Nitric oxide production is enhanced in patients with heat stroke

Alzeer, Abdulaziz H.; Alarifi, Abdullah; Warsy, Arjumand S.; Ansari, Ziauddin; Zhang, Haibo; Vincent, Jean‐Louis

doi:10.1007/s001340050787

Cited by 40 publications

(1 citation statement)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These observations tend to indicate that iNOS-derived NO plays a role in the development of the inflammatory response by altering key components of the inflammatory cascade. In fact, both plasma or brain NO levels have been elevated in heatstroke patients [37] and rats [1, 38]. Aminoguanidine, an iNOS inhibitor, improves heat tolerance in rats by preserving splanchnic blood [1] and cerebral blood flow [38].…”

Section: Discussionmentioning

confidence: 99%

Attenuation of Acute Lung Inflammation and Injury by Whole Body Cooling in a Rat Heatstroke Model

Yang

Chang

Cheng

et al. 2009

BioMed Research International

View full text Add to dashboard Cite

Whole body cooling is the current therapy of choice for heatstroke because the therapeutic agents are not available. In this study, we assessed the effects of whole body cooling on several indices of acute lung inflammation and injury which might occur during heatstroke. Anesthetized rats were randomized into the following groups and given (a) no treatment or (b) whole body cooling immediately after onset of heatstroke. As compared with the normothermic controls, the untreated heatstroke rats had higher levels of pleural exudates volume and polymorphonuclear cell numbers, lung myloperoxidase activity and inducible nitric oxide synthase expression, histologic lung injury score, and bronchoalveolar proinflammatory cytokines and glutamate, and PaCO2. In contrast, the values of mean arterial pressure, heart rate, PaO2, pH, and blood HCO3− were all significantly lower during heatstroke. The acute lung inflammation and injury and electrolyte imbalance that occurred during heatstroke were significantly reduced by whole body cooling. In conclusion, we identified heat-induced acute lung inflammation and injury and electrolyte imbalance could be ameliorated by whole body cooling.

show abstract

Section: Discussionmentioning

confidence: 99%

Attenuation of Acute Lung Inflammation and Injury by Whole Body Cooling in a Rat Heatstroke Model

Yang

Chang

Cheng

et al. 2009

BioMed Research International

View full text Add to dashboard Cite

show abstract

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

View full text Add to dashboard Cite

This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

show abstract