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Biomedical subjects

F Gotoh

Publications and source records attributed to F Gotoh.

At least 55 records · Page 3Linked to original sources
PubMed1988

Trial of the RBC aggregometer head for estimating blood flow in veins in vivo.

The whole blood RBC aggregometer head reported previously for measuring the degree of RBC aggregation in whole blood was tested for its usefulness as a flowmeter of blood vessels in situ. Modifications to its construction were made so that it became readily attachable and detachable without damage to the vessels. In ex vivo experiments employing a transparent vinyl tube and freshly drawn heparinized human whole blood, the RBC aggregometer head was applicable for evaluating semiquantitative flow changes within a limited flow range based on the degree of RBC aggregation. A linear relationship was observed between the logarithm of blood flow in a low shear range (below approximately 180/s) and changes in the light transmission of the flowing blood. The RBC aggregometer head with or without an electromagnetic flowmeter (EMF) was applied to the jugular vein and femoral vein in cats. A stop-flow change of whole blood in the jugular vein was detected by the RBC aggregometer head as a dramatic change in light transmission (LT). The aggregometer head recorded a similar LT change consistently, whereas the EMF was found to be rather discrepant, indicating the occurrence of anomalous flow. It is concluded that the RBC aggregometer head can be used as an semiquantitative flowmeter for relative changes in blood flow in veins in situ.

Animals↗
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

Evolution of criteria for determination of brain death in Japan.

In 1974, the Japanese EEG Society's Ad Hoc Committee on Brain Death published criteria for determining brain death only in cases of acute gross primary brain lesions. In 1983, a new brain death study group was organized to re-evaluate these criteria. During a 6-month period from March 1, 1984, 217 neurosurgical and neurological clinics and emergency services throughout Japan reported 718 brain deaths caused not only by primary lesions but also by secondary brain lesions and diagnosed as such on the basis of the 1974 criteria excluding the condition of "abrupt fall of blood pressure followed by persistent hypotension". The data derived from the 718 cases in this collaborative study were pooled and analyzed, and it became known that the 1974 criteria still are generally reliable. Some changes have been made, however, and new criteria for determination of brain death adopted.

Advisory Committees↗
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↗
PubMed1987

Brainstem auditory evoked responses and CT findings in multiple system atrophy.

Brainstem auditory evoked responses (BAERs) and CT findings were comparatively studied in 11 patients with Shy-Drager syndrome and 10 patients with olivopontocerebellar atrophy. The I-III interpeak latencies (IPLs) were prolonged in 6 patients with Shy-Drager syndrome and in 6 patients with olivopontocerebellar atrophy. Mean values of the I-III IPLs were 2.54 +/- 0.28 ms (Shy-Drager syndrome) and 2.62 +/- 0.15 ms (olivopontocerebellar atrophy). In each disease, the I-III IPLs correlated well with the degree of the pontine atrophy estimated from the CT scan. The patients with Shy-Drager syndrome could be clinically divided into two varieties. In addition to autonomic dysfunction, one variety (4 patients) was linked with parkinsonism, and the other (7 patients) with signs of multiple nervous systems involvement. Prolongation of I-III IPLs and pontine atrophy were noted in 6 out of the latters patients, whereas the former patients did not show such abnormalities. The combination of BAERs and CT scan provides useful clinical information on multiple system atrophy.

Adult↗
PubMed1986

Dual effect of naloxone on blood platelet aggregation and cerebral blood flow in gerbils.

The effect of naloxone on blood platelet aggregation and cerebral blood flow in gerbils was studied. Administration of naloxone in dose 1 mg/kg to intact gerbils resulted in a marked increase in platelet aggregability accompanied by 27% reduction in cerebral blood flow. Focal cerebral ischemic injury significantly enhanced platelet aggregatory response and treatment with naloxone was without any additional effect on platelet aggregation. Cerebral blood flow in ischemic hemisphere, however, increased following naloxone injection by 46%. In vitro naloxone in millimolar concentrations inhibited platelet aggregation in a dose-dependent way. Apparent decrease in fluorescence of platelet membranes tagged with fluorescence probe due to naloxone suggests conformational changes in platelet membrane as a primary mechanism for the antiaggregatory effect of naloxone in vitro.

Animals↗
PubMed1986

Effects of a stable enkephalin analogue, (D-Met2,Pro5)-enkephalinamide, and naloxone on cortical blood flow and cerebral blood volume in experimental brain ischemia in anesthetized cats.

The effects of intracarotid injection of the stable enkephalin analogue (D-Met2,Pro5)-enkephalinamide (ENK) and intravenous administration of naloxone on the cerebrocortical blood flow (dye dilution method) and cerebral blood volume (CBV) (photoelectric method) were investigated during unilateral brain ischemia in anesthetized cats. Both parameters were measured simultaneously in the intact and ischemic (middle cerebral artery occluded) hemispheres. An intracarotid injection of ENK 0.5 mg/kg induced a significant increase in cortical vascular resistance and a -87% decrease in cerebrocortical blood flow from 25 +/- 3 to 4 +/- 3 ml/100 g/min, without CBV alteration in the ischemic hemisphere. Naloxone (1 mg/kg i.v.), on the other hand, induced a marked two-fold increase in cerebrocortical blood flow and a significant elevation of CBV from 5.9 +/- 0.5 to 7.4 +/- 0.7 vol% in the ischemic hemisphere. No change in cerebrocortical blood flow or CBV was observed in the intact hemisphere either after ENK or after naloxone administration. Arterial blood gases and hematocrit remained unchanged. On the basis of the present findings, we conclude that besides other factors, endogenous opioid mechanisms may also participate in ischemic cerebrovascular reactions and the cerebral circulatory effects of naloxone probably reflect its opiate receptor blocking property and not simply its other non-opiate-related actions.

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↗
PubMed1986

Whole-blood red blood cell aggregometer for human and feline blood.

A whole-blood aggregometer of red blood cells (RBC) is described. It consists of a transparent 0.26-cm ID vinyl tube of approximately 30 cm in length containing freshly drawn heparinized blood and a densitometer head that is attached to the tube. The densitometer head consists of an infrared light source of gallium arsenide and a light detector (silicon photodiode) to monitor changes in optical density of the blood in the tube. The tube and densitometer head were installed in a temperature-controlled box at 37 degrees C. The blood in the tube was first subjected to rapid flow with a solenoid so that the wall shear rate of the blood was approximately 500 s-1. The shear gave rise to a rapid increase in optical density of the blood due to dispersion of the blood corpuscles. The blood was then brought abruptly to a full stop. After the flow had stopped the densitometer head revealed a gradual decrease in optical density in association with RBC aggregate formation. The resultant pattern was termed by us an "RBC aggregogram." The RBC aggregogram exhibited an exponential decay in its initial part, which was followed by an asymptotic decrease. A simple mathematical procedure was employed to calculate the rate constant of the initial decrease from the two values on the RBC aggregogram at 10 and 20 s. The rate constant k10 was 0.192 +/- 0.028 (5.2 s as time constant; 3.6 s as half time) for feline blood and 0.129 +/- 0.012 (7.7 s as time constant; 5.3 s as half time) for human blood. The RBC aggregation rate varied linearly with the hematocrit below 40%.

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↗
PubMed1985

Fisher's syndrome following trigeminal herpes zoster.

A case of Fisher's syndrome associated with trigeminal herpes zoster is reported for the first time. Retrograde propagation of the virus to the brainstem through the trigeminal root was thought to be the most probable pathogenic mechanism. We provide additional evidence suggesting that the focus of Fisher's syndrome is in the brainstem.

Adult↗