Renal and cutaneous vasomotor and respiratory rate adjustments to peripheral cold and warm stimuli and to bacterial endotoxin in conscious rabbits

Riedel, Walter; Kozawa, Emi; Iriki, Masami

doi:10.1016/0165-1838(82)90038-8

Cited by 58 publications

(32 citation statements)

References 32 publications

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“…*P Ͻ 0.05 vs. control. scious rabbits demonstrated that LPS caused an initial decrease in RSNA that was attributed to compensatory renal vasodilatation in response to peripheral vasoconstriction (14). In this context, it is possible that the renal sympathoinhibition is part of a central patterned response that is evoked to raise body temperature in response to the infection.…”

Section: Discussionmentioning

confidence: 99%

Septic shock induces distinct changes in sympathetic nerve activity to the heart and kidney in conscious sheep

Ramchandra

Wan

Hood

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Sepsis and septic shock are the chief cause of death in intensive care units, with mortality rates between 30 and 70%. In a large animal model of septic shock, we have demonstrated hypotension, increased cardiac output, and tachycardia, together with renal vasodilatation and renal failure. The changes in cardiac sympathetic nerve activity (CSNA) that may contribute to the tachycardia have not been investigated, and the changes in renal SNA (RSNA) that may mediate the changes in renal blood flow and function are unclear. We therefore recorded CSNA and RSNA during septic shock in conscious sheep. Septic shock was induced by administration of Escherichia coli, which caused a delayed hypotension and an immediate, biphasic increase in heart rate (HR) associated with similar changes in CSNA. After E. coli, RSNA decreased for over 3 h, followed by a sustained increase (180%), whereas renal blood flow progressively increased and remained elevated. There was an initial diuresis, followed by oliguria and decreased creatinine clearance. There were differential changes in the range of the arterial baroreflex curves; it was depressed for HR, increased for CSNA, and unchanged for RSNA. Our findings, recording CSNA for the first time in septic shock, suggest that the increase in SNA to the heart is not driven solely by unloading of baroreceptors and that the increase has an important role to increase HR and cardiac output. There was little correlation between the changes in RSNA and renal blood flow, suggesting that the renal vasodilatation was mediated mainly by other mechanisms. acute renal failure; renal blood flow SEPSIS AND SEPTIC SHOCK remain a major challenge in medicine; they are the chief cause of death in intensive care units with mortality rates between 30 and 70% (15). A cardiovascular hallmark of septic shock is systemic vasodilatation and hypotension, which has been proposed to be mediated largely by increased production of nitric oxide (5, 16). The fall in arterial pressure is accompanied by increases in heart rate (HR) and renal sympathetic nerve activity (RSNA) (12,18).Although these are well-established responses to bacterial infection, the mechanisms have not been fully elucidated, and recordings of cardiac sympathetic nervous activity (CSNA) have not been made in septic shock. An important role for increased CSNA as a cause of the tachycardia is the finding that ␤-blockade returned the elevated HR to control levels in conscious rabbits treated with lipopolysaccharide (LPS) (10) and prevented the tachycardia in febrile humans (2). The factors leading to an increase in CSNA in septic shock have not been investigated but may include unloading of arterial baroreceptors in response to the hypotension and altered baroreflex control.The majority of studies that have investigated the changes in SNA during sepsis have shown increases in RSNA in response to endotoxemia induced by administration of LPS (17, 18). The relevance of LPS models of sepsis in rodents to human sepsis is uncertain as LPS administration in rode...

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Section: Discussionmentioning

confidence: 99%

Septic shock induces distinct changes in sympathetic nerve activity to the heart and kidney in conscious sheep

Ramchandra

Wan

Hood

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Parallel rises and falls of core temperatures in exercising men at rest and during work, although with core temperature starting from higher levels under febrile conditions [63], or parallel shifts of metabolic rate to higher values in response to hypothalamic heating and cooling in febrile rabbits [64], suggest that whole-body thermal reception remains rather unaltered during fever and that the elevation of core temperature is caused by another, most likely nonthermal, mechanism. The external environment has been found to modulate the fever pattern considerably [58,65]. This finding might be taken in support of the hypothesis that the sensitivity of the temperature-sensing elements is not altered during fever.…”

Section: Thermosensors In Fevermentioning

confidence: 54%

Temperature Homeostasis and Redox Homeostasis

Riedel

2001

Thermotherapy for Neoplasia, Inflammation, and Pain

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Summary. It appears that the constancy of body temperature, among other metabolic equilibria, depends to a certain extent on a homeostatically regulated ratio of brain redox buffer components, which are in virtually all animal cells, glutathione and its disulfide. Glutathione serves additionally as an antioxidant by directly reacting with radicals. Pyrogens have been found to cause oxidative stress by increasing oxygen radical formation after they entered the circulation and reacted with cells of the immune system. Oxidative stress is then sensed in the brain by alteration of the ratio of reduced versus oxidized thiol groups of the redox modulatory site of the NMDA subtype of glutamate receptors, which control Ca 2 + influx. All neurons excited by glutamate contain NOS, which is activated by Ca 2 +. NO acts as a negative feedback regulator of NMDA-receptor activity by oxidizing its thiol groups and thus prevents Ca 2 + influx and overstimulation by glutamate. The redox-sensitive site of the NMDAreceptor complex is involved in temperature regulation; its oxidation by NO or other agents able to oxidize thiol groups elicits the autonomic pattern of cold defense and elevates core temperature, whereas thiol reduct ants elicit the pattern of heat defense and lower core temperature. It is conceivable that lowering cerebral NO levels, as observed in fever, are part of a defense mechanism by which in the presence of oxygen radicals the production of dangerous molecules such as peroxynitrite is avoided. If so, then the physiological role of fever might be considered not only as a component of the host's defense against microbial invasion, but also as an adaptative process sacrificing body temperature homeostasis to minimize cerebral injury. Temperature HomeostasisThere is some evidence that the evolutionary process of attaining a high and stable body temperature could not have occurred without the simultaneous development of increasingly more efficient metabolic pathways that enabled living systems to aquire and utilize free energy to carry out the various energy-consuming bodily functions. Because energy production is primarily a function of mitochondrial oxidative phosphorylation, continuous uptake and delivery of oxygen to the heat-producing tissues and removal of carbon dioxide from them is of utmost importance. It is obvious that the lung and the circulatory system playa pivotal role not only for the transport of blood gases and metabolites but also for the transfer of heat. Full homeothermy has therefore developed in air-breathing terrestrial vertebrates together with their capability of high energy production and of heat insulation of the integument. There is general agreement that homeothermy cannot be achieved without participation of the central nervous system (CNS). All concepts concerned with homeothermic temperature regulation rely on the existence of thermosensory inputs located in the skin, in the body core, and in various parts of the brain. Conveying these signals to special structures within the CNS adju...

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“…These responses can be related to local inflammatory responses which are induced by mononuclear cell factor (MCF). The elevation of circulating PG's and enhanced renal excretion of PG metabolites, especially during the early phase of fever, might further bear some relationship with altered organ functions during fever, e.g., the sequence of antidiuresis and diuresis observed in goats during endotoxin fever [30] or the dissociation of renal blood flow and local sympathetic activity [41].…”

Section: A Response Components Of the Fever Syndromementioning

confidence: 99%