Directly Cooling Gut Prevents Mortality in the Rat Model of Reboa Management of Lethal Hemorrhage

Liu, Chunli; Ye, Dong; Crawford, Robert S.; Sarkar, Rajabrata; Hu, Bingren

doi:10.1097/shk.0000000000001744

Cited by 5 publications

(21 citation statements)

References 30 publications

(52 reference statements)

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“…This technique, because of its simplicity of use, could potentially be used in any clinical scenario in which temporary aortic clamping is needed. 1 …”

Section: Discussionmentioning

confidence: 99%

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Transrectal intracolon cooling prevents paraplegia and mortality in a rat model of aortic occlusion-induced spinal cord ischemia

Crawford

Liu

et al. 2021

JVS-Vascular Science

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Objective Spinal cord ischemia–reperfusion injury (SC-IRI) occurs in many medical conditions such as aneurysm surgical repair but no treatment of SC-IRI is available in clinical practice. The objective of the present study was to develop a novel medical device for the treatment of SC-IRI. Methods A rat model of SC-IRI was used. A novel transrectal intracolon (TRIC) temperature management device was developed to maintain an intracolon wall temperature at either 37°C (TRIC37°C) or 12°C (TRIC12°C). The upper body temperature was maintained as close as possible to 37°C in both groups. A 2F Fogarty balloon catheter was inserted via the left common carotid artery to block the distal aortic blood flow to the spinal cord. The proximal blood pressure was controlled by the withdrawal and infusion of blood via the jugular vein catheter, such that the distal tail artery blood pressure was maintained at ∼10 mmHg for 13 and 20 minutes, respectively. Next, the balloon was deflated, and TRIC temperature management was continued for an additional 30 minutes to maintain the colon wall temperature at either 37°C or 12°C during the reperfusion period. Results All the rats subjected to 13 minutes of spinal cord ischemia in the TRIC37°C group had developed paraplegia during the postischemic phase. In striking contrast, TRIC at 12°C completely prevented the paraplegia, dramatically improved the arterial blood gas parameters, and avoided the histopathologic injuries to the spinal cord in rats subjected to 13 minutes of spinal cord ischemia. Furthermore, TRIC12°C allowed for the extension of the ischemia duration from 13 minutes to 20 minutes, with significantly reduced functional deficits. Conclusions Directly cooling the intestine focally with the TRIC device offered an exceptional survival rate and functional improvement after aortic occlusion-induced spinal cord ischemia.

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“…This technique, because of its simplicity of use, could potentially be used in any clinical scenario in which temporary aortic clamping is needed. 1 …”

Section: Discussionmentioning

confidence: 99%

“…Spinal cord ischemia–reperfusion injury (SC-IRI) is a devastating complication of many medical conditions such as acute aortic pathology or aortic surgery. 1 , 2 , 3 , 4 , 5 , 6 At present, no effective treatment is available for clinical patients with SC-IRI.…”

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confidence: 99%

Transrectal intracolon cooling prevents paraplegia and mortality in a rat model of aortic occlusion-induced spinal cord ischemia

Crawford

Liu

et al. 2021

JVS-Vascular Science

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“…As described above, the depletion or disappearance of intra-neuronal NSF immunoreactivity was mainly due to NSF deposition into a detergent (Triton X100)/salt-insoluble aggregates after both global and focal brain ischemia (Liu and Hu, 2004 ; Yuan et al, 2018b , 2021 ; Liu et al, 2021 ). These NSF aggregates are such dense structures that they were not accessible by the NSF antibody during the immunostaining of brain sections (Hu et al, 2000b ; Liu and Hu, 2004 ; Zhang et al, 2006 ; Yuan et al, 2018b , 2021 ).…”

Section: Part 3 Interruption Of Endolysosomal Trafficking Leads To Stroke Brain Injurymentioning

confidence: 92%

Interruption of Endolysosomal Trafficking After Focal Brain Ischemia

Gaire

Subedi

et al. 2021

Front. Mol. Neurosci.

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A typical neuron consists of a soma, a single axon with numerous nerve terminals, and multiple dendritic trunks with numerous branches. Each of the 100 billion neurons in the brain has on average 7,000 synaptic connections to other neurons. The neuronal endolysosomal compartments for the degradation of axonal and dendritic waste are located in the soma region. That means that all autophagosomal and endosomal cargos from 7,000 synaptic connections must be transported to the soma region for degradation. For that reason, neuronal endolysosomal degradation is an extraordinarily demanding and dynamic event, and thus is highly susceptible to many pathological conditions. Dysfunction in the endolysosomal trafficking pathways occurs in virtually all neurodegenerative diseases. Most lysosomal storage disorders (LSDs) with defects in the endolysosomal system preferentially affect the central nervous system (CNS). Recently, significant progress has been made in understanding the role that the endolysosomal trafficking pathways play after brain ischemia. Brain ischemia damages the membrane fusion machinery co-operated by N-ethylmaleimide sensitive factor (NSF), soluble NSF attachment protein (SNAP), and soluble NSF attachment protein receptors (SNAREs), thus interrupting the membrane-to-membrane fusion between the late endosome and terminal lysosome. This interruption obstructs all incoming traffic. Consequently, both the size and number of endolysosomal structures, autophagosomes, early endosomes, and intra-neuronal protein aggregates are increased extensively in post-ischemic neurons. This cascade of events eventually damages the endolysosomal structures to release hydrolases leading to ischemic brain injury. Gene knockout and selective inhibition of key endolysosomal cathepsins protects the brain from ischemic injury. This review aims to provide an update of the current knowledge, future research directions, and the clinical implications regarding the critical role of the neuronal endolysosomal trafficking pathways in ischemic brain injury.

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“…The ABG parameters (pH, pCO 2 , pO 2 , electrolytes, lactate, base deficit, bicarbonate, glucose, and potassium) were measured via an ABL90 FLEX blood gas analyzer (Radiometer, Brea, CA). Prothrombin time (PT)/international normalized ratio (INR) were measured or calculated in whole blood with the Coag-Sense PT/INR Professional System according to the manufacturer's instructions (CoaguSense, Inc, Fremont, CA), as described in our previous studies (8,18).…”

Section: Arterial Blood Gas and Coagulation Analysismentioning

confidence: 99%

“…A TRIC device was inserted via the rectum into the descending colon at about 10 cm of length from the anus and activated 15 min after the start of bleeding according to the technique described in our previous studies (8,18). The TRIC temperature management was continued post-HS for additional 3 h. In the TRIC10 + Res group, rewarming was initiated at the end of a 3-h post-HS with a rewarming rate of 0.15°C/min until the esophageal temperature reached a range of 30°C to 32°C, which took about an additional 60 to 90 min.…”

Section: Temperature Managementmentioning

confidence: 99%

Intracolon Cooling Increases Survival Rate in the Rat Model of Lethal Hemorrhage

Arya,

Hu,

Chen

et al. 2023

Shock

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Background The objective of this study is to investigate whether Trans-Rectal Intra-Colon (TRIC) cooling can prolong the survival duration in a rat hemorrhagic shock (HS) model. Methods A lethal-HS was induced by bleeding 47% of the total blood volume. A TRIC device was placed into the colon to maintain the intra-colon temperature either at 37 °C (TRIC37°C) or TRIC10°C pos-HS. In the surface cooling (SC) rats, the body temperatures were maintained at the same level as the esophageal temperature of the TRIC10°C rats. A separated group of TRIC10°C rats were resuscitated (Res) at 90 minutes post-HS. A total six groups were: (i) Sham-TRIC37°C (n = 5); (ii) Sham-TRIC10°C (n = 5); (iii) HS-TRIC37°C (n = 5); (iv) HS-TRIC10°C (n = 6); (v) HS-SC (n = 6); and (vi) HS-TRIC10°C + Res (n = 6). Results An average post-HS survival time was 18.4 ± 9.4 minutes in HS TRIC37°C and 82 ± 27.82 minutes in the HS SC group. In striking contrast, the HS TRIC10°C group exhibited an average survival time of 150.2 ± 66.43 minutes. The post-HS blood potassium level rose significantly in the HS-TRIC37°C and HS-SC, whereas remained unchanged in the TRIC10°C groups. Post-HS intestinal damage occurred in HS-TRIC37°C and HS-SC groups but virtually absent in HS TRIC10°C groups. Following resuscitation at 90 min post-HS, all HS-TRIC10°C rats were fully recovered from the lethal HS. Conclusions TRIC10°C reversed the high blood potassium level, prevented the intestinal damage, and prolonged the survival duration by 6-fold relative to normothermia and by 2-fold compared to SC post-HS. All TRIC10°C rats were successfully resuscitated at 90 min post-HS.

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Directly Cooling Gut Prevents Mortality in the Rat Model of Reboa Management of Lethal Hemorrhage

Cited by 5 publications

References 30 publications

Transrectal intracolon cooling prevents paraplegia and mortality in a rat model of aortic occlusion-induced spinal cord ischemia

Transrectal intracolon cooling prevents paraplegia and mortality in a rat model of aortic occlusion-induced spinal cord ischemia

Interruption of Endolysosomal Trafficking After Focal Brain Ischemia

Intracolon Cooling Increases Survival Rate in the Rat Model of Lethal Hemorrhage

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