Yazar "Ulvi, Hizir" seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim
    Öğe
    The Relationship Between the Neuron Density of the Trigeminal Ganglion and the Posterior Communicating Artery Vasospasm in Subarachnoid Hemorrhage: An Experimental Study
    (Lippincott Williams & Wilkins, 2012) Aydin, Mehmet Dumlu; Serarslan, Yurdal; Gundogdu, Cemal; Aydin, Nazan; Aygul, Recep; Kotan, Dilcan; Ulvi, Hizir
    Objective: Posterior communicating arteries (PComAs) are innervated by vasodilatatory fibers of the trigeminal ganglion (TGG). We examined whether there is a relationship between the neuron density of the TGG and the severity of PComA vasospasm in a subarachnoid hemorrhage (SAH). Methods: This study was conducted on 20 rabbits. Five were used as a baseline control group. Five were used as a sham group by injecting 1 mL of serum physiologic, and experimental SAH was applied to 10 animals by injecting homologous blood into the cisterna magna. After 10 days, PComAs and TGGs were examined histopathologically. PComA volumes and the neuron density of TGGs were estimated stereologically, and the results were analyzed statistically. Results: In control group, the mean volume of the PComAs was 66,500 +/- 8500 mu m(3), and the mean neuronal density of the TGGs was 8650 +/- 950/mm(3). In the serum physiologic group, the mean volume of the PComAs was 65,000 +/- 6550 mu m(3), and the mean neuronal density of the TGGs was 8600 +/- 800/mm(3). In the SAH group, the mean volume of the PComAs was 46,500 +/- 5500 mu m(3), and the mean neuronal density of the TGGs was 4200 +/- 500/mm(3). The results reveal an inverse relationship between the neuronal density in the TGG and the severity of the PComA vasospasm. Conclusions: The neuron density of the TGG may be an important factor in the regulation of PComA volume and in the continuation of cerebral blood flow. Low neuron density in the TGG may play an important role in the pathogenesis of PComA vasospasm in SAH.
  • [ N/A ]
    Öğe
    The Role of Trigeminal Ganglion Neuron Density in the Prevention of Subarachnoid Hemorrhage-induced Basilar Artery Vasospasm: An Experimental Study
    (Lippincott Williams & Wilkins, 2009) Onder, Arif; Serarslan, Yurdal; Aydin, Mehmet Dumlu; Aydin, Nazan; Ulvi, Hizir; Kotan, Dilcan; Aygul, Recep
    Objective: Cerebral arteries innervated by several systems contribute to the control of cerebral blood flow. Sensory fibers of the trigeminal nerve have a vasodilatory effect on the basilar artery. Subarachnoid hemorrhage (SAH) causes severe cerebral vasospasm by various neurochemical mechanisms. We examined possible relationships between the neuron density of the trigeminal ganglion and the severity of basilar artery vasospasm in SAH. Methods: In this study, 28 rabbits were used. The animals were randomly divided into 3 groups: SAH (n = 18), serum physiologic (n = 5) and control (n = 5) groups. Experimental SAH was induced by injecting homologous blood into the cisterna magna. After 20 days, the basilar arteries and trigeminal ganglions were examined histopathologically. Basilar artery volumes and the neuron density of the ophthalmic divisions of the trigeminal ganglions were estimated stereologically, and the results were statistically analyzed. Results: The mean basilar artery volume was 4.15 +/- 0.19 mm(3) and the mean neuronal density of the trigeminal ganglion was 6500 +/- 750/mm(3) for the control group. These values were 4.05 +/- 0.29 mm(3) and 6400 +/- 584/mm(3) for the serum physiologic group, 3.80 +/- 0.35 mm(3) and 4600 +/- 300/mm(3) for living animals in the SAH group, and 2.26 +/- 0.29 mm(3) and 2950 +/- 618/mm(3) for dead animals in SAH group, respectively. A linear relationship was found between the neuronal density of the trigeminal ganglion and basilar artery volumes. Conclusions: The neuron density of the trigeminal ganglion may be an important factor in the regulation of basilar artery volume and for the continuation of cerebral blood flow. The low neuron density of the trigeminal ganglion may be involved in the pathogenesis of severe basilar artery vasospasm induced by SAH.