Changes in Arachidonic Acid Metabolite Patterns in Alloxan-Induced Diabetic Rats

Hui, S.‐C. G.; Ogle, C. W.; Wang, Z.; An, Yingli; Hu, Yonghe

doi:10.1159/000138612

Cited by 10 publications

(4 citation statements)

References 15 publications

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“…In pentobarbitone anaesthetized rats with alloxan-induced diabetes of 14 days duration, reduced sensitivity occurred to the depressor effects of AA (1 -2 mg/kg), and AH23848 (5 mg/ kg) significantly potentiated depressor responses to low doses of AA (0.125-0.25 mg/kg) (Boura et al 1986). Reduced depressor responses to AA in anaesthetized STZ-induced diabetic rats have also been reported by workers in our laboratory (Law & King 1990), and similar changes in alloxan-treated rats have since been found by Hui et al (1989). Both studies used diabetic rats of 14 days duration.…”

Section: Anaesthetized Ratssupporting

confidence: 78%

“…Hui et al found that this change in responsiveness to AA was not due to a non-specific decrease in diabetic vasculature sensitivity, as there was no change in responsiveness to the vasodilator sodium nitroprusside, which acts directly on smooth muscle. There also appeared to be a temporal factor in these changes as there was no alteration in AA responses in diabetic rats of 1 week duration (Hui et al 1989). Quilley and McGiff (1985) have already drawn attention to the fact that the proportion of urinary AA metabolites in rats with experimental diabetes varies depending on the time after induction of diabetes.…”

Section: Anaesthetized Ratsmentioning

confidence: 99%

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Cardiovascular Sensitivity Changes to Eicosanoids in Rats With Experimentally Induced Diabetes Mellitus

Hodgson

Sikorski

King

1992

Clin Exp Pharma Physio

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This paper attempts to provide a short review of the evidence for: 1. Increased platelet production of thromboxane A2 and reduced vascular production of prostacyclin in the human and also animal models of diabetes. 2. Reduced depressor responsiveness to arachidonic acid of anaesthetized alloxan- and streptozotocin-induced diabetic rats. 3. Enhanced constrictor responsiveness to arachidonic acid in blood-perfused hindquarters of alloxan-induced diabetic rats. 4. Potentiation by the thromboxane A2-mimetic, U46619, of constrictor responses to 5-hydroxytryptamine in Krebs'-perfused hindquarters and kidneys of both control and alloxan-induced diabetic rats. 5. Alterations during diabetes in production of, and responsiveness to, eicosanoids may contribute to the cardiovascular changes which occur in this disease.

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Section: Anaesthetized Ratssupporting

confidence: 78%

Section: Anaesthetized Ratsmentioning

confidence: 99%

Cardiovascular Sensitivity Changes to Eicosanoids in Rats With Experimentally Induced Diabetes Mellitus

Hodgson

Sikorski

King

1992

Clin Exp Pharma Physio

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“…The EDSS [8, 9] is the most used clinical tool for longitudinal observation of stability, improvement or worsening of the disability [4]. …”

Section: Introductionmentioning

confidence: 99%

Multiple Sclerosis: Relapses and Timing of Remissions

Iuliano¹,

Napoletano²,

Esposito³

2007

Eur Neurol

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Background: Relapse is a relatively sudden worsening of neurological status in multiple sclerosis patients. The aim of this paper is to describe the frequency and timing of the subsequent clinical remission, and factors linked to a possible lack of recovery. Methods: Two hundred and twenty-three relapses in 62 multiple sclerosis patients were examined retrospectively. Kurtzke’s Expanded Disability Status Scale (EDSS) scores were calculated every 3 months from 1 year before to 1 year after. Remission was defined as improvement vs. the EDSS as scored during the relapse. Recovery was defined as return to the EDSS as scored before the relapse. Results: The frequency of improvement was 78% at 3 months, 86% at 6, and lower in males (65 vs. 81%). The frequency of recovery was 55% at 3 months, 71% at 6. Kaplan-Meier curves showed stabilization after 6 months, with improvement in 90% of patients, 100% without further relapses. Relapses without recovery were only 30%; 15% excluding short-term relapses. Conclusions: Incomplete remissions do not appear to be linked to the evolution of the relapse, but to further relapses in the following months; in other words, to the short-term relapse rate.

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“…These include impaired uptake of AA (Watts et al, 1982), reduced levels of cyclooxygenase (COX)-1 (Fang et al, 1997), and diminished eicosanoid production (Watts et al, 1982;Qvist and Larkins, 1983;Hui et al, 1989;Greco et al, 1991;Nakagawa and Ishii, 1996). In addition, Qvist and Larkins (1983) verified that the production of prostaglandin (PG) E 2 and thromboxane (Tx) B 2 is reduced in leukocytes from diabetic patients in response to Staphylococcus aureus or zymosan.…”

Section: Introductionmentioning

confidence: 89%