Naltrexone Modifies Thermoregulatory Symptoms and Lessens the Severity of Heat Stroke in Guinea Pigs<sup>a</sup>

Romanovsky, Andrej A.; Blatteis, Clark M.

doi:10.1111/j.1749-6632.1997.tb51745.x

Cited by 5 publications

(4 citation statements)

References 17 publications

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“…For example, an increase in brain levels of β‐endorphin 19 or dynorphin 87 was noted in rats with heat stroke. Naltrexone, a wide‐spectrum opioid receptor antagonist, has been shown to attenuate the severity of heat stroke 88–90 . The heat stroke‐induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral hypoperfusion and hypoxia, as well as increased levels of extracellular ischaemia and damage markers in the brain, were all significantly attenuated by prior antagonism of mu‐opioid receptors, but not kappa‐ or delta‐opioid receptors 91 .…”

Section: Mu‐opioid Receptor Blockade Protects Against Heat Strokementioning

confidence: 99%

CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE^¶

Chen

Niu²,

Lin

2006

Clin Exp Pharma Physio

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2. All heat-stressed rodents, even under general anaesthesia, have hyperthermia, systemic inflammation, hypercoagulable state, arterial hypotension and tissue ischaemia and injury in multiple organs. These findings demonstrate that rodent heat stroke models can nearly mirror the full spectrum of human heat stroke. Experimental heat stroke fulfills the empirical triad used for the dignosis of classical human heat stroke, namely hyperthermia, central nervous system alterations and a history of heat stress.3. These physiological dysfunctions and survival during heat stroke can be improved by whole-body or brain cooling therapy adopted immediately after the onset of heat stroke.4. However, in the absence of body or brain cooling, these heat stroke reactions can still be reduced by the following measures: (i) fluid replacement with 3% NaCl solution, 10% human albumin or hydroxyethyl starch; (ii) intravenous delivery of antiinflammatory drugs, free radical scavengers or interleukin-1 receptor antagonists; (iii) hyperbaric oxygen therapy; or (iv) transplantation of human umbilical cord blood cells.5. In addition, before initiation of heat stress, prior manipulations with one of the following measures was found to be able to protect against heat stroke reactions: (i) systemic delivery of α α α α-tocopherol, mannitol, inducible nitric oxide synthase inhibitors, mu-opioid receptor antagonists, endothelin ET A receptor antagonists, serotoninergic nerve depletors or receptor antagonists, or glutamate receptor antagonists; or (ii) heat shock portein 72 preconditioning.6. There is compelling evidence that cerebrovascular dysfunction is an attractive target for therapy in heat stroke.

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Section: Mu‐opioid Receptor Blockade Protects Against Heat Strokementioning

confidence: 99%

CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE^¶

Chen

Niu²,

Lin

2006

Clin Exp Pharma Physio

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“…Most of the data on heatstroke have been derived from experimentally induced models of heatstroke in rodents, baboons and dogs, and from clinical studies in humans. [1][2][3][4][5][6][7][8][9][10][11][12] Only a single study of naturally occurring heat-induced illness in 42 dogs has been published until year 2006. 13 Since then, different aspects of this devastating syndrome have been investigated in dogs with naturally occurring heatstroke, admitted to the Hebrew University Veterinary Teaching Hospital, and are presented in this review.…”

mentioning

confidence: 99%

Pathophysiology of heatstroke in dogs – revisited

2017

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Heatstroke results from a failure to dissipate accumulated heat during exposure to hot environments, or during strenuous physical exercise under heat stress. It is characterized by core body temperatures > 41°C, with central nervous system dysfunction. Functional morphology and thermoregulatory effectors differences between dogs and humans may require special heatstroke protective adaptations in dogs, however, the risk factors for developing heatstroke are similar in both. In dogs, these include hot, especially highly humid environments, excessive physical activity, obesity, large (>15 kg) body weight, being of certain breed (e.g., Labrador retrievers and brachycephalic breeds), upper airway obstruction and prolonged seizures. Lack of acclimation to heat and physical fitness decreases the survival of heat stroked dogs. At the systemic level, blood pooling within the large internal organs (e.g., spleen, liver) is a major contributor to the development of shock and consequent intestinal ischemia, hypoxia and endothelial hyperpermeability, commonly occurring in heatstroke patients. Evoked serious complications include rhabdomyolysis, acute kidney injury, acute respiratory distress syndrome and ultimately, sepsis and disseminated intravascular coagulation. The most common clinical signs in dogs include acute collapse, tachypnea, spontaneous bleeding, shock signs and mental abnormalities, including depression, disorientation or delirium, seizures, stupor and coma. In such dogs, presence of peripheral blood nucleated red blood cells uniquely occurs, and is a highly sensitive diagnostic and prognostic biomarker. Despite early, appropriate body cooling, and intensive supportive treatment, with no available specific treatment to ameliorate the severe inflammatory and hemostatic derangements, the mortality rate is around 50%, similar to that of human heatstroke victims. This review discusses the pathophysiology of canine heatstroke from a veterinarian's point of view, integrating new and old studies and knowledge.

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“…An increase in the serum concentrations of b-endorphin have also been observed in patients with heat stroke (13). Naltrexone, a wide-spectrum opioid-receptor antagonist with a strong anti-m -opioid receptor activity, has been demonstrated to attenuate the severity of heat stroke (7,8,10,14,15). However, the mechanism underlying the therapeutic effects of naltrexone on heat stroke remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Naltrexone Protects Against Hypotension, Hyperthermia, and β-Endorphin Overproduction During Heatstroke in the Rat

et al. 2005

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Abstract. Heat stroke is characterized by hyperthermia, arterial hypotension, decreased baroreflex sensitivity, and increased serum levels of b-endorphin. Whereas naltrexone may have therapeutic potential in heat stroke, the underlying mechanism remains unclear. We tested the hypothesis that naltrexone may attenuate heat stroke by reducing hyperthermia, hypotension, decreased baroreceptor sensitivity, and / or increased serum levels of b-endorphin. Heat stroke was induced by exposing the anesthetized adult Sprague-Dawley rats in an incubator at 43°C. The moment in which the mean arterial pressure dropped irreversibly from the peak level was taken as the onset of heat stroke. Control rats were exposed to 24°C. Mean arterial pressure, baroreceptor sensitivity, and maximal reflex bradycardia, after the onset of heat stroke, were all significantly lower than in control rats. However, rectal temperature and serum levels of bendorphin were all greater after the onset of heat stroke. Intravenous delivery of naltrexone (10 mg / kg) 20 min before the initiation of heat stress, but not immediately at the onset of heat stroke, significantly attenuated the above-mentioned reactions. Accordingly, naltrexone improved survival during heat stroke. These results suggest that naltrexone protects against hypotension and decrement of both baroreceptor sensitivity and maximal reflex bradycardia during heat stroke by reducing both hyperthermia and increment of serum b-endorphin and thus improves survival.

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Naltrexone Modifies Thermoregulatory Symptoms and Lessens the Severity of Heat Stroke in Guinea Pigs^a

Cited by 5 publications

References 17 publications

CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE^¶

CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE^¶

Pathophysiology of heatstroke in dogs – revisited

Naltrexone Protects Against Hypotension, Hyperthermia, and β-Endorphin Overproduction During Heatstroke in the Rat

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Naltrexone Modifies Thermoregulatory Symptoms and Lessens the Severity of Heat Stroke in Guinea Pigsa

Cited by 5 publications

References 17 publications

CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE¶

CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE¶

Pathophysiology of heatstroke in dogs – revisited

Naltrexone Protects Against Hypotension, Hyperthermia, and β-Endorphin Overproduction During Heatstroke in the Rat

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Product

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Naltrexone Modifies Thermoregulatory Symptoms and Lessens the Severity of Heat Stroke in Guinea Pigs^a

CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE^¶

CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE^¶