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Biomedical subjects

Y Fukuuchi

Publications and source records attributed to Y Fukuuchi.

At least 181 records · Page 10Linked to original sources
PubMed1988

Effects of the new calcium antagonist 2-nitratopropyl 3-nitratopropyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate on cerebral circulation in cats.

Effects of CD-349 (2-nitratopropyl 3-nitratopropyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate) on cerebral circulation were studied in 10 cats. The cats were fixed in a stereotactic head-holder, and two burr holes were made at 3-mm intervals over the left parietal cortex. Through one cranial window, the pial artery and vein diameters were measured continuously by a newly developed videocamera system in conjunction with a width analyzer, and the other one was used for measurement of cerebral blood volume (CBV). The pial artery (141 +/- 14 micron) was dilated by 16.6 +/- 4.9% (p less than 0.01) 1 min and 24.8 +/- 5.1% (p less than 0.01) 5 min after the CD-349 injection. The pial vein (101 +/- 20 micron) was also dilated with the percent increase of the diameter being 11.4 +/- 4.0% (p less than 0.01) 1 min and 11.3 +/- 4.9% (p less than 0.05) 5 min after the CD-349 administration. The CBV was also increased. The mean arterial blood pressure was decreased by 39.8 +/- 7.3 mmHg (p less than 0.01) 1 min and 34.4 +/- 5.5 mmHg (p less than 0.01) 5 min after drug injection. Thereafter, the blood pressure gradually returned to the pre-drug level. Form these results it is suggested that CD-349 exerts direct vasodilatory action via inhibition of calcium influx across vascular cell membranes into cerebral vessels.

Animals↗
PubMed1987

Comparison between pial and intraparenchymal vascular responses to sympathetic stimulation under hypercapnic conditions. With special reference to the mechanism for escape phenomenon.

We have shown that secondary vasodilation ('escape' phenomenon) during sympathetic nerve stimulation occurs in the intraparenchymal vessels but not remarkable in the pial vessels. To test a possible role of CO2 accumulation in the brain tissue in this phenomenon, the responses of pial and intraparenchymal vessels to sympathetic nerve stimulation were investigated during hypercapnia in 9 cats by using a video camera photoelectric system. The ipsilateral superior cervical ganglion was electrically stimulated for 5 min during hypercapnia (PaCO2 = 50 +/- 2 mm Hg). The intraparenchymal vessels as well as pial vessels remained constricted throughout the stimulation. Secondary dilation of the intraparenchymal vessels as seen at the later stage of sympathetic stimulation during normocapnia was not observed under the hypercapnic conditions. We assume that the arterial CO2 tension was so high that the constriction of inflow vessels could not result in accumulation of CO2 in the brain parenchyma. The accumulation of chemical metabolites as represented by CO2 is therefore considered to be the most probable mechanism underlying the escape phenomenon of the intraparenchymal vessels.

Animals↗
PubMed1986

Comparison between pial and intraparenchymal vascular responses to cervical sympathetic stimulation in cats. Part 1. Under normal resting conditions.

To investigate the role of sympathetic regulation in both resistance and capacitance vessels in cerebral circulation, the response of pial and intraparenchymal vessels to sympathetic nerve stimulation were simultaneously examined in 14 cats by means of a newly developed video camera photoelectric system. The system consisted of a video camera system for measurement of pial vascular diameters and a photoelectric apparatus for estimating regional cerebral blood volume in the intraparenchymal vessels. The ipsilateral superior cervical ganglion was electrically stimulated for 5 min. Initially, both the pial and intraparenchymal vessels constricted. The large pial arteries (173 +/- 25 micron, mean +/- SEM) remained constricted throughout the stimulation, whereas the intraparenchymal vessels began to dilate after the initial constriction and exceeded the control level at 175 +/- 25 s despite continued stimulation. In conclusion, such sympathetic nerve stimulation is considered to exert a constrictive effect on the intraparenchymal as well as the pial vessels at the early stage. The compensatory dilation of the intraparenchymal vessels was delayed 3 min after initiation of the stimulation.

Animals↗
PubMed1985

Effects of (D-Met2,Pro5)-enkephalinamide and naloxone on pial vessels in cats.

To elucidate the fundamental actions of endogenous opioids and naloxone on the cerebral circulation, the effects of (D-Met2,Pro5)-enkephalinamide and naloxone on pial vessels were investigated in cats. Pial arteries (165.7 +/- 24.9 microns) were found to dilate after the intravenous administration of 1 mg/kg of (D-Met2,Pro5)-enkephalinamide, and a definite dilatation of 7.1-7.6% persisted for 15 min. Pial veins (100.6 +/- 20.2 microns) also dilated but to a lesser degree. The MABP (118.7 +/- 10.5 mm Hg) decreased by 20 mm Hg immediately after the injection, but gradually returned to the initial value 15 min later. The observed cerebral vasodilatation may be attributable to sympathetic inhibition mediated either by the presynaptic opiate receptors of the cerebral vessels or by the opiate receptors in the brainstem. After the intravenous administration of 1 mg/kg of naloxone, pial arteries (122.0 +/- 17.2 microns) showed a slight but significant dilatation of 2.3-5.3%. There were no significant changes in pial veins (87.0 +/- 12.4 microns). MABP (130.4 +/- 12.3 mm Hg) was slightly increased after the injection. Although the mechanism involved was unclear, the cerebral vasodilatation occurring after the administration of naloxone may contribute to its ameliorating effect on the neurological symptoms following cerebral ischemia.

Animals↗
PubMed1984

Blood flow velocity in the pial arteries of cats, with particular reference to the vessel diameter.

The blood flow velocity and diameter of feline pial arteries, ranging in diameter from 20 to 200 microns, were measured simultaneously using a newly developed video camera method under steady-state conditions for all other parameters. There was a linear relationship between blood flow velocity and pial artery diameter (y = 0.340x + 0.309), the correlation coefficient being 0.785 (p less than 0.001). The average values for blood flow velocity in pial arteries less than 50 microns, greater than or equal to 50 but less than 100 microns, greater than or equal to 100 but less than 150 microns, and greater than or equal to 150 microns in diameter were 12.9 +/- 1.3, 24.6 +/- 3.4, 42.1 +/- 4.7, and 59.9 +/- 5.3 mm/s, respectively. Blood flow rate was calculated as a product of the cross-sectional area and the flow velocity. The blood flow rate increased exponentially as the pial artery diameter increased (y = 2.71 X 10(-4) x2.98). The average values for blood flow rate in pial arteries less than 50 microns, greater than or equal to 50 but less than 100 microns, greater than or equal to 100 but less than 150 microns and greater than or equal to 150 microns in diameter were 12.8 +/- 1.5, 122.1 +/- 24.8, 510.2 +/- 74.8, and 1524.2 +/- 174.4 10(-3) mm3/s, respectively. Hemorheological parameters such as the wall shear rate and Reynolds' number were also calculated. The data obtained provide a useful basis for further investigations in the field of cerebral circulation.

Animals↗
PubMed1982

Video camera method for simultaneous measurement of blood flow velocity and pial vessel diameter.

A new method for the simultaneous measurement of blood flow velocity and pial vessel diameter is described. The system consists basically of a high-sensitivity vidicon camera, camera control, width analyzer, video densitometer, TV monitor, desktop computer, and multi-pen recorder. The pial vessels are visualized through a cranial window at 25-200x magnification on the TV monitor. The diameter of three target vessels can be recorded simultaneously on the recorder by adjustment of controllable video signal gates using the width analyzer. At the same time, the optical densities of two targets at points upstream and downstream of the pial vessel are measured continuously with video densitometers, and their outputs are recorded on the polygraph and analyzed by the computer. The time difference in the two peaks of time--concentration curves, produced very 2-3 s at the highest frequency by the injection of a small amount of saline through the lingual artery, is measured on-line using the computer. The flow velocity in the vessel is calculated from the time difference and the distance between the two targets. The system was shown to be stable, reliable, and rapid in response. This method may provide a useful tool for research in the field of blood circulation in the brain or any other organ.

Animals↗
PubMed1982

Effect of nimodipine, a calcium antagonist, on cerebral vasospasm after subarachnoid hemorrhage in cats.

Effect of a calcium antagonist, isopropyl-(2-methoxyethyl)-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5- pyridinedicarboxylate (nimodipine) on the cerebral vasospasm after experimental subarachnoid hemorrhage (SAH) was studied in ten adult cats. The vasospasm was induced by injecting of 0.2-0.3 ml fresh autologous whole blood into the cisterna magna. Diameter of pial vessels was continuously measured by means of the vidicon camera system developed in our laboratory. Intravenous administration of nimodipine (0.1 mg/kg) 20-30 min after SAH resulted in a complete disappearance of the spasm with the reduction of blood pressure. The dilatory response was more marked in the smaller arteries (less than 100 microns) than in the larger ones (greater than or equal to 100 microns). Administration of smaller dose of nimodipine (0.01 mg/kg) also produced dilation of the pial vessels, although the effect was less remarkable in the smaller arteries. These data suggest that nimodipine might be useful in the treatment of the cerebral vasospasm after SAH. The mechanism underlying the action of nimodipine was discussed.

Animals↗
PubMed1980

Effects of nimodipine (Bay e 9736) on cerebral circulation in cats.

The response of feline pial arteries to i.v. administration of isopropyl-(2-methoxyethyl)-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate (nimodipine, Bay e 9736) was studied by means of the vidicon camera system developed in our laboratory. Pial arteries showed a dose-dependent dilation with a reduction of systemic arterial blood pressure in the dose range of 0.001 mg/kg to 0.1 mg/kg of nimodipine. The dilatory response was more marked in the smaller arteries (< 100 mu) than in the larger ones (greater than or equal to 100 mu).

Animals↗
PubMed1979

[A case of bilateral spontaneous external carotid-cavernous fistulae with intrahepatic gallbladder (author's transl)].

A 55-year-old female presented bilateral external ophthalmoplegias and a hypesthesia in the left face and then an intracranial bruit, bilateral conjunctival injections and bilateral chemosis. In her past history, there were right retinal hemorrhage, diabetes mellitus and hypertension but no cranial trauma. The arteriographical aspects were almost identical in both sides: selective external carotid arteriography revealed an opacification of the cavernous sinus through the ascending pharyngeal artery, the accessory meningeal artery and the middle meningeal artery, but the internal carotid arteries and the vertebral arteries did not participate in these fistulae. The association in our case of spontaneous external carotid-cavernous fistulae with intrahepatic gallbladder derived from a developmental arrest in the early stage of embryonic life suggests that spontaneous external carotid-cavernous fistula is derived from communications between extra-cranial vessels and the sinuses in the early stage of embryonic life.

Arteriovenous Fistula↗
PubMed1978

Tolosa-Hunt syndrome. Arteriographic evidence of improvement in carotid narrowing.

Diagnosis of Tolosa-Hunt syndrome was made in a 25-year-old woman on the basis of unilateral third and sixth nerve paresis and possible involvement of the first branch of the ipsilateral trigeminal nerve, accompanied by headaches and ocular pain, which responded promptly to corticosteroid administration. Irregular narrowing of the right carotid siphon and occlusion of the homolateral superior ophthalmic vein were observed. During steroid therapy this stenosis improved in association with almost complete clinical recovery, although the vein was not recanalized. Of ten reported cases with contrast radiographic abnormalities, including our own, only two showed pupillary involvement. We hypothesize that the third nerve paresis with pupillary sparing in this syndrome may be attributable to the same underlying mechanism as that of diabetic ophthalmoplegia.

Adult↗