The Measurement of Brainstem Blood Flow in the Experimental Recirculation Model of Brainstem Ischemia in the Rat

This report describes a surgical approach and measurement of brainstem blood flow (BBF) used in experimental ischemic model of the brainstem. The vertebral artery of Wistar rat was exposed and prepared embolic thread was inserted into the vertebral artery. The lesions of the baselar artery occuleded animals were restricted to the brainstem which, in the rat, is normally supplied by the vertebrobasilar artery. Using the hydrogen clearance techniques, blood flow of the brainstem was measured in 21 rats. The mean value of mean blood pressure (MBP) was 96.2±6.2 mmHg before ischemia. It dropped to 62.0±12.4 mmHg after transient hypertension. The preischemic BBF was 35.5±2.4 ml/100g/min. This was followed by a gradual increase to hyperperfusion after recirculation. After 1 hour of recirculation, BBF rose to a level above 78.9±5.9 ml/100g/min. These findings suggest that this model may be useful in the evaluation of pathophysiogical changes in brainstem ischemia

Traumatic Cerebral Aneurysm -- Surgical Manafement and mportance of Post-Traumatic Cerebral Angiography Before Delayed Rupture --

We report rare case of traumatic cerebral aneurysm. A 36-year-old man fell and struck the right pariental region of his head. He lost consciousness for 10 min but had no neurological deficits on admission. CT scan revealed right acute subdural hematoma. On the eighth day, we anticipativery performed precautionary cerebral angiography, which ahowed a traumatic cerebral aneurysm on the peripheral branch of the right middle cerebral artery. This aneurysm was cured by microneurosurgery and the patient was discharged without deficits. The most important aspect of the present case was the aneurysm was discovered in advance by cerebral angiography and cured by microneurosurgery. We review previous cases of traumatic cerebral aneurysm and discuss the importance of cerebral angiography after head injury and the surgical management of traumatic cerebral aneurysm

Establishment of an abnormal vascular patterning model in the mouse retina

Abnormalities in retinal blood vessels and neuronal function persist in eyes undergoing retinopathy of prematurity. In this study, we examined morphological and functional changes in retinal blood vessels and neurons in mice that had undergone short-term interruption of retinal vascular development through inhibition of vascular endothelial growth factor (VEGF) signaling. In mice treated with the VEGF receptor tyrosine kinase inhibitor KRN633 on postnatal day (P) 0 and 1, the vascular density in the retinal surface increased by P12, but development of deep retinal vascular plexus and choroidal vasculature was delayed until P14. Overall retinal morphology was mostly normal in KRN633-treated mice during the observation period (∼P28), with the exception of P8 and P14. On P28, abnormalities in retinal vascular patterns were evident, but electroretinogram and retinal blood perfusion were within the normal range. Abnormal architecture of retinal vasculature disturbs retinal hemodynamics; therefore, mice treated postnatally with VEGF receptor inhibitors could serve as an animal model for studying the regulatory mechanism of local retinal blood flow and the effect of persistent abnormal retinal vascular patterns on the risk of onset of retinal ischemia. Keywords: Endothelial cell, Neuronal cell, Vascular endothelial growth factor, Vascular patterning, Retin

Impairment of endothelium-dependent vasodilator function of retinal blood vessels in adult rats with a history of retinopathy of prematurity

Retinopathy of prematurity (ROP) is a proliferative retinal vascular disease, initiated by delayed retinal vascular growth after premature birth. In the majority of cases, ROP resolves spontaneously; however, a history of ROP may increase the risk of long-term visual problems. In this study, we evaluated the endothelial function of retinal blood vessels in adult rats with a history of ROP. ROP was induced in rats by subcutaneous injection of a vascular endothelial growth factor receptor tyrosine kinase inhibitor (KRN633) on postnatal day (P) 7 and P8. On P56, vasodilator responses to acetylcholine, GSK1016790A (an activator of transient receptor potential vanilloid 4 channels), NOR3 (a nitric oxide [NO] donor), and salbutamol (a β2-adrenoceptor agonist) were assessed. Compared to age-matched controls, retinal vasodilator responses to acetylcholine and GSK1016790A were attenuated in P56 rats with a history of ROP. No attenuation of acetylcholine-induced retinal vasodilator response was observed under inhibition of NO synthase. Retinal vasodilator responses to NOR3 and salbutamol were unaffected. These results suggest that the production of and/or release of NO is impaired in retinal blood vessels in adult rats with a history of ROP. A history of ROP might increase the risk of impaired retinal circulation in adulthood