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Biomedical subjects

K Katsumata

Publications and source records attributed to K Katsumata.

At least 73 records · Page 4Linked to original sources
PubMed1994

Acute and chronic effect of ethanol on the occurrence of alloxan diabetes in rats.

We investigated the chronic and acute effect of ethanol on alloxan-induced diabetes in rats. When 1 ml/100 g b.w. of 35% ethanol solution was intraperitoneally injected into rats 10 min before intramuscular injection of alloxan, the alloxan-induced diabetes was completely prevented at the alloxan dosis (150, 200 mg/kg b.w.) at which the disease is unfailingly induced in control rats. This finding confirmed the results of Heikkila, Barden and Cohen. On the other hand, when rats were given 10% ethanol solution instead of water for 40 straight days, alloxan at a dose of 130 or 140 mg/kg caused diabetes in all cases, whereas no controls developed diabetes. This demonstrable effect of the promotion of alloxan-induced diabetes by chronic alcohol administration was the exact opposite of the acute effect of alcohol. We discussed the contradictory action of ethanol in relation to the occurrence of alloxan diabetes in rats.

Alloxan↗
PubMed1993

Antinociceptive effects in the formalin and capsaicin tests after intrathecal administration of substance P analogues in mice.

The antinociceptive effect of substance P- and substance P-(6-11) analogues containing D-histidine (D-His) in position 9 was examined in mice in the formalin and capsaicin tests. [D-Arg1,D-Trp7,9,Leu11]substance P (spantide) was used as reference drug. Intrathecal injections of the [D-His9]substance P and substance P-(6-11) analogues at 4.0 nmol resulted in no significant antinociception as measured in the 2.0% formalin test, although spantide was antinociceptive in the early and late phases. The early response induced by 0.0625% formalin was reduced significantly by the [D-His9]substance P and substance P-(6-11) analogues at 4.0 nmol, which were less potent than spantide. The antinociception induced by spantide and a few analogues of substance P and substance P-(6-11) containing D-His was reversed significantly by pretreatment with 2 mg/kg naloxone, an opioid antagonist. The nociceptive response to capsaicin was inhibited significantly by lower doses (2.0 nmol) of the analogues. The antinociception evoked by the analogues was not reversed by naloxone in the capsaicin test. Co-injection of the [D-His9]substance P and substance P-(6-11) analogues at 2.0 nmol selectively decreased substance P-induced licking, biting and scratching without affecting the behavioural responses to NK2 and NK3 receptor agonists. Spantide non-selectively inhibited the behavioural responses produced by not only substance P, but also neurokinin A, D-septide, neurokinin B and eledoisin. The data show that the capsaicin test may be a better method for evaluating neurokinin antagonists than the formalin test.

Analgesics↗
PubMed1993

Antinociception induced by CP 96,345, a non-peptide NK-1 receptor antagonist, in the mouse formalin and capsaicin tests.

The non-peptide NK-1 receptor antagonist, CP 96,345, has been evaluated for antinociceptive activity in two chemical pain models in the mouse. CP 96,345, injected intrathecally (i.t.) 5 min prior to 2.0% formalin, produced significant antinociception in both the early and late phases of the formalin-induced paw licking procedure. Antinociception could also be observed during the late phase by treatment with CP 96,345 after formalin. In the capsaicin (CAP) test, i.t. injection of CP 96,345 produced a dose-dependent reduction of the paw-licking response at doses much less than antinociceptive doses in the formalin test. Naloxone did not affect antinociception in either test. CP 96,345 evoked a reversible deficit in motor performance as assayed by the rotarod test. The results indicate that i.t. CP 96,345 is antinociceptive in the capsaicin test at doses showing no overt behavioural effects but there is an overlap in doses producing antinociceptive and motor effects in the formalin test.

Analgesics↗
PubMed1992

Naloxone-reversible effect of spantide on the spinally mediated behavioural response induced by neurokinin-2 and -3 receptor agonists.

[D-Arg1, D-Trp7,9, Leu11]-substance P (spantide) was tested for antagonism against the licking, biting and scratching response induced by various neurokinin (NK) receptor agonists and bombesin (Bom) in mice. When co-administered with substance P (SP) intrathecally, spantide reduced the SP-induced behavioural responses in a dose-dependent manner. The duration of this antagonistic effect was approximately 30 min. Behavioural responses induced by physalaemin (Phy), [pGlu6, L-Pro9]-SP (6-11) (septide), [pGlu6, D-Pro7]-SP (6-11) (D-septide) and eledoisin (Ele) were also dose-dependently decreased by relatively small doses of spantide. Higher doses of spantide were needed to reduce the behavioural responses induced by [Sar9, Met (O2)11]-SP, neurokinin A (NK A) and neurokinin B (NK B). No significant effect of spantide was observed against the behavioural responses elicited by Bom. Pretreatment with naloxone, an opioid antagonist, resulted in a reversible effect on the behavioural reduction of NK-2 and NK-3 receptor agonists produced by spantide. However, the effect of spantide on the NK-1 receptor agonist-induced response was unchanged by naloxone. In homogenates of mouse spinal cord, competition studies confirmed that the binding of the opioid ligand [3H]naloxone was displaced by spantide with a low but measurable affinity. These results suggest that the behavioural response to NK-2 and NK-3 receptor agonists may be partially inhibited by spantide through the activation of opioid system in the mouse spinal cord.

Analgesics↗
PubMed1992

The capsaicin test in mice for evaluating tachykinin antagonists in the spinal cord.

A capsaicin test involving peripheral nociception, which produces behaviour similar to that elicited by formalin, is described in mice. Capsaicin was injected subcutaneously (s.c.) into the dorsal surface of a hindpaw and the time the animals spent licking the paw was recorded. Doses of capsaicin of 6.25-1600 ng induced nociception, during a period of 5 min, starting immediately after injection and disappearing completely at 10 min. Intrathecally (i.t.) administered [D-Arg1,D-Trp7,9,Leu11]substance P (spantide), a tachykinin antagonist and [D-Phe7,D-His9]substance P (6-11), a selective antagonist of substance P (SP), inhibited the capsaicin-induced behaviour, in a dose-dependent manner. This licking behaviour was also inhibited by intrathecal administration of SP antiserum but not by somatostatin (SOM) antiserum. Intrathecal pretreatment with capsaicin resulted in a marked reduction of the licking response, following subcutaneous injection of capsaicin into the paw. Capsaicin-induced licking was not affected by intrathecal administration of cyclo[7-aminoheptanoyl-Phe-D-Trp-Lys-(OBz)-Thr], a SOM antagonist and by intrathecal pretreatment with cysteamine, a SOM depletor. This nociceptive test may allow discrimination between SP- and SOM-mediated responses in the spinal cord of the mouse.

Analgesics↗
PubMed1992

Protective effect of diltiazem hydrochloride on the occurrence of alloxan- or streptozotocin-induced diabetes in rats.

This study demonstrated that 20 mg/kg of the Ca2+ channel blocker, diltiazem hydrochloride, administered by intraperitoneal injection 15 min before 200 mg/kg of alloxan given by the same route to induce diabetes, served to suppress disease onset completely in rats. Even though 48-h fasting promoted the onset of alloxan diabetes, 40 mg/kg of diltiazem hydrochloride completely prevented the occurrence of diabetes induced by intraperitoneal injection of 200 mg/kg of alloxan. Forty mg/kg of the same agent, however, failed to prevent the onset of diabetes induced by the intravenous injection of streptozotocin (50 mg/kg). From the fact that Ca2+ channel blockers such as nicardipine, verapamil and bepridil have a similar suppressive effect on the occurrence of alloxan diabetes, one may readily infer that this action is characteristic of Ca2+ channel blockers. Moreover, the results suggest the close connection of Ca2+ in the occurrence of alloxan diabetes in rats.

Alloxan↗
PubMed1992

Sudden death of a diabetic patient during Holter monitoring.

The sudden death of a diabetic patient (NIDDM) during Holter monitoring is described. The patient was a 64-yr-old male with an 11-yr history of diabetic nephropathy, retinopathy, autonomic nervous dysfunction, and old myocardial infarction. In spite of all these complications, he remained asymptomatic and eventually resumed his normal activities, including a daily 1-h walk, until his sudden death. The cause of death was considered to be cardiac disease, but was not confirmed by autopsy. A detailed analysis of his Holter monitoring is given.

Arrhythmias, Cardiac↗
PubMed1992

[A case of systemic lupus erythematosus complicated with monoclonal CD5 + B cell proliferation suspected as chronic lymphocytic leukemia].

A case of systemic lupus erythematosus (SLE) complicated with monoclonal CD5 + B cell proliferation in peripheral blood and bone marrow is reported. A 59-year-old man suffering from left chest pain was admitted to the hospital because of thrombocytopenia (platelets 1.9 x 10(4)/mm3). The diagnosis of SLE was made from (1) pleuritis (2) autoimmune thrombocytopenia (3) positive anti-DNA antibodies, positive LE cell preparation (4) positive antinuclear antibodies. Prednisolone 60mg per day was started. From that time monoclonal CD5 + B cells began to increase in peripheral blood (maximum lymphocyte counts 11000/mm3, CD5 + B cells 77.6%) and bone marrow, and the complication of chronic lymphocytic leukemia (CLL) was suspected. It is said that patients of CLL often have various autoantibodies, and in about 15% of CLL patients complicate autoimmune hemolytic anemia, but those who develop collagen diseases are rare. And while lymphoid malignancies occur more often in the patients of SLE in comparison with normal subjects, the reports of the patients who complicate the proliferation of monoclonal CD5 + B cells like CLL are very few. But from many facts that indicate the relation between CD5 + B cell or its proliferation and the production of autoantibodies or autoimmune diseases, we consider this case worth to be reported.

Antigens, CD↗
PubMed1991

High incidence of sleep apnea syndrome in a male diabetic population.

In order to study the possible relationship between sleep apnea syndrome (SAS) and diabetes mellitus, we first examined the prevalence of SAS among 12,787 general patients (6554 males and 6233 females) who visited Katsumata Hospital at Nagoya, Japan. Among them, thirty-five males and five females were diagnosed as having SAS. The male patients were statistically analysed by the corrected Mantel-Haenszel chi-square test taking the body type into account, and it was found that the prevalence of SAS was significantly high both in a diabetic population and in a hypertensive one. Among 40 SAS patients of both sexes, 34 were given a glucose tolerance test (GTT) with oral administration of 75 g glucose. Thirteen showed a diabetic pattern, 12 a borderline pattern and only 9 had a normal pattern. All 13 diabetic patients had non-insulin-dependent type diabetes (NIDDM). The present results showed that SAS has a close relationship not only to hypertension but also to NIDDM.

Adolescent↗
PubMed1991

[Pneumoperitoneum without perforation of the gastrointestinal tract in a patient with systemic lupus erythematosus].

Pneumoperitoneum often occurs after the perforation of the gastrointestinal tract. However, pneumoperitoneum without the perforation has been reported as one of the complications of collagen diseases, the cause of which is usually the rupture of pneumatosis cystoides intestinalis (PCI). PCI is sometimes observed in the patients with scleroderma and mixed connective tissue disease but rarely in the patients with systemic lupus erythematosus. We reported here a case of systemic lupus erythematosus developed the pneumoperitoneum without the perforation of gastrointestinal tract. A 51-year-old female who had been diagnosed as systemic lupus erythematosus and taken steroid for 12 years, visited our hospital because of general malaise. She had no abdominal symptoms but the roentgenographic examinations revealed the pneumoperitoneum. The laparotomy was performed and there were no findings of the perforation of the gastrointestinal tract. Because PCI is hardly recognized macroscopically after the rupture and the pneumoperitoneum due to PCI is often asymptomatic, we considered the cause of the pneumoperitoneum in this case was the rupture of PCI. The mechanisms of the formation of PCI in patients with collagen diseases were also discussed in this paper.

Female↗