7 research outputs found
Concentrations of argon gas (µl/ml) in blood in home cage controls, animals ventilated under normoxic conditions, animals ventilated with argon after hypoxia, and animals ventilated with argon after hypoxia that subsequently underwent hypothermia.
<p>Separate animals within one experimental setup are displayed with different symbols (open circles and closed squares).</p
Schematic representation of the three steps of the experimental setup.
<p>Schematic representation of the three steps of the experimental setup.</p
Calculated differences in monitored parameters (normoventilation – argon ventilation) displayed as absolute difference.
<p>For reference, the median value of the 6 animals during baseline is added to the right of each panel. Each dot represents a single switch from argon to normoventilation or vice versa. Ag: argon, HI: hypoxia-ischemia, HT: hypothermia.</p
Recorded physiological data from representative animal receiving therapeutic hypothermia.
<p>Black horizontal bars represent periods of argon ventilation.</p
Coefficients of argon, hypoxia and hypothermia after multivariable analysis of mean arterial blood pressure (MABP), heart rate, aEEG voltage and regional cerebral saturation (rScO<sub>2</sub>).
<p>Coefficients of argon, hypoxia and hypothermia after multivariable analysis of mean arterial blood pressure (MABP), heart rate, aEEG voltage and regional cerebral saturation (rScO<sub>2</sub>).</p
data_sheet_1_Nitric Oxide Synthase Inhibition as a Neuroprotective Strategy Following Hypoxic–Ischemic Encephalopathy: Evidence From Animal Studies.docx
Background<p>Hypoxic–ischemic encephalopathy following perinatal asphyxia is a leading cause of neonatal death and disability worldwide. Treatment with therapeutic hypothermia reduced adverse outcomes from 60 to 45%. Additional strategies are urgently needed to further improve the outcome for these neonates. Inhibition of nitric oxide synthase (NOS) is a potential neuroprotective target. This article reviews the evidence of neuroprotection by nitric oxide (NO) synthesis inhibition in animal models.</p>Methods<p>Literature search using the EMBASE, Medline, Cochrane, and PubMed databases. Studies comparing NOS inhibition to placebo, with neuroprotective outcome measures, in relevant animal models were included. Methodologic quality of the included studies was assessed.</p>Results<p>26 studies were included using non-selective or selective NOS inhibition in rat, piglet, sheep, or rabbit animal models. A large variety in outcome measures was reported. Outcome measures were grouped as histological, biological, or neurobehavioral. Both non-selective and selective inhibitors show neuroprotective properties in one or more outcome measures. Methodologic quality was either low or moderate for all studies.</p>Conclusion<p>Inhibition of NO synthesis is a promising strategy for additional neuroprotection. In humans, intervention can only take place after the onset of the hypoxic–ischemic event. Therefore, combined inhibition of neuronal and inducible NOS seems the most likely candidate for human clinical trials. Future studies should determine its safety and effectiveness in neonates, as well as a potential sex-specific neuroprotective effect. Researchers should strive to improve methodologic quality of animal intervention studies by using a systematic approach in conducting and reporting of these studies.</p