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Biomedical subjects

S Sugimoto

Publications and source records attributed to S Sugimoto.

At least 181 records · Page 10Linked to original sources
PubMed1986

Susceptibility to ischemic insult in hypertensive rats: correlation between degree of ischemia and hypertension.

The Wistar rat, with a blood pressure range of 120-160 mmHg, and two strains of spontaneously hypertensive rats (SHR), stroke-prone (SHRSP, range 210-270 mmHg) and stroke-resistant (SHRSR, range 160-240 mmHg), were used to determine the degree of damage after ischemic insult induced by bilateral carotid artery ligation (BLCL). The survival rate and McGraw Stroke Index correlated well with the degree of hypertension. After BLCL, impairment of cerebral blood flow is abrupt and residual flow is near zero in rats with initial blood pressures greater than 200 mmHg. A markedly deteriorated aerobic metabolism, as measured by the concentrations of ATP, c-AMP and lactate, is seen to precipitate in rats with initial blood pressures greater than 180 mmHg and severe edema occurs if the pressure is more than 160 mmHg. The degree of hypertension that produces high vulnerability to stroke and severe damage to the brain after ischemic insult is indicated as beginning at about 180 mmHg.

Adenosine Triphosphate↗
PubMed1986

[Effect of long-term prior antihypertensive treatment on cerebral ischemia induced by bilateral common carotid artery ligation in SHRSR].

The susceptibility to cerebral ischemia was studied in stroke-resistant spontaneously hypertensive rats (SHRSR) treated by a long-term antihypertensive treatment, and compared with untreated SHRSR and Wistar rats (WR). Male SHRSR, aged 8 weeks, were divided into two groups and a long-term antihypertensive treatment for 4-6 weeks was started on one group (treated SHRSR: T-SHR) while the other group was left untreated as control (untreated SHRSR: U-SHR). The changes of blood pressure were checked on these rats. The prior treatment of hypertension was achieved by administration of hydroflumethiazide (120 mg/kg/day) and captopril (15-30 mg/kg/day) orally for 4-6 weeks by mixing in drinking water. All the experiments were performed at the age of 12-16 weeks and WR of similar age served as normotensive untreated control. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and blood pressure was always checked before BLCL. The survival ratio was observed from 1 hour to 24 hours after BLCL. The regional cerebral blood flow (rCBF) were measured before and 4 hours after BLCL periodically. The brain energy metabolites were measured 4 hours after BLCL. rCBF were measured at the thalamus by the hydrogen clearance method. ATP concentrations were determined by luciferine-luciferase method, c-AMP was measured by RIA and lactate by enzymatic method. The brain water content was measured by freeze-dry method.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1986

Arachidonic acid-induced brain ischaemia: different severity between stroke-resistant spontaneously hypertensive rats and Wistar-Kyoto rats.

A thrombo-embolic stroke model was produced by the internal carotid artery (ICA) infusion of arachidonic acid (AA). The differences in responses to AA ICA infusion were investigated in stroke-resistant spontaneously hypertensive rats (SHRSR) and Wistar-Kyoto (WKY) rats. The SHRSR showed a higher mortality, more severe brain oedema and brain metabolic impairment, more prominent elevation of TXB2 and 6-keto-PGF1 alpha. Electron microscopic observation revealed more severe endothelial damage, mitochondrial swelling and perivascular oedema and earlier thrombus formation in SHRSR than in WKY rats.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

[Effect of bilateral common carotid artery ligation on prostaglandin levels (TXA2, PGI2) in spontaneously hypertensive rats (SHRSP, SHRSR) and normotensive rats (WKY)].

Three different levels of global forebrain ischemia were induced in rats and their plasma levels of Thromboxane B2 (TXB2) and 6 Keto PGF1 alpha were determined to investigate the relation between severity of ischemia and eicosanoid production. Ischemia stimulates the activity of cellular lipase whose actions cause deacylation of brain phospholipids and release of free fatty acids. Arachidonic acid (A.A.) is one of the predominant fatty acids which is liberated in brain after ischemia. A.A. is the primary substrate for the synthesis of prostaglandins (PGs), Thromboxane A2 (TXA2) and Prostacyclin (PGI2), which play an important role in regulation of platelet aggregation and vasotonus. Thromboxane is a potent platelet aggregator and vasoconstrictor. On the other hand, PGI2 has the opposite nature. Therefore it can be considered that PGs and moreover, the balance of TXA2 and PGI2 may have an intimate relation to the development of cerebral ischemia. Three different levels of ischemia were produced by bilateral carotid artery ligation (BLCL) using three kinds of rats with different blood pressure ranges, namely, SHRSP (Stroke-prone spontaneously hypertensive rats), SHRSR (Stroke-resistant spontaneously hypertensive rats) and WKY (Wistar kyoto rats). It is known that higher pressure groups suffer severe ischemia by BLCL procedure. Hypertensive rats (SHRSP, SHRSR) were originally produced from WKY. The experimental animals used were about 300 gr and 16 weeks old male rats. The plasma and brain TXB2 and 6 Keto-PGF1 alpha, stable metabolites of TXA2 and PGI2 were measured by radioimmunoassay. The chronological changes of brain and plasma PGs levels after ischemia using SHRSR were also investigated.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1986

[A neurochemical study of rat brain maldevelopment induced by MAM treatment at different stages of gestation].

The regional levels of several cell marker proteins in the brain and the ability of operant discrimination learning on a multiple fixed ratio (FR), fixed interval (FI) schedule were determined in rats with microencephaly induced by prenatal treatment with methylazoxymethanol (MAM), an antimitotic agent, on the 11 th to 13 th days (Group A) or on the 15 th day (Group B) of gestation. The cell marker proteins were determined with a sensitive enzyme immunoassay. Neuron-specific enolase (NSE; gamma gamma-enolase) had a significantly lowered level in the neocortex anterior in Group A. Non-neuronal enolase (NNE; alpha alpha-enolase) was significantly reduced in the superior colliculus, lateral geniculate body and optic nerve, but increased 1.5 fold in the retina in Group A. S-100b protein, a marker of astroglial cells, showed no significant change. As for the learning performance, the Group B animals showed an elevated behavioral activity and made evident discrimination between the FI and FR schedule. But Group A animals had prolonged FR components requiring responses to light on, and their spontaneous activity counts recorded by Automex showed an inhibition of behavior in light environments. These findings suggest a causative role of some developmental abnormality in the central visual system, indicated by the aberrant cell marker levels, in the disturbed learning ability of the Group A animals.

Abnormalities, Drug-Induced↗
PubMed1986

[CT-myelography of cervical cord injury].

UNLABELLED: We reported seven cases of acute cervical cord injuries who were examined by CT-Myelography (CTM) within 7 days after trauma. The presence or absence of spinal cord enlargement, the initial neurological status and the neurological prognosis of these patients were studied. The neurological status of each patient was graded by the method of Frankel who defined five grades from A to E according to the severity of neurological deficits. Seven patients were all males. The youngest was 18 and the oldest was 73 years old, with a mean age of 40.7 years. Follows up periods ranged from 7 to 23 months. RESULT: CTM revealed the enlargement of spinal cord in two cases, who had severe neurological deficits and were graded to A. No neurological improvements were obtained in these cases. Five cases without cord enlargement were graded to A in one patient, B in one patient and C in three patients. Four of these five patients improved neurologically. One grade C patient remained grade C. Complete block of subarachnoid space was observed in two out of seven cases. Cord enlargement was present in one of them. Another case of complete block improved from C to D. CONCLUSION: We consider the presence of cord enlargement which can be demonstrated by CTM well correlates the severity of the cord damage and presume poor neurological prognosis. Internal decompression, such as posterior longitudinal myelotomy may be recommended to the case of cord enlargement. When the cord enlargement is absent, improvement of neurological grade is expected although the initial neurological status shows severe deficits.

Adolescent↗
PubMed1986

[Protective effect of thromboxane A2 synthetase inhibitor (trapidil) on acutely-induced cerebral ischemia].

The experimental study presented was undertaken to evaluate the role of thromboxane A2 contributing to aggravating cerebral ischemia, and to examine the effect of a thromboxane A2 synthetase inhibitor, trapidil on cerebral ischemia. Cerebral ischemia model was induced in 16 week old spontaneously hypertensive rats (SHR) by bilateral common carotid artery ligation (BLCL). Two doses of trapidil 15 mg/kg was intraperitoneally administered one dose 2 hr before and one dose 15 min after BLCL in SHR. While control animals only underwent BLCL. Brain tissue metabolites such as ATP, lactate and pyruvate, brain water content and plasma thromboxane B2 and 6 Keto PGF1 alpha were determined 3 hr after BLCL. Scanning electron microscopic observations were also recorded. ATP concentrations were 1.36 +/- 0.23 n moles/mg wet tissue in the trapidil treated group, 0.61 +/- 0.26 n moles/mg wet tissue in the control group, the difference between the treated and the control being significant (P less than 0.001). Lactate concentrations were 4.70 +/- 1.20 n moles/mg wet tissue in the treated group, 12.17 +/- 8.53 n moles/mg wet tissue in the control group, the difference between the treated and the control being significant (P less than 0.02). Pyruvate concentrations were 0.59 +/- 0.11 n moles/mg wet tissue in the treated group, 0.43 +/- 0.16 n moles/mg wet tissue in the control, the difference was also significant (P less than 0.05). Average water content was 78.87 +/- 0.59% in the treated group, 79.82 +/- 0.33% in the control.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1985

Anomalous atlantoaxial portions of vertebral and posterior inferior cerebellar arteries.

In a review of the vertebral angiograms of 300 patients free from disease at the craniovertebral junction, we found atlantoaxial arterial anomalies in 2,3%. These were: 2 cases in which the vertebral artery ran in the spinal canal below C1, 3 cases of duplication of the vertebral artery above and below C1, and 2 cases of origin of the posterior inferior cerebellar artery at C2. Although these arteries ran in the spinal canal between C1 and C2, they never encroached upon the posterior third of the canal. From the survey of another 21 patients having bony abnormalities at the craniovertebral junction, the first type of arterial anomaly described above was seen in 4 patients and associated with failure of segmentation of the embryonic sclerotome such as occipitalization of the atlas or Klippel-Feil syndrome. It is possible to relate the development of these anomalous vessels to malarrangement of the embryonic segmental arteries. Our results indicate that one must be cautious with lateral C1/2 puncture or surgical exposure of the region.

Adult↗
PubMed1985

Effects of lesions of prefrontal cortex and dorsomedial thalamus on delayed go/no-go alternation in rats.

The effect of prefrontal cortex (PFC) and/or dorsomedial thalamus (DMT) lesions on a delayed go/no-go alternation task was studied in the rat. The lesion gave rise to the impairment of smooth alternation of one response to another, resulting in the generation of some successive repetitions of either response. However, either type of response was generated in virtually equal frequencies during pre- and post-surgery sessions. These results suggest that the DMT and PFC are involved in the memory and response control process for generating the alternation response, and they do not mediate either one type of response. Furthermore, DMT or DMT/PFC lesions induced a larger behavioral impairment than PFC lesions indicating that the DMT plays a major role in generating the alternation behavior based on the memory for the previous response.

Animals↗