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Biomedical subjects

M Shishido

Publications and source records attributed to M Shishido.

33 records · Page 2Linked to original sources
PubMed1983

[Chronic subdural hematoma associated with arachnoid cyst--study of the mechanism of its development].

A significant number of cases of chronic subdural hematoma associated with middle fossa arachnoid cyst has been reported in literature, but sufficiently tenable explanation for co-occurrence of both lesions has not yet proposed. In this study, authors try to elucidate mechanisms involved in development of chronic subdural hematoma and arachnoid cyst in the same patient. Eighteen cases with arachnoid cyst in the middle fossa were diagnosed by CT scan during last 5 years in our institute. Among these, five patients had chronic subdural hematoma additionally to their middle fossa arachnoid cyst. Analysis of clinical, roentgenological data and operative findings in our five cases and reviewing of cases reported so far in the literature makes clear the following characteristics in this pathological condition. 1) Patients of chronic subdural hematoma associated with arachnoid cyst were obviously younger than patients with usual chronic subdural hematoma. 2) Chronic subdural hematoma developed in the same side to the associated arachnoid cyst. 3) Characteristic changes in the skull on x-ray films indicated the long lasting existence of middle fossa arachnoid cyst. On the other hand, history of cases suggested that chronic subdural hematomas had developed within recent 1-3 months. 4) Intracranial pressure tended to remain normal or slightly elevate. 5) Abnormal, small veins which run on the surface of the membranous capsule of arachnoid cyst and bridge the Sylvian fissure were not infrequently found at operation. These veins were not able to visualized on routine angiography. On the basis of these clinical and pathological characteristics, authors infer a mechanism for development of subdural hematoma associated with arachnoid cyst. The presence of middle fossa arachnoid cyst must increase a compressibility of the intracranial content, especially of the ipsilateral cerebral hemisphere and it predisposes for development of chronic subdural hematoma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1982

Manipulation of thrombus formation in the hamster cheek pouch with drugs that interact with PGI2 in vitro.

A single platelet thrombus was formed in an arteriole of the hamster cheek pouch by electrical stimulation followed by topical application of ADP. The sizes of the thrombi were continuously recorded with a photocell placed on a TV monitor screen and quantified by areas on the record. Repeated application of small doses of ADP (5-15 nmole/10 microliters) resulted in very reproducible formation of the thrombi, and the size of the thrombi was reduced dose-dependently by topical application of PGI2. Three drugs were tested in this model. Cyclooxygenase inhibitor (indomethacin 10 mg/kg, i.p.) increased the formation of thrombi, while a smaller dose (3 mg/kg) did not have any significant effect. This could be explained by inhibition of the generation of endogenous PGI2, since aggregation of hamster platelets by ADP was not inhibited by indomethacin in vitro. EG-626 (phthalazinol, a phosphodiesterase inhibitor) (300 mg/kg, i.p.) decreased the size of thrombus. AI-122 (1.0 mg/kg, i.p.), which has been proven to enhance PGI2 biosynthesis from isolated rat aortae, also decreased the formation. Thus, drugs such as EG-626 or AI-122 are quite promising as anti-thrombotic drugs.

Adenosine Diphosphate↗
PubMed1980

Reduced responses of renin release to three different stimuli in essential hypertensive patients of stage II (WHO stage classification).

The responses of renin release to three different stimuli, such as 1) head-up tilt, 2) administration of loop diuretics(bumetanide) and 3) low sodium diet + administration of bumetanide + ambulation were examined in essential hypertensive patients and normotensive subjects. Essential hypertensive patients were classified as stage I and II according to WHO stage classification. Groups studied were age-matched. The responses of renin release to three stimuli did not significantly differ in normotensive subjects (n = 13, 42 +/- 2(SEM) years old) and essential hypertensive patients of stage I (n = 15, 44 +/- 2). However, essential hypertensive patients of stage II (n = 20, 44 +/- 1) showed significantly lower responses of renin release to all three stimuli than essential hypertensive patients of stage I and normotensive subjects. The results suggest that the suppression of renin release is related in part to the development of hypertension.

Adult↗