Effects of ibuprofen on the physiology and survival of hypothermic sepsis

Arons, Murray M.; Wheeler, Arthur P.; Bernard, Gordon R.; Christman, Brian W.; Russell, James A.; Schein, Roland M. H.; Summer, Warren R.; Steinberg, Kenneth P.; Fulkerson, W. J.; Wright, Patrick E.; Dupont, William D.; Swindell, Bridgett B.

doi:10.1097/00003246-199904000-00020

Cited by 208 publications

(142 citation statements)

References 24 publications

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“…Whereas the majority (ϳ90%) of patients with systemic inflammation have an increased T b , a number of them (ϳ10%) have a lowered T b (6,17). Thermoregulatory manifestations are also present in animal models of systemic inflammation.…”

mentioning

confidence: 99%

Cyclooxygenase-1 or -2—which one mediates lipopolysaccharide-induced hypothermia?

Steiner

Hunter²,

Phipps³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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DL, Romanovsky AA. Cyclooxygenase-1 or -2-which one mediates lipopolysaccharide-induced hypothermia? Am J Physiol Regul Integr Comp Physiol 297: R485-R494, 2009. First published June 10, 2009 doi:10.1152/ajpregu.91026.2008.-Systemic inflammation is associated with either fever or hypothermia. Fever, a response to mild systemic inflammation, is mediated by cyclooxygenase (COX)-2 and not by COX-1. However, it is still disputed whether COX-2, COX-1, neither, or both mediate(s) responses to severe systemic inflammation, and, in particular, the hypothermic response. We compared the effects of SC-236 (COX-2 inhibitor) and SC-560 (COX-1 inhibitor) on the deep body temperature (Tb) of rats injected with a lower (10 g/kg iv) or higher (1,000 g/kg iv) dose of LPS at different ambient temperatures (Tas). At a neutral Ta (30°C), the rats responded to LPS with a polyphasic fever (lower dose) or a brief hypothermia followed by fever (higher dose). SC-236 (2.5 mg/kg iv) blocked the fever induced by either LPS dose, whereas SC-560 (5 mg/kg iv) altered neither the febrile response to the lower LPS dose nor the fever component of the response to the higher dose. However, SC-560 blocked the initial hypothermia caused by the higher LPS dose. At a subneutral T a (22°C), the rats responded to LPS with early (70 -90 min, nadir) dose-dependent hypothermia. The hypothermic response to either dose was enhanced by SC-236 but blocked by SC-560. The hypothermic response to the higher LPS dose was associated with a fall in arterial blood pressure. This hypotensive response was attenuated by either SC-236 or SC-560. At the onset of LPS-induced hypothermia and hypotension, the functional activity of the COX-1 pathway (COX-1-mediated PGE2 synthesis ex vivo) increased in the spleen but not liver, lung, kidney, or brain. The expression of splenic COX-1 was unaffected by LPS. We conclude that COX-1, but not COX-2, mediates LPS hypothermia, and that both COX isoforms are required for LPS hypotension. body temperature; thermoregulation; fever; inflammation SO STRONGLY IS SYSTEMIC INFLAMMATION associated with changes in deep body temperature (T b ) that every clinical definition of the systemic inflammatory response syndrome includes a change in T b (11,48). Whereas the majority (ϳ90%) of patients with systemic inflammation have an increased T b , a number of them (ϳ10%) have a lowered T b (6, 17). Thermoregulatory manifestations are also present in animal models of systemic inflammation. In a rat model of systemic inflammation induced by bacterial LPS, the pattern of T b change depends on the ambient temperature (T a ) and the LPS dose. At a neutral or supraneutral T a (warm environment), fever is the prevailing response; the fever is monophasic when the dose of LPS is low (just suprathreshold), but it turns polyphasic as the dose increases (66, 68, 69, 71, 79); a mild hypothermia may precede the polyphasic fever when the dose of LPS is high (68). At a subneutral T a (cool environment), hypothermia followed by fever is the predominant response; th...

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mentioning

confidence: 99%

Cyclooxygenase-1 or -2—which one mediates lipopolysaccharide-induced hypothermia?

Steiner

Hunter²,

Phipps³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Increase in mortality 28,51,52 CAD Increase incidence of vasopressor and/or inotropic support 11 Increase occurrence of arrhythmia 3 Increase rate of angina or myocardial ischemia 3,10 Increase in mortality 11 …”

Section: Sepsismentioning

confidence: 99%

“…Hypothermia has specifically been shown to be detrimental in patients with certain comorbidities as emphasized in Table 3. In septic patients, hypothermia is associated with a much higher incidence in mortality [28,51,52]. This is likely because fever--a form of autologous hyperthermia--functions as an immunologic defense that combats infection [28,[33][34][35].…”

Section: Traumamentioning

confidence: 99%

Perioperative temperature measurement and management: moving beyond the Surgical Care Improvement Project

Sappenfield¹,

Hong²,

Galvagno³

2013

J Anesthesiol Clin Sci

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Intraoperative management of patient body temperature is a standard of care for practicing anesthesiologists. Merely complying with the Surgical Care Improvement Project (SCIP) measurement is inadequate for optimizing perioperative outcomes. Clinicians should have a sound understanding of available temperature monitoring sites, deleterious effects of hypothermia, and indications for therapeutic hypothermia. This foundation will help physicians use indicated modalities to improve patient outcomes throughout the perioperative period. The purpose of this paper is to review appropriate intraoperative temperature monitoring, the importance of maintaining normothermia, and indications for intraoperative hypothermia.

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“…Moreover, several studies have shown that hypothermia delays the induction of proinflammatory cytokines in vitro (7). At the same time, however, several studies have reported that the mortality rate of hypothermic patients with sepsis is twice that of febrile septic patients (2,4,9). We studied the effects of hypothermia on mortality rate, concentrations of TNF-␣ and IL-6 in plasma, and the end products of NO in endotoxin-exposed rats.…”

mentioning

confidence: 97%

Effects of Hypothermia on Mortality and Inflammatory Responses to Endotoxin-Induced Shock in Rats

Taniguchi¹,

Kanakura

Takemoto

et al. 2003

Clin Vaccine Immunol

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We studied the effects of hypothermia on mortality rate, concentrations of tumor necrosis factor alpha and interleukin 6 in plasma, and the end products of nitric oxide (NO) in endotoxemia. It was found that moderate and mild hypothermia improved the mortality rate and attenuated cytokine responses and the elevation of the end products of NO after endotoxin injection and that these beneficial effects were similar for moderate and mild hypothermia.Endotoxin shock, a common problem in patients with endotoxemia that often resists even intensive medical treatment, is characterized by profound hypotension, progressive metabolic acidosis, and dysfunction of multiple organs. Although its pathophysiology is not well defined, cytokines and nitric oxide (NO) are considered important in mediating the cardiovascular disturbance (10,11,17). Circulating endotoxin increases the production and release of tumor necrosis factor alpha (TNF-␣) and interleukin 6 (IL-6), which are dilators of resistance vessels in skeletal muscle (5). When macrophages are activated by endotoxin or cytokines, the inducible NO synthase gene is expressed. This, in turn, leads to the production of NO synthase, which, once activated, continuously releases large amounts of NO, with a vasodilating effect (13,14). Enhanced production of NO thus contributes importantly to cardiovascular dysfunction.Several investigators have documented that hypothermia has an organ-protective effect in controlled hemorrhagic shock and provides myocardial protection (6, 18). Moreover, several studies have shown that hypothermia delays the induction of proinflammatory cytokines in vitro (7). At the same time, however, several studies have reported that the mortality rate of hypothermic patients with sepsis is twice that of febrile septic patients (2, 4, 9). We studied the effects of hypothermia on mortality rate, concentrations of TNF-␣ and IL-6 in plasma, and the end products of NO in endotoxin-exposed rats. MATERIALS AND METHODSAnimal preparation. All experimental procedures were approved by the Animal Care Committee of Kanazawa University School of Medicine and were in accordance with the National Institutes of Health guidelines for animal use. Male Wistar rats (n ϭ 36) weighing 375 Ϯ 15 g (mean Ϯ standard deviation [SD]) were anesthetized with an intraperitoneal injection of pentobarbital sodium (30 mg/kg of body weight). Ventilation was performed through a tracheotomy. The femoral artery was cannulated to monitor blood pressure and to draw blood samples. Lactated Ringer's solution containing a muscle relaxant (0.02 mg of pancuronium bromide/ml) and pentobarbital sodium (0.5 mg/ml) was infused continuously at a rate of 10 ml ⅐ kg Ϫ1 ⅐ h Ϫ1 through a femoral vein cannula because animals anesthetized with this dose of pentobarbital alone did not demonstrate escape behavior. The heart rate (HR) was recorded from lead II of the electrocardiogram. The rats were connected to a pressure-controlled ventilator (Servo 900B; Siemens-Elema, Solna, Sweden) delivering 100% oxygen at a fr...

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Effects of ibuprofen on the physiology and survival of hypothermic sepsis

Cited by 208 publications

References 24 publications

Cyclooxygenase-1 or -2—which one mediates lipopolysaccharide-induced hypothermia?

Cyclooxygenase-1 or -2—which one mediates lipopolysaccharide-induced hypothermia?

Perioperative temperature measurement and management: moving beyond the Surgical Care Improvement Project

Effects of Hypothermia on Mortality and Inflammatory Responses to Endotoxin-Induced Shock in Rats

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