitude (N1/P1, spinal, 38 ± 7 μV; cortical 19 ± 3 μV) data for the EP responses were consistent with those in the published literature. Reliable and reproducible EP recordings were obtained with the attachment of the electrodes to the rectal mucosa at predetermined locations between 16 and 8 cm above the anal verge, and the distance between the attachment sites of the electrodes (the optimal distance being approximately 3.0 cm between the two electrodes). CONCLUSION: This technique can be used to assess potential abnormalities in primary afferent neural pathways innervating the rectum in several neurodegenerative and functional pain disorders.展开更多
文摘Sepsis is a systemic inflammatory response representing the leading cause of death in critically ill patients,mostly due to multiple organ failure.The gastrointestinal tract plays a pivotal role in the pathogenesis of sepsisinduced multiple organ failure through intestinal barrier dysfunction,bacterial translocation and ileus.In this review we address the role of the gastrointestinal tract,the mediators,cell types and transduction pathways involved,based on experimental data obtained from models of inflammation-induced ileus and (preliminary) clinical data.The complex interplay within the gastrointestinal wall between mast cells,residential macrophages and glial cells on the one hand,and neurons and smooth muscle cells on the other hand,involves intracellular signaling pathways,Toll-like receptors and a plethora of neuroactive substances such as nitric oxide,prostaglandins,cytokines,chemokines,growth factors,tryptases and hormones.Multidirectional signaling between the different components in the gastrointestinal wall,the spinal cord and central nervous system impacts inflammation and its consequences.We propose that novel therapeutic strategies should target inflammation on the one hand and gastrointestinal motility,gas-trointestinal sensitivity and even pain signaling on the other hand,for instance by impeding afferent neuronal signaling,by activation of the vagal anti-inflammatory pathway or by the use of pharmacological agents such as ghrelin and ghrelin agonists or drugs interfering with the endocannabinoid system.
文摘Objective To study the arrhythmia induced by stimulation of nicotine-sensitive neurons in cardiac ganglial plexuses. Methods When nicotine (100 μg ) was injected into canine right atrial ganglial plexus (RAGP) and ganglial plexus between aorta and pulmonary artery (A-PGP) in 33 anesthetized open-chest dog, electrocardiogram, atrial force and ventricular intramyocardial pressures (IMP) were recorded. The responses were also recorded following administration of atropine or propranolol and after heart acute decentralization. Results Ventricular arrhythmia (VA) was induced by injections of nicotine into A-PGP, but not by injections of nicotine into RAGP in 13 dogs. Atrioventricilar (A-V) block was induced by nicotine activating RAGP in 10 dogs, but not by nicotine activating A-PGP. Propranolol could reduce the frequency of VA elicited by stimulating A-PGP, atropine could reduce the frequency of A-V block elicited by stimulating RAGP. After acute decentralization, VA was still induced by activation of A-PGP in 9 dogs, but A-V block elicited by stimulating RAGP was decreased. Conclusion VA is induced by stimulating N receptor in cardiac nicotine-sensitive efferent sympathetic neurons of ventricular ganglial plexus (A-PGP), and then modifying β receptor of ventricles. A-V block is elicited by stimulating N receptor in atrial ganglial plexus (RAGP), then modifying M receptor of A-V node not only via efferent parasympathetic neurons, but also via afferent pathway.
基金grant from the Liaoning Provincial Education Bureau, No. 20060890
文摘A previous study by our research group showed that nerve growth factor is involved in the onset of asthma through regulating SH2-Bβ expression in the lung and visceral primary afferent neurons of asthmatic mice. This study sought to assess the expression level of interleukin-1β in primary afferent neurons in C7-T5 spinal ganglia, spinal cord and lung in asthmatic mice after blockage of SH2-Bβ. The levels of interleukin-1β protein in primary afferent neurons in the C7-T5 spinal ganglia and lung were decreased, and interleukin-1β mRNA expression also down-regulated in the spinal cord, medulla oblongata and lung tissue after blockage of SH2-Bβ. Our findings indicate that SH2-Bβ can upregulate the expression of interleukin-1β in C7-T5 spinal ganglia, spinal cord and lung of asthmatic mice.
基金Supported by Grants from the National Institutes of Health M01-RR-00042UL1RR024986 (to Wiley JW)
文摘AIM: To study a novel technique to record spinal and cortical evoked potentials (EPs) simultaneously in response to electrical stimulation in the human rectum. METHODS: Eight male and nine female healthy volunteers participated. Stimulating electrodes were attached to the rectal mucosa at 15 cm and 12 cm above the dentate line. Recording skin electrodes were positioned over vertebrae L4 through S2. The electrical stimulus was a square wave of 0.2 ms duration and the intensity of the stimulus varied between 0 and 100 mA. EP responses were recorded using a Nicolet Viking IV programmable signal conditioner.RESULTS: Simultaneous recording of cortical and spinal EPs was obtained in > 80% of the trials. The EP responses increased with the intensity of the electrical stimulation, were reproducible overtime, and were blocked by application of Lidocaine jelly at the site of stimulation. The morphology (N1/P1), mean ± SD for latency (spinal N1, 4.6 ± 0.4 ms; P1, 6.8 ± 0.5 ms; cortical N1, 136.1 ± 4.2 ms; P1, 233.6 ± 12.8 ms) and amplitude (N1/P1, spinal, 38 ± 7 μV; cortical 19 ± 3 μV) data for the EP responses were consistent with those in the published literature. Reliable and reproducible EP recordings were obtained with the attachment of the electrodes to the rectal mucosa at predetermined locations between 16 and 8 cm above the anal verge, and the distance between the attachment sites of the electrodes (the optimal distance being approximately 3.0 cm between the two electrodes). CONCLUSION: This technique can be used to assess potential abnormalities in primary afferent neural pathways innervating the rectum in several neurodegenerative and functional pain disorders.
