Differential Responses of the Nitric Oxide Synthase (NOS) Gene to Immunological Challenges in Noble Scallop Chlamys nobilis

Infarct volume and edema were assessed after transient focal ischemia in mice lacking neuronal nitric oxide synthase (NOS) gene expression. With use of an 8–0 coated monofilament, the middle cerebral artery (MCA) of mutant (n = 32) and wild-type mice [SV-129 (n = 31), C57Black/6 (n = 18)] were occluded for 3 h and reperfused for up to 24 h. Regional CBF (rCBF), neurological deficits, water content, and infarct volume were examined in all three strains. rCBF, blood pressure, and heart rate did not differ between groups when measured for 1 h after reperfusion. Neurological deficits were less severe in mutant mice after MCA occlusion. Brain water content at 3 h after reperfusion and infarct volume at 24 h after reperfusion were greater in wild-type mice. These data indicate that genetic deletion of neuronal NOS confers resistance to focal ischemic injury in a reperfusion model. The findings agree with previous studies showing that tissue injury is less extensive after both permanent MCA occlusion and global ischemia in mice lacking neuronal NOS gene expression. Hence, NO may play a pivotal role in the pathogenesis of ischemic brain damage.

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OVARIAN NITRIC OXIDE SYNTHASE (NOS) GENE EXPRESSION DURING PERIPUBERTAL DEVELOPMENT

Life Sciences ◽

10.1016/s0024-3205(97)00710-8 ◽

1997 ◽

Vol 61 (15) ◽

pp. 1507-1516 ◽

Cited By ~ 9

Author(s):

Vinod Srivastava ◽

Benjamin J Jones ◽

Hugh Dookwah ◽

Jill K Hiney ◽

W Les Dees

Keyword(s):

Gene Expression ◽

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Oxide Synthase ◽

Nos Gene

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Hemodilutional anemia is associated with increased cerebral neuronal nitric oxide synthase gene expression

Journal of Applied Physiology ◽

10.1152/japplphysiol.00931.2002 ◽

2003 ◽

Vol 94 (5) ◽

pp. 2058-2067 ◽

Cited By ~ 40

Author(s):

Gregory M. T. Hare ◽

C. David Mazer ◽

William Mak ◽

Reginald M. Gorczynski ◽

Kathryn M. Hum ◽

...

Keyword(s):

Gene Expression ◽

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Oxygen Delivery ◽

Tissue Hypoxia ◽

Tissue Oxygen ◽

Cerebral Tissue ◽

Acute Anemia ◽

Oxide Synthase ◽

Nos Gene

Severe hemodilutional anemia may reduce cerebral oxygen delivery, resulting in cerebral tissue hypoxia. Increased nitric oxide synthase (NOS) expression has been identified following cerebral hypoxia and may contribute to the compensatory increase in cerebral blood flow (CBF) observed after hypoxia and anemia. However, changes in cerebral NOS gene expression have not been reported after acute anemia. This study tests the hypothesis that acute hemodilutional anemia causes cerebral tissue hypoxia, triggering changes in cerebral NOS gene expression. Anesthetized rats underwent hemodilution when 30 ml/kg of blood were exchanged with pentastarch, resulting in a final hemoglobin concentration of 51.0 ± 1.2 g/l ( n = 7 rats). Caudate tissue oxygen tension (PbrO2 ) decreased transiently from 17.3 ± 4.1 to 14.4 ± 4.1 Torr ( P < 0.05), before returning to baseline after ∼20 min. An increase in CBF may have contributed to restoring PbrO2 by improving cerebral tissue oxygen delivery. An increase in neuronal NOS (nNOS) mRNA was detected by RT-PCR in the cerebral cortex of anemic rats after 3 h ( P < 0.05, n = 5). A similar response was observed after exposure to hypoxia. By contrast, no increases in mRNA for endothelial NOS or interleukin-1β were observed after anemia or hypoxia. Hemodilutional anemia caused an acute reduction in PbrO2 and an increase in cerebral cortical nNOS mRNA, supporting a role for nNOS in the physiological response to acute anemia.

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