Involvement of Nitric Oxide in the Pathophysiology of Acute Heat Stress in the Rat

Sharma, H. S.; Westman, Jan; Alm, Per; Sjöquist, Per-Ove; Cervós-Navarro, J; Nyberg, Fred

doi:10.1111/j.1749-6632.1997.tb51749.x

Cited by 72 publications

(27 citation statements)

References 36 publications

(68 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Intestinal mucosal permeability to endotoxin increases during heatstroke in the rat (26); this alteration enhances production of cytokines that induce nitric oxide (NO) overproduction in the rat (27). Indeed, plasma or cerebral levels of NO are elevated in heatstroke rats (27,28; present results).…”

Section: Stress Accordingly Cd34supporting

confidence: 52%

See 1 more Smart Citation

Human Umbilical Cord Blood–Derived CD34+ Cells Can Be Used as a Prophylactic Agent for Experimental Heatstroke

Hwang¹,

Chen²,

Lin³

et al. 2008

J Pharmacol Sci

View full text Add to dashboard Cite

Abstract. We attempted to assess the prophylactic effect of human umbilical cord bloodderived CD34+ cells in experimental heatstroke. Anesthetized rats, 1 day before heat stress, were divided into 2 major groups and given CD34 − cells (defined by 1 × 10 6 human cord blood lymphocytes and monocytes that contained <0.2% CD34 + cells) or CD34 + cells (defined by 1 × 10 6 human cord blood lymphocytes and monocytes that contained >95% CD34 + cells). They were exposed to ambient temperature of 43°C for 70 min to induce heatstroke. When the CD34 − cells-treated or untreated rats underwent heat stress, their survival time values were found to be 20 -24 min. Pretreatment with CD34+ cells significantly increased survival time (123 -351 min). As compared with normothermic controls, all CD34− cells-treated heatstroke animals displayed hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. However, these heatstroke reactions all were significantly suppressed by CD34 + cells pretreatment. In addition, the levels of interlukin-10 in plasma and glial cell line-derived neurotrophic factors in brain were all significantly increased after CD34 + cell administration during heatstroke. Our data indicate that human umbilical cord-derived CD34 + cells can be used as a prophylactic agent for experimental heatstroke.

show abstract

Section: Stress Accordingly Cd34supporting

confidence: 52%

“…Indeed, plasma or cerebral levels of NO are elevated in heatstroke rats (27,28; present results). Aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, improves heat tolerance in the rat by preserving the splanchnic blood flow (29) and reducing intracranial hypertension and cerebral ischemia and damage (30).…”

Section: Stress Accordingly Cd34mentioning

confidence: 81%

Human Umbilical Cord Blood–Derived CD34+ Cells Can Be Used as a Prophylactic Agent for Experimental Heatstroke

Hwang¹,

Chen²,

Lin³

et al. 2008

J Pharmacol Sci

View full text Add to dashboard Cite

show abstract

“…nNOS mRNA expression is tightly regulated, consistent with its role in development (28) and in the adaptation to environmental stress (45,46). This level of fine control is imposed, in part, through the cell-and tissue-specific production of different RNA transcripts (47).…”

Section: Figurementioning

confidence: 82%

Hypoxia induces a functionally significant and translationally efficient neuronal NO synthase mRNA variant

Ward

Toporsian²,

Scott³

et al. 2005

J. Clin. Invest.

102

View full text Add to dashboard Cite

We tested the hypothesis that induction of neuronal NO synthase (nNOS) impairs vascular smooth muscle contractility after hypoxia. nNOS protein was increased in aorta, mesenteric arterioles, pulmonary arteries, brain, and diaphragm from rats exposed to 8% O 2 for 48 hours and in human aortic SMCs after hypoxic incubation (1% O 2 ). Ca 2+ -dependent NO synthase activity was increased in endothelium-denuded aortic segments from hypoxia-exposed rats. N G -nitro-l-arginine methyl ester enhanced the contractile responses of endothelium-denuded aortic rings and mesenteric arterioles from hypoxia-exposed but not normoxic rats (P < 0.05). The hypoxia-inducible mRNA transcript expressed by human cells was found to contain a novel 5′-untranslated region, consistent with activation of transcription in the genomic region contiguous with exon 2. Translational efficiency of this transcript is markedly increased compared with previously described human nNOS mRNAs. Transgenic mice possessing a lacZ reporter construct under control of these genomic sequences demonstrated expression of the construct after exposure to hypoxia (8% O 2 , 48 hours) in the aorta, mesenteric arterioles, renal papilla, and brain. These results reveal a novel human nNOS promoter that confers the ability to rapidly upregulate nNOS expression in response to hypoxia with a functionally significant effect on vascular smooth muscle contraction.

show abstract

“…Both pyrogenic cytokines and endothelium-derived factors can interfere with normal thermoregulation, thereby precipitating arterial hypotension, hyperthermia, and heatstroke (4). Plasma or brain nitrite / nitrate levels are elevated in heatstroke patients (5) and rats (6,7). A more recent report has also shown that aminoguanidine (AG) slows the rate of NO production, preserves the splanchnic blood flow, and improves heat tolerance in rats (2).…”

Section: Introductionmentioning

confidence: 93%

Aminoguanidine Protects Against Intracranial Hypertension and Cerebral Ischemic Injury in Experimental Heatstroke

et al. 2004

View full text Add to dashboard Cite

Abstract. The aim of the present study was to ascertain whether aminoguanidine attenuated intracranial hypertension and cerebral ischemic injury in experimental heatstroke. Urethaneanesthetized rats were exposed to heat stress (ambient temperature of 43°C) to induce heatstroke. Control rats were exposed to 24°C. Mean arterial pressure, cerebral perfusion pressure, and cerebral blood flow after the onset of heatstroke were all significantly lower than in control rats. However, colonic temperature, intracranial pressure, heart rate, cerebral inducible nitric oxide synthase (iNOS)-dependent NO, and neuronal damage score were greater after the onset of heatstroke. Aminoguanidine (30 mmol / kg, i.v.; 30 min before the start of heat exposure) pretreatment significantly attenuated the heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral ischemia and neuronal damage, and increased iNOS-dependent NO formation in the brain. The extracellular concentrations of ischemic (e.g., glutamate and lactate / pyruvate ratio) and damage (e.g., glycerol) markers in the hypothalamus were also increased after the onset of heatstroke. Aminoguanidine pretreatment significantly attenuated the increase in hypothalamic ischemia and damage markers associated with heatstroke. Delaying onset of aminoguanidine administration (i.e., 0 or 30 min after the start of heat exposure) reduced the preventive efficiency on heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral ischemia, and increased iNOS-dependent NO formation in brain. These results suggest that aminoguanidine protects against heatstroke-induced intracranial hypertension and cerebral ischemic injury by inhibition of cerebral iNOS-dependent NO production.

show abstract

Involvement of Nitric Oxide in the Pathophysiology of Acute Heat Stress in the Rat

Cited by 72 publications

References 36 publications

Human Umbilical Cord Blood–Derived CD34+ Cells Can Be Used as a Prophylactic Agent for Experimental Heatstroke

Human Umbilical Cord Blood–Derived CD34+ Cells Can Be Used as a Prophylactic Agent for Experimental Heatstroke

Hypoxia induces a functionally significant and translationally efficient neuronal NO synthase mRNA variant

Aminoguanidine Protects Against Intracranial Hypertension and Cerebral Ischemic Injury in Experimental Heatstroke

Contact Info

Product

Resources

About