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Biomedical subjects

T Kitano

Publications and source records attributed to T Kitano.

At least 109 records · Page 6Linked to original sources
PubMed1978

Intracranial pressure in patients with diffuse cerebral arterial spasm following ruptured intracranial aneurysms.

Intracranial pressure (ICP) was recorded continuously in 12 pre-operative patients with angiographic evidence of diffuse cerebral arterial spasm due to a ruptured intracranial aneurysm. Recordings were made for 1 to 7 days, starting within 13 days after the haemorrhage. 1. An increased ICP was observed in the first week after subarachnoid haemorrhage (SAH) in 4 of the patients without any signs of angiographic arterial spasm. 2. This initial increase was regularly followed by a depression of ICP in between 7--12 days after SAH. In 11 out of 12 patients such a depression was concomitant with the beginning of arterial spasm. During the period of depressed ICP pattern, 6 patients showed little or no neurological deterioration, whereas 5 patients showed impaired consciousness or neurological deficits. 3. A secondary rise of ICP thereafter always followed due to ischaemic brain swelling or infarction, and was usually associated with a serious neurological deterioration. 4. Continuous ventricular drainage was performed to control the secondary increased ICP in 7 patients who survived, 4 of them with good clinical improvement and 3 with severe neurological deficits. 5. In the stage of depressed ICP, the administration of isoproterenol and steroids is recommended in order to try to alleviate the secondary rise of ICP.

Acute Disease↗
PubMed1978

[General pharmacological studies on tramadol, a potent analgetic agent (author's transl)].

The general pharmacological properties of 1-(m-methoxyphenyl)-2-(dimethylaminomethyl)-cyclohexan-1-ol (tramadol; Tramal) are described and compared with those of other strong narcotic analgetics. In behavioral studies tramadol in high doses had a primarily stimulating effect in mice and rats and a sedative effect in rabbits and dogs. The Straub tail phenomenon, a reaction typical for mice administered morphine, was observed only after subtoxic doses of tramadol. In i.v. doses tramadol generally caused a weak central inhibition of non-stimulated and electrically stimulated brain activity in unanesthetized rabbits. Muscle tone and motor coordination in rats and mice were only slightly affected by the drug, in contrast to the effect of morphine. Unlike other strong analgesics tramadol in doses of 5--20 mg/kg i.v. did not cause respiratory depression and even clearly increased respiratory volume and rate in conscious rabbits and anesthetized dogs. In cats and dogs i.v. doses of tramadol up to 10 mg/kg were well tolerated in the cardiovascular system. Tramadol has a slight, papaverine-like spasmolytic effect and no effect on gastrointestinal motility or urinary and electrolyte excretion. The drug showed no antipyretic properties in rabbits. It inhibited edema in rats and guinea pigs but had no antiproliferative effect in the cotton pellet test in rats. Tramadol did not inhibit monoamine oxidase activity or cause enzyme induction in the rat liver.

Analgesics↗
PubMed1978

[Intracranial pressure in patients with diffuse cerebral arterial spasm following ruptured intracranial aneurysms (author's transl)].

Intracranial pressure (ICP) was recorded continuously for 2 to days in 12 pre-operative patients with angiographic evidence of diffuse cerebral arterial spasm due to ruptured intracranial aneurysm. The ICP pattern of the low level (below 15 mmHg) and flat type was registered in the early stage of the arterial spasm in 11 patients in whom the ICP recording was made within 11 days after the hemorrhagic attack. During the period of low and flat ICP pattern, 6 patients showed little or no neurological deterioration whereas 5 patient showed impaired consciousness or neurological deficits. In 9 out 11 patients, the low level of ICP was followed by an abnormal deterioration. Continuous ventricular drainage was performed to control the secondary increased ICP in 7 patients and they survived, 4 of them with good results but remaining 3 with severe neurological deficits.

Adult↗
PubMed1977

Interaction of non-specific inhibitor and rabies virus haemagglutinim.

In order to elucidate the properties of an inhibitor of rabies virus haemagglutinin in normal animal sera, experiments were made with the HEP Flury strain and calf serum which contains the inhibitor. The results of physico-chemical treatment, gel-filtration and density analysis suggested lipoprotein involvement. When inhibitor and haemagglutinin were mixed, the separate activities could be recovered from the mixture by centrifuging on a sucrose density gradient. By contrast, neither haemagglutinin nor inhibitor could be recovered by this treamtnet when the inhibitor was added at the start of virus growth. The binding of inhibitor with rabies virus during virus growth seems irreversible and different from the binding of inhibitor with pre-formed rabies haemagglutinin.

Animals↗
PubMed1977

Intracranial hypertension in patients with ruptured intracranial aneurysm.

Simultaneous continuous recording of intracranial pressure (ICP) and systemic blood pressure was carried out in 26 patients admitted within 1 week after subarachnoid hemorrhage (SAH) due to a ruptured intracranial aneurysm. The patients were graded as described by Hunt and Hess. Recordings were made for 1 to 5 days. The more impaired the consciousness, the higher the rate of ICP. In Grade III, IV, and V patients, the mean ICP level was in the range of 15 to 40 mm Hg, 30 to 75 mm Hg, and exceeded 75 mm Hg, respectively. A definite correlation between vasospasm shown by cerebral arteriogram and the clinical grade was not observed. In our series of ICP recordings, we never observed a typical plateau wave. The variations of ICP seen in Grade III and IV patients were the B- and C-waves (15 to 45 mm Hg in amplitude) described by Lundberg, and those in Grade V patients were the high amplitude monotonous waves synchronous with the arterial pulses (15 to 40 mm Hg in amplitude). These phenomena may indicate that Grade III and IV patients with SAH are in a condition of cerebral vasomotor instability, and Grade V patients have cerebral vasomotor paralysis.

Adult↗
PubMed1977

Enhanced affinity of opiate receptors for naloxone in striatal slices of morphine-dependent mice.

Slices of corpus striatum were allowed to accumulate 3H-morphine and then they were placed in a small chamber and superfused with Krebs-Ringer bicarbonate solution. 100 to 1 pM of naloxone caused an immediate increase in the release of morphine from the slices when it was placed in the superfusion fluid at 0, 5 or 15 min after the the start of the superfusion. Slices from morphine-dependent mice were more sensitive to the naloxone-induced release of morphine than those of control mice. The data suggest that the affinity of the opiate receptors in the corpus straitum for naloxone is increased in morphine-dependent mice.

Animals↗
PubMed1976

[Effects of norepinephrine and phentolamine on acute intracranial hypertension].

It is accepted that cerebrovascular dilatation is a constant response during the advanced stage of intracranial hypertension. Severe intracranial hypertension ultimately associates with profound vasodilatation and reduces cerebral blood flow to zero. This irreversible state is called cerebral vasomotor paralysis by Langfitt et al (1965). The rich adrenergic nerve supply of the cerebral vessels suggests that pressor amines possibly affect the cerebral circulation and the cerebral vascular tone. This study is to investigate the reactivity of norepinephrine and phentolamine on intracranial pressure (ICP) in patients with severe intracranial hypertension. The ICP and systemic blood pressure (SBP) monitorings were carried out continuously after the evacuation of intracerebral hematomas due to ruptured intracranial aneurysms. Severe intracranial hypertension due to brain swelling was observed in these patients. Three stages were defined according to the reactivity to norepinephrine and phentolamine on the ICP. In Stage I, norepinephrine caused a transient decrease in the ICP and phentolamine caused a marked rise in the ICP. Stage II was marked by the absence of the ICP response to norepinephrine and phentolamine. During Stage III, the ICP changes synchronously with a variation of the SBP after the administration of norepinephrine and phentolamine. In Stage I patients, the mean ICP level was between 500-1000 mmH2O. Tracing of the ICP in this group showed transient rises called pressure waves and the waves were recurring increases in the ICP to value of 300-500 mmH2O superimposed on an elevated level of the ICP. On the other hand, in Stage II and III patients, the ICP level exceeded 1000 mmH2O. Tracing of the ICP in these groups showed only variations by the arterial pulses. The patients in Stage I had a well prognosis for life if proper treatments such as continuous ventricular drainage were carried out. The patients in Stage II and III had a poor prognosis for life inspite of continuous ventricular drainage. There are varying stages in cerebrovascular dilatation accompanying intracranial hypertension. We have no information on the mechanism of this cerebrovascular dilatation at present. However, we speculate that the pressor amines such as norepinephrine may partly participate in the mechanism responsible for the vasodilation. So, we attempt to grade the degree of this vasodilatation according to the reactivity of norepinephrine and phentolamine on the ICP. It is presumed that cerebrovascular dilatation is slight and reversible in Stage I patients, whereas cerebrovascular dilatation is profund and irreversible in Stage II and III patients. Continuous ICP recording and examination of the reactivity to norepinephrine and phentolamine on the ICP are valuable when considering the prognosis for life in patients with severe intracranial hypertension.

Adult↗
PubMed1974

Morphological, chemical, and biological characterization of Japanese encephalitis virus virion and its hemagglutinin.

Three morphologically distinct structures, inner core, envelope, and surface projections, were observed in purified Japanese encephalitis virus virions by electron microscopy. The average diameter of each structure was 29.8 +/- 2.5, 44.8 +/- 3.2, and 53.1 +/- 4.5 nm, respectively. Double staining with uranyl acetate and phosphotungstic acid preserved these structures well. Treatment of virions with proteolytic enzymes resulted in the loss of hemagglutinating activity, surface projections, and the major polypeptide band in polyacrylamide gel electrophoresis, which corresponds to glycoprotein, one of the three virion polypeptides. Surface projections were purified by cesium chloride density gradient centrifugation after treatment of virions with Nonidet P-40. The purified materials had a density of 1.256 g/cm(3) and were composed of only glycoprotein, as revealed by polyacrylamide gel electrophoresis. Purified surface projections carried hemagglutinating activity, as well as neutralizing antibody-blocking activity, and induced neutralizing antibody in mice.

Animals↗