Rapid cooling after acute hyperthermia alters intestinal morphology and increases the systemic inflammatory response in pigs

Johnson, Jay S; Sapkota, A.; Lay, D. C.

doi:10.1152/japplphysiol.00685.2015

Cited by 39 publications

(33 citation statements)

References 49 publications

(86 reference statements)

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“…This ischemic insult aggravates intestinal damage and dysfunction of the intestinal barrier. As reported in previous studies ( 25 , 34 ), the results of the present study showed that intestinal damage was aggravated following cooling treatment. This may result from gut reperfusion during the cooling treatment and the sustained systemic inflammatory cascade ( 35 , 36 ).…”

Section: Discussionsupporting

confidence: 89%

Cryptdin-2 predicts intestinal injury during heatstroke in mice

et al. 2017

Int J Mol Med

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Intestinal injury-induced bacterial translocation and endotoxemia are important in the pathophysiological process of heatstroke. However, the underlying mechanism remains to be fully elucidated. Previous studies using 2D-gel electrophoresis found that defensin-related cryptdin-2 (Cry-2), an intestinal α-defensin, is upregulated in intestinal tissues during heatstroke in mice, and that treatment with ulinastatin, a multivalent enzyme inhibitor, reduced heat-induced acute lung injury. To investigate the association between Cry-2 and heat stress (HS)-induced intestinal injury and the probable protective role of ulinastatin, the present study examined the intestinal expression of Cry-2 via histopathologic analysis and reverse transcription-quantitative polymerase chain reaction analysis in mice with heatstroke. The heat-stressed mice were exposed to different core temperatures and cooling treatments, and intestinal pathological changes and Chiu scores were determined. Chemical markers of intestinal injury, serum and intestinal concentrations of diamine oxidase (DAO) and D-lactic acid (D-Lac), and serum and intestinal concentrations of Cry-2 were also determined. Correlations were analyzed using Spearman's correlation analysis. It was found that HS upregulated the expression of Cry-2, and the serum and intestinal concentrations of Cry-2 were correlated with the severity of HS-induced intestinal damage, indicated by pathology scores and concentrations of DAO and D-lac. Ulinastatin protected the intestines from HS-induced injury and downregulated the expression of Cry-2, which was also correlated with the extent of intestinal injury. Therefore, ulinastatin administration may be beneficial for patients with heatstroke, and Cry-2 may be a novel predictor of HS-induced intestinal injury.

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Section: Discussionsupporting

confidence: 89%

Cryptdin-2 predicts intestinal injury during heatstroke in mice

et al. 2017

Int J Mol Med

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“…Hyperthermia causes an increase in intestinal damage due to ischemic injury (Arieli et al, 2003) and hypoxia (Horowitz, 2007) resulting in greater permeability and endotoxin translocation (Lambert, 2009;Johnson et al, 2016) and morphological alterations such as reduced villus height and crypt depth, and a reduction in the villus height to crypt depth ratio (Pearce et al, 2013a; Johnson et al, 2016).…”

Section: Daymentioning

confidence: 99%

Early life thermal stress: Impact on future thermotolerance, stress response, behavior, and intestinal morphology in piglets exposed to a heat stress challenge during simulated transport1

Johnson

Duttlinger

et al. 2018

Journal of Animal Science

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Study objectives were to evaluate the impact of early life thermal stress (ELTS) on thermoregulation, stress response, and intestinal health of piglets subjected to a future heat stress (HS) challenge during simulated transport. From d 7 to 9 post-farrowing, 12 first-parity sows and their litters were exposed to thermoneutral (ELTN; 25.4 ± 1.1 °C w/heat lamp; n = 4), HS (ELHS; cycling 32-38 °C w/heat lamp; n = 4), or cold stress (ELCS; 25.4 ± 1.1 °C w/no heat lamp; n = 4) conditions, and then from d 10 until weaning all piglets were exposed to thermoneutral (TN) conditions (25.3 ± 1.9 °C w/heat lamp). During the ELTS period, respiration rate, rectal temperature (TR), and skin temperature (TS) of three mixed-sex piglets per dam were monitored daily (0800, 1200, 1600, 2000 h). At 13 ± 1.3 d of age, temperature recorders were implanted intra-abdominally into all piglets. At weaning (20.0 ± 1.3 d of age), piglets were bled and then herded up a ramp into a simulated transport trailer and exposed to HS conditions (cycling 32-38 °C) for 8 h. During the 8 h simulated transport, core body temperature (TC) and TS were assessed every 15 min. After the simulated transport, piglets were unloaded from the trailer, bled, weighed, and then housed individually in TN conditions (28.5 ± 0.7 °C) for 7 d. During this time, ADFI and ADG were monitored, blood samples were taken on d 1, 4, and 7, and piglets were video-recorded to assess behavior. Piglets were sacrificed on d 8 post-simulated transport and intestinal morphology was assessed. Data were analyzed using PROC MIXED in SAS 9.4. In the ELTS period, piglet TR was increased overall (P = 0.01) in ELHS (39.77 ± 0.05 °C) compared to ELTN (39.34 ± 0.05 °C) and ELCS (39.40 ± 0.05 °C) litters. During simulated transport, TC was greater (P = 0.02) in ELHS (40.84 ± 0.12 °C) compared to ELTN (40.49 ± 0.12 °C) and ELCS (40.39 ± 0.12 °C) pigs. Following simulated transport, BW loss was greater (P = 0.01; 40%) for ELHS compared to ELTN and ELCS pigs and ADFI was reduced (P = 0.05; 28.6%) in ELHS compared to ELTN pigs. Sitting behavior tended to be increased (P = 0.06; 47.4%) in ELHS vs. ELCS or ELTN pigs. Overall, circulating cortisol was greater for ELHS (P ≤ 0.01; 38.8%) compared to ELCS and ELTN pigs. Goblet cells per villi were reduced (P = 0.02; 20%) in the jejunum of ELHS vs. ELCS and ELTN pigs. In summary, ELHS reduced thermotolerance and increased the future stress response of piglets compared to ELCS and ELTN.

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“…Indeed, basing treatment strategies on that index alone might inadvertently expose hyperthermic humans to unforeseen complications. For instance, Johnson, Sapkota, and Lay () investigated the impact of rapidly (ice‐cold water douche; 4°C) and gradually cooling (staged air cooling to 20.7°C) hyperthermic pigs. Faster rectal temperature reductions accompanied the rapid cooling, with animals experiencing higher circulating endotoxin concentrations (lipopolysaccharide) than either the gradually cooled or normothermic pigs.…”

Section: Discussionmentioning

confidence: 99%

“…Not surprisingly, the optimal manner in which cooling might be achieved has been debated (Casa, Kenny, & Taylor, 2010), with some recommending ice-cold water immersion Binkley, Beckett, Casa, Kleiner, & Plummer, 2002;Casa et al, 2007), a method first advocated by Ferris, Blankenhorn, Robinson, and Cullen (1938), whereas others advocate less aggressive cooling strategies (Caldwell et al, 2009;Taylor, Caldwell, van den Heuvel, & Patterson, 2008a;Weiner & Khogali, 1980;Wyndham et al, 1959). One aspect of the former approach is the possibility of exposure to adverse, cold-induced pathophysiological sequelae, including cardiac arrhythmia, reduced cerebral blood flow, hypertension and endotoxaemia (Johnson et al, 2016;Mantoni, Belhage, Pedersen, & Pott, 2007;Shattock & Tipton, 2012;Tipton, 1989).…”

Section: Introductionmentioning

confidence: 99%

A vascular mechanism to explain thermally mediated variations in deep‐body cooling rates during the immersion of profoundly hyperthermic individuals

Caldwell

Heuvel

Kerry

et al. 2018

Experimental Physiology

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Physiologically trivial time differences for cooling the intrathoracic viscera of hyperthermic individuals have been reported between cold- and temperate-water immersion treatments. One explanation for that observation is reduced convective heat delivery to the skin during cold immersion, and this study was designed to test both the validity of that observation, and its underlying hypothesis. Eight healthy men participated in four head-out water immersions: two when normothermic, and two after exercise-induced, moderate-to-profound hyperthermia. Two water temperatures were used within each thermal state: temperate (26°C) and cold (14°C). Tissue temperatures were measured at three deep-body sites (oesophagus, auditory canal and rectum) and eight skin surfaces, with cutaneous vascular responses simultaneously evaluated from both forearms (laser-Doppler flowmetry and venous-occlusion plethysmography). During the cold immersion of normothermic individuals, oesophageal temperature decreased relative to baseline (-0.31°C over 20 min; P < 0.05), whilst rectal temperature increased (0.20°C; P < 0.05). When rendered hyperthermic, oesophageal (-0.75°C) and rectal temperatures decreased (-0.05°C) during the transition period (<8.5 min, mostly in air at 22°C), with the former dropping to 37.5°C only 54 s faster when immersed in cold rather than in temperate water (P < 0.05). Minimal cutaneous vasoconstriction occurred during either normothermic immersion, whereas pronounced constriction was evident during both immersions when subjects were hyperthermic, with the colder water eliciting a greater vascular response (P < 0.05). It was concluded that the rapid intrathoracic cooling of asymptomatic, hyperthermic individuals in temperate water was a reproducible phenomenon, with slower than expected cooling in cold water brought about by stronger cutaneous vasoconstriction that reduced convective heat delivery to the periphery.

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Rapid cooling after acute hyperthermia alters intestinal morphology and increases the systemic inflammatory response in pigs

Cited by 39 publications

References 49 publications

Cryptdin-2 predicts intestinal injury during heatstroke in mice

Cryptdin-2 predicts intestinal injury during heatstroke in mice

Early life thermal stress: Impact on future thermotolerance, stress response, behavior, and intestinal morphology in piglets exposed to a heat stress challenge during simulated transport1

A vascular mechanism to explain thermally mediated variations in deep‐body cooling rates during the immersion of profoundly hyperthermic individuals

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