Biomedical subjects

Hirofumi Nakatomi

Publications and source records attributed to Hirofumi Nakatomi.

5 recordsLinked to original sources

PubMed2004

A model of global cerebral ischemia in C57 BL/6 mice.

A reproducible model of global cerebral ischemia in mice is essential for elucidating the molecular mechanism of ischemic neuronal injury. Such a model is particularly important in the mouse because many genetically engineered mutant animals are available. In C57BL/6 and SV129/EMS mice, we evaluated a three-vessel occlusion model. Occlusion of the basilar artery with a miniature clip was followed by bilateral carotid occlusion. The mean cortical cerebral blood flow was reduced to less than 10% of the preischemic value, and the mean anoxic depolarization was attained within 1 minute. In C57BL/6 mice, there was CA1 hippocampal neuronal degeneration 4 days after ischemia. Neuronal damage depended upon ischemic duration: the surviving neuronal count was 78.5 +/- 8.5% after 8-minute ischemia and 8.4 +/- 12.7% after 14-minute ischemia. In SV129/EMS mice, similar neuronal degeneration was not observed after 14-minute ischemia. The global ischemia model in C57BL/6 mice showed high reproducibility and consistent neuronal injury in the CA1 sector, indicating that comparison of ischemic outcome between wild-type and mutant mice could provide meaningful data using the C57BL/6 genetic background. Strain differences in this study highlight the need for consideration of genetic background when evaluating ischemia experiments in mice.

Animals↗

PubMed2004

Prospective risk of hemorrhage in patients with vertebrobasilar nonsaccular intracranial aneurysm.

OBJECT: Nonsaccular intracranial aneurysms (NIAs) are characterized by dilation, elongation, and tortuosity of intracranial arteries. Dilemmas in management exist due to the limited regarding the natural history of this disease entity. The objective of this study was to determine the prospective risk of subarachnoid hemorrhage (SAH) in patients with vertebrobasilar NIAs. METHODS: All patients with vertebrobasilar fusiform or dolichoectatic aneurysms that had been radiographically demonstrated between 1989 and 2001 were identified. These patients' medical records were retrospectively reviewed. A prospective follow-up survey was sent and death certificates were requested. Based on results of neuroimaging studies, the maximal diameter of the involved artery, presence of SAH, and measurements of arterial tortuosity were recorded. Nonsaccular intracranial aneurysms were classified according to their radiographic appearance: fusiform, dolichoectatic, and transitional. Dissecting aneurysms were excluded. The aneurysm rupture rate was calculated based on person-years of follow up. Predictive factors for rupture were evaluated using univariate analysis (p < 0.05). One hundred fifty-nine patients, 74% of whom were men, were identified. The mean age at diagnosis was 64 years (range 20-87 years). Five patients (3%) initially presented with hemorrhage; four of these patients died during follow up. The mean duration of follow up was 4.4 years (692 person-years). Nine patients (6%) experienced hemorrhage after presentation; six hemorrhages were definitely related to the NIA. The prospective annual rupture rate was 0.9% (six patients/692 person-years) overall and 2.3% in those with transitional or fusiform aneurysm subtypes. Evidence of aneurysm enlargement or transitional type of NIA was a significant predictor of lesion rupture. Six patients died within 1 week of experiencing lesion rupture. CONCLUSIONS: Risk of hemorrhage in patients harboring vertebrobasilar NIAs is more common in those with evidence of aneurysm enlargement or a transitional type of aneurysm and carries a significant risk of death.

Adult↗

PubMed2003

Microsuture-tying forceps with attached scissors for bypass surgery.

BACKGROUND: Bypass surgery requires the shortest temporary occlusion time of a recipient artery during anastomosis. For this purpose, we have devised a microforceps with attached scissors that makes it possible to perform the multiple steps involved in anastomosis without exchanging instruments. This microforceps avoids having to exchange instruments twice in one suturing, such as that between a microsuture-tying forceps or a microneedle holder and microscissors in conventional methods. METHODS: The instrument is made of stainless steel and is 15.5 cm long. Using this microforceps with scissors, we can suture, tie, and cut a ligature fluently for consecutive sutures without exchanging instruments. The mean time during one suturing was compared between two patient groups treated by conventional method and with use of this instrument. RESULTS: This instrument was used for 34 patients with ischemic cerebrovascular disease (including three who needed deep-site anastomoses) and allowed us to perform superficial temporal artery-middle cerebral artery (STA-MCA) anastomoses uneventfully. This instrument saved 15.2 s in the mean time during one suturing. CONCLUSIONS: Although it is of paramount importance to practice tying sutures well, this new instrument removes the need to exchange conventional instruments, and we believe it will save time and, therefore, decrease complications during bypass surgery.

Anastomosis, Surgical↗

PubMed2002

Regeneration of hippocampal pyramidal neurons after ischemic brain injury by recruitment of endogenous neural progenitors.

The adult brain is extremely vulnerable to various insults. The recent discovery of neural progenitors in adult mammals, however, raises the possibility of repairing damaged tissue by recruiting their latent regenerative potential. Here we show that activation of endogenous progenitors leads to massive regeneration of hippocampal pyramidal neurons after ischemic brain injury. Endogenous progenitors proliferate in response to ischemia and subsequently migrate into the hippocampus to regenerate new neurons. Intraventricular infusion of growth factors markedly augments these responses, thereby increasing the number of newborn neurons. Our studies suggest that regenerated neurons are integrated into the existing brain circuitry and contribute to ameliorating neurological deficits. These results expand the possibility of novel neuronal cell regeneration therapies for stroke and other neurological diseases.

Animals↗

PubMed2002

Cardiac arrest cerebral ischemia model in mice failed to cause delayed neuronal death in the hippocampus.

Global cerebral ischemia models for genetically engineered mice are of particular importance for the study of delayed neuronal death, but have been complicated by variability of vascular anatomy. Here we developed a 5-min cardiac arrest model that was not affected by vascular anatomy, and evaluated the hippocampal neuronal injury in BL/6 and SV129 mice. Despite prolonged anoxic depolarization for approximately 7 min, however, no consistent ischemic neuronal injury was noted in the CA1 sector of the hippocampus in both strains. Thus, our observations suggested that murine hippocampal neurons are relatively resistant to ischemia compared with those in other rodents.

Animals↗