Role of Nociceptin/Orphanin FQ in Age-Dependent Cerebral Hemodynamic Effects of Brain Injury

2000 ◽  
Vol 17 (9) ◽  
pp. 751-764 ◽  
Author(s):  
WILLIAM M. ARMSTEAD
Keyword(s):  
Brain Injury ◽  
Orphanin Fq ◽  
Hemodynamic Effects ◽  
Cerebral Hemodynamic ◽  
Age Dependent

scholarly journals NOC/oFQ contributes to age-dependent impairment of NMDA-induced cerebrovasodilation after brain injury

2000 ◽  
Vol 279 (5) ◽  
pp. H2188-H2195 ◽  
Author(s):  
William M. Armstead
Keyword(s):  
Cerebrospinal Fluid ◽  
Amino Acid ◽  
Brain Injury ◽  
Excitatory Amino Acid ◽  
Age Groups ◽  
Orphanin Fq ◽  
Pial Artery ◽  
Age Related ◽  
Age Dependent

This study characterized the effects of fluid percussion brain injury (FPI) on N-methyl-d-aspartate (NMDA)-induced vasodilation and determined the role of nociceptin/orphanin FQ (NOC/oFQ) in such changes as a function of age and time postinsult. FPI elevated cerebrospinal fluid (CSF) NOC/oFQ from 70 ± 3 to 444 ± 56 pg/ml (≈10−10 M) within 1 h and to 1,931 ± 112 pg/ml within 8 h, whereas values returned to control levels within 168 h in the newborn pig. In contrast, FPI elevated CSF NOC/oFQ from 77 ± 4 to 202 ± 16 pg/ml within 1 h and values returned to control levels within 8 h in the juvenile pig. Topical NOC/oFQ (10−10 M) had no effect on pial artery diameter but attenuated NMDA (10−8, 10−6M)-induced dilation (9 ± 1 and 16 ± 1 vs. 5 ± 1 and 10 ± 1%) in both age groups. In the newborn, NMDA-induced pial artery dilation was reversed to vasoconstriction within 1 h post-FPI and responses remained impaired for 72 h, but such vasoconstriction was attenuated by pretreatment with [F/G]NOC/oFQ(1–13)-NH2 (10−6 M, 1 mg/kg iv), an NOC/oFQ antagonist (9 ± 1 and 16 ± 1 vs. −7 ± 1 and −12 ± 1 vs −2 ± 1 and −3 ± 1% for control, FPI, and FPI pretreated with the NOC/oFQ antagonist). In contrast, in the juvenile, NMDA-induced vasodilation was only attenuated within 1 h post-FPI and returned to control within 8 h. Such dilation was also partially restored by the NOC/oFQ antagonist. These data indicate that NOC/oFQ contributes to impaired NMDA pial artery dilation after FPI. These data suggest that the greater NOC/oFQ release in the newborn versus the juvenile may contribute to age-related differences in FPI effects on excitatory amino acid-induced pial dilation.

Age-dependent cerebral hemodynamic effects of indomethacin in the newborn piglet

2004 ◽  
Vol 97 (5) ◽  
pp. 1880-1887 ◽  
Author(s):  
Derek W. Brown ◽  
David Lee ◽  
Vazhkudai S. Kumaran ◽  
Ting-Yim Lee
Keyword(s):  
Near Infrared ◽  
Cerebral Blood Volume ◽  
Ductus Arteriosus ◽  
Hemodynamic Response ◽  
Oxygen Extraction Fraction ◽  
Postnatal Life ◽  
Dependent Manner ◽  
Hemodynamic Effects ◽  
Cerebral Hemodynamic ◽  
Age Dependent

With recent discussions in the literature regarding prophylactic use of early (within the first 12 h after birth), low-dose indomethacin to reduce the incidence and severity of intraventricular hemorrhage, knowledge pertaining to the cerebral hemodynamic effects of indomethacin in this age group is of significant interest. The cerebral circulation is known to undergo significant changes during the first few days of postnatal life. In the present study, we have investigated the hypothesis that postnatal adaptive changes influence the cerebral hemodynamic response to indomethacin in an age-dependent manner. Near-infrared spectroscopy with indocyanine green was used to measure cerebral hemodynamics, cerebral metabolic rate of oxygen, and cerebral oxygen extraction fraction in 39 newborn piglets. Piglets were grouped by age and received either 0.2 mg/kg indomethacin (14 were <13 h of age and 12 were >13 h of age) or saline (8 were <13 h of age and 5 were >13 h of age) infusions. In a subgroup of indomethacin-treated piglets (9 less than and 7 greater than 13 h of age), Doppler flow ultrasound was used to diagnose and monitor the presence and persistence of patent ductus arteriosus. Age was a significant factor in the cerebral hemodynamic response to indomethacin with piglets <13 h of age exhibiting delayed increases in cerebral blood flow and cerebral blood volume at 150 min post-indomethacin infusion.

Role of Nociceptin/Orphanin FQ in the Physiologic and Pathologic Control of the Cerebral Circulation

2002 ◽  
Vol 227 (11) ◽  
pp. 957-968 ◽  
Author(s):  
William M. Armstead
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Circulation ◽  
Cerebral Hemodynamics ◽  
Present Review ◽  
Cerebral Hypoxia ◽  
Orphanin Fq ◽  
Hypoxia Ischemia

Nociceptin/orphanin FQ is a newly described member of the opioid family. Previous minireviews in this series have described the contribution of important factors, including opioids, in the regulation of the cerebral circulation during physiologic and pathologic conditions. The present review extends these initial comments to an opioid whose vascular actions have only very recently been appreciated. In particular, this review discusses the contribution of nociceptin/orphanin FQ to impaired cerebral hemodynamics after cerebral hypoxia/ischemia and traumatic brain injury.

Role of endothelin-1 in age-dependent cerebrovascular hypotensive responses after brain injury

1999 ◽  
Vol 277 (5) ◽  
pp. H1884-H1894 ◽  
Author(s):  
William M. Armstead
Keyword(s):  
Blood Pressure ◽  
Brain Injury ◽  
Cerebral Autoregulation ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Age Dependent ◽  
Cerebrovascular Regulation

This study was designed to compare the effect of fluid percussion brain injury (FPI) on the hypotensive cerebrovascular response in newborn and juvenile pigs as a function of time postinsult and to determine the role of endothelin-1 (ET-1) in any age-dependent differences in hypotensive cerebrovascular regulation after injury. Ten minutes of hypotension (10–15 ml blood/kg) decreased mean arterial blood pressure uniformly in both groups (∼45%). In the newborn, hypotensive pial artery dilation (PAD) was blunted within 1 h, remained diminished for at least 72 h, but was resolved within 168 h postinjury (66 ± 4, 69 ± 4, 71 ± 4, and 64 ± 4% inhibition at 1, 4, 8, and 72 h post-FPI). During normotension, regional cerebral blood flow (rCBF) was decreased by FPI, and hypotension further reduced the already decremented rCBF for at least 72 h. Cerebrospinal fluid (CSF) ET-1 was increased from 26 ± 4 to 206 ± 25 pg/ml within 72 h post-FPI, whereas an ET-1 antagonist partially restored impaired hypotensive PAD and altered hypotensive rCBF. In contrast, hypotensive PAD and altered CBF were only inhibited for 4 h post-FPI in the juvenile (56 ± 3 and 34 ± 4% inhibition at 1 and 4 h post-FPI). CSF ET-1 was only increased from 27 ± 4 to 67 ± 9 pg/ml at 4 h, whereas the concentration returned to preinjury value by 8 h post-FPI. ET-1 antagonism similarly partially restored impaired hypotensive PAD and altered hypotensive rCBF. These data show that FPI disturbs cerebral autoregulation during hypotension both to a greater magnitude and for a longer duration in the newborn than in the juvenile. These data suggest that the greater FPI-induced ET-1 release in the newborn could contribute to age-dependent differences in impaired hypotensive cerebral autoregulation after FPI.

scholarly journals Cerebral Hemodynamic Effects of Acute Hyperoxia and Hyperventilation after Severe Traumatic Brain Injury

2010 ◽  
Vol 27 (10) ◽  
pp. 1853-1863 ◽  
Author(s):  
Leonardo Rangel-Castilla ◽  
Lucia Rivera Lara ◽  
Shankar Gopinath ◽  
Paul R. Swank ◽  
Alex Valadka ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Hemodynamic Effects ◽  
Cerebral Hemodynamic
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