Small animal model species are not created equal

Dobson, Geoffrey P.

doi:10.1097/ccm.0b013e31823c8965

Cited by 7 publications

(5 citation statements)

References 7 publications

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“…Saline control hearts had increased vacuolation, PMN infiltration, and congestion compared to ALM treatment group. Heart injury scores (median [range]) were 10 [6-12] for Saline (P ¼ 0.006 vs ALM survivors), 7 [4][5][6][7][8][9][10][11] for ALM non-survivors, and 4 [3][4] for ALM survivors (see Results). and lower HF in Saline animals also support a greater contribution of sympathetic innervation to autonomic control of cardiovascular function in non-survivors, or a parasympathetic withdrawal, or both (Table 2).…”

Section: Mortality and Sympathetic-parasympathetic Imbalancementioning

confidence: 99%

“…Following surgery Saline Control and ALM therapy animals were singly housed in divided Tecniplast cages to protect wound sites but allow for visual, auditory, and olfactory contact. The rat is chosen over the mouse because the mouse can enter a dormant state called torpor when subjected to traumatic stress (10), and may invoke different mechanisms of adaptation compared to rats and humans who do not share this metabolic-lowering ability.…”

Section: Animals and Ethicsmentioning

confidence: 99%

“…Heart injury scores (median [range]) were 10 [6-12] for Saline, 7 [4][5][6][7][8][9][10][11] for ALM non-survivors, and 4 [3][4] for ALM survivors (H ¼ 9.579; df ¼ 2; P ¼ 0.008). All Saline controls had mild-to-moderate evidence of vacuolation, hyperemia, hemorrhage/congestion, and interstitial edema (Fig.…”

Section: Heart Histopathologymentioning

confidence: 99%

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ALM Fluid Therapy Shifts Sympathetic Hyperactivity to Parasympathetic Dominance in the Rat Model of Non-Compressible Hemorrhagic Shock

Letson

Biroš

Morris

et al. 2021

Shock

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Excessive sympathetic outflow following trauma can lead to cardiac dysfunction, inflammation, coagulopathy, and poor outcomes. We previously reported that buprenorphine analgesia decreased survival after hemorrhagic trauma. Our aim is to examine the underlying mechanisms of mortality in a non-compressible hemorrhage rat model resuscitated with saline or adenosine, lidocaine, magnesium (ALM). Anesthetized adult male Sprague-Dawley rats were randomly assigned to Saline control group or ALM therapy group (both n ¼ 10). Hemorrhage was induced by 50% liver resection. After 15 min, 0.7 mL/kg 3% NaCl AE ALM intravenous bolus was administered, and after 60 min, 0.9% NaCl AE ALM was infused for 4 h (0.5 mL/kg/h) with 72 h monitoring. Animals received 6-12-hourly buprenorphine for analgesia. Hemodynamics, heart rate variability, echocardiography, and adiponectin were measured. Cardiac tissue was analyzed for adrenergic/cholinergic receptor expression, inflammation, and histopathology. Four ALM animals and one Saline control survived to 72 h. Mortality was associated with up to 97% decreases in adrenergic (b-1, a-1A) and cholinergic (M2) receptor expression, cardiac inflammation, myocyte Ca 2þ loading, and histopathology, indicating heart ischemia/failure. ALM survivors had higher cardiac output and stroke volume, a 30-fold increase in parasympathetic/sympathetic receptor expression ratio, and higher circulating adiponectin compared to Saline controls. Paradoxically, Saline cardiac adiponectin hormone levels were higher than ALM, with no change in receptor expression, indicating intra-cardiac synthesis. Mortality appears to be a ''systems failure'' associated with CNS dysregulation of cardiac function. Survival involves an increased parasympathetic dominance to support cardiac pump function with reduced myocardial inflammation. Increased cardiac a-1A adrenergic receptor in ALM survivors may be significant, as this receptor is highly protective during heart dysfunction/failure.

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Section: Mortality and Sympathetic-parasympathetic Imbalancementioning

confidence: 99%

Section: Animals and Ethicsmentioning

confidence: 99%

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ALM Fluid Therapy Shifts Sympathetic Hyperactivity to Parasympathetic Dominance in the Rat Model of Non-Compressible Hemorrhagic Shock

Letson

Biroš

Morris

et al. 2021

Shock

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“…It is with great interest that I have read the paper by Lima et al (1), together with its accompanying editorial (2), so the more since we use the near-infrared spectroscopy (NIRS) technology in research (3)(4)(5) and in everyday clinical practice.…”

Section: To the Editormentioning

confidence: 99%

The author replies

Haouzi¹

2012

Critical Care Medicine

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“…Reduced VO 2 can be observed during hemorrhagic shock or severe hypoxia in rats [ 10 ], but this response is less pronounced in adult individuals [ 11 , 12 ]. In other words, even “small animal model species are not created equal” [ 13 ]. Hence, whenever interventions target or affect cellular energy metabolism [ 14 , 15 ], results obtained in mouse models may be misleading.…”

mentioning

confidence: 99%