UMLS:C0011849 - FACTA Search

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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a prospective and experimental trial with the objective of treating pregnancies complicated with symptomatic polyhydramnios. Patients with pregnancies between 24 and 25 weeks, index of amniotic fluid greater than 24 and with symptoms associated to polyhydramnios such as abdominal discomfort, respiratory distress and premature uterine contractions, were entered into the trial. The medication utilized was Indomethacin 25 mg p.o. every six hours until symptoms disappear and the index of amniotic fluid was less than 24. Eight patients were treated during an eight months period. The average age was 30 years, with a rank between 25 and 37 years. There were only two nulliparous and the average gestational age was 30 weeks. The patients were classified in this way: three with idiopathic polyhydramnios, two with twin pregnancies, one with diabetes mellitus and two pregnancies, one with diabetes mellitus and two pregnancies with fetal malformations. 18 trisomy was diagnosed in the newborn from one of the patients with idiopathic polyhydramnios. The average index of amniotic fluid upon initiating the treatment was of 33.6 and 18 upon finishing. The maximum treatment time was six days with average four. Ultrasonographic control was obtained every 24 hours and fetal echocardiogram at 24 and 96 hours of treatment. There were no maternal nor fetal side effects. Success rate correcting symptomatic polyhydramnios with Indomethacin was 100%.
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PMID:[Pregnancy complicated with symptomatic polyhydramnios: treatment with indomethacin]. 907 5

We hypothesized that in diabetes arterial reactivity to constrictors is attenuated by certain endothelium-derived substances. We examined the vasoconstriction induced by methoxamine (alpha1-agonist) in isolated mesenteric arterial beds from streptozotocin (STZ)-induced diabetic rats and age-matched control rats. The dose-response curve for methoxamine was shifted to the right and the maximum contractile response was impaired in mesenteric arterial beds from diabetic rats. The methoxamine vasoconstriction was reduced in endothelium-denuded preparations from controls rats, but increased in those from diabetic rats. Treatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine enhanced the vasoconstrictions induced by methoxamine in both control and diabetic rats. Indomethacin had no effect on the methoxamine vasoconstriction in control rats, but it shifted the dose-response curve to the left in diabetic rats. Whether given with or without indomethacin, BQ-123, (an ET(A)-receptor antagonist) plus BQ-788 (an ET(B)-receptor antagonist) shifted the dose-response curve for methoxamine to the right in control rats (while reducing the maximum response) but to the left in diabetic rats. The methoxamine-stimulated release of 6-keto-prostaglandin F1alpha from the mesenteric arterial bed in diabetic rats was approximately four times that seen in the control rats, while the methoxamine-induced release of thromboxane B2 (TXB2), a metabolite of thromboxane A2 (TXA2), was less in diabetic rats than in the control animals. These results suggest that an increased production of prostaglandin I2 (PGI2) and decreased formation of TXA2 could be responsible for the attenuation of the methoxamine-induced mesenteric vasoconstriction seen in diabetic rats, and these changes in the diabetic state could be partly responsible for the lower blood pressure seen in our diabetic rats.
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PMID:Possible modulation by endothelin-1, nitric oxide, prostaglandin I2 and thromboxane A2 of vasoconstriction induced by an alpha-agonist in mesenteric arterial bed from diabetic rats. 986 7

The purpose of this study was to analyse the influence of experimental diabetes on vascular response of rabbit carotid artery to acetylcholine (Ach). We compared the Ach-induced relaxant response of isolated arterial segments obtained from both control and diabetic animals. To assess the influence of the endothelium, this cell layer was mechanically removed in some of the arterial segments ("rubbed arteries") from each experimental group. Ach induced a concentration-related endothelium-mediated relaxation of carotid artery from control rabbits that was significantly higher with respect to that obtained in diabetic animals. Pre-treatment with N(G)-nitro-L-arginine (L-NA) induced a concentration-dependent inhibition of relaxant response to Ach, which was significantly higher in carotid arteries isolated from diabetic rabbits. Incubation of rubbed arteries with L-NA almost abolished the relaxant response to Ach in arterial segments from both control and diabetic animals. Indomethacin potentiated Ach-induced response of carotid arteries from control rabbits, without modifying that obtained in those from diabetic animals. Aminoguanidine did not significantly inhibit the relaxant action of Ach in arterial segments from either control or diabetic rabbits. These results suggest that diabetes impairs endothelial modulatory mechanisms of vascular response of rabbit carotid artery to Ach. This endothelial dysfunction is neither related with a lower release of nitric oxide (NO) or prostacyclin. Diabetes impairs the production of some arachidonic acid vasoconstrictor derivative. There has been observed an increased modulatory activity of NO, but this is not related with the expression of an inducible isoform of NO synthase.
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PMID:Influence of experimental diabetes on regulatory mechanisms of vascular response of rabbit carotid artery to acetylcholine. 1082 46

The influence of diabetes on endothelial mechanisms implicated in the response of isolated rabbit carotid arteries to 5-hydroxytryptamine (5-HT) was studied. 5-HT induced a concentration-dependent contraction that was potentiated in arteries from diabetic rabbits with respect to that in arteries from control rabbits. Endothelium removal potentiated 5-HT contractions in arteries from both control and diabetic rabbits but increased the maximum effect only in arteries from diabetic rabbits. Incubation of arterial segments with N(G)-nitro-L-arginine (L-NA) enhanced the contractile response to 5-HT. This L-NA enhancement was greater in arteries from diabetic rabbits than in arteries from control rabbits. Aminoguanidine did not modify the 5-HT contraction in arteries from control and diabetic rabbits. Indomethacin inhibited the 5-HT-induced response, and this inhibition was higher in arteries from control rabbits than in arteries from diabetic rabbits. In summary, diabetes enhances the sensitivity of the rabbit carotid artery to 5-HT. In control animals, the endothelium modulated the arterial response to 5-HT by the release of both nitric oxide (NO) and a vasoconstrictor prostanoid. Diabetes enhances endothelial constitutive NO activity and impairs the production of the endothelial vasoconstrictor.
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PMID:Diabetes-induced changes in endothelial mechanisms implicated in rabbit carotid arterial response to 5-hydroxytryptamine. 1093 99

An arteriograph was used to assess myogenic tone, smooth muscle contractility and the influence of endothelial function on mesenteric resistance artery reactivity in insulin-resistant mice (C57BL/KsJ-db/db) and age- and gender-matched wild-type mice. Increases in transmural pressure induced myogenic tone in arteries from both control and db/db mice. At 12 and 16 weeks of age, greater tone developed in diabetic than in control mice. In control, but not in db/db mice, pretreatment of arteries with L-NAME potentiated myogenic tone. Indomethacin and SQ29548 (PGH2/TXA2 receptor antagonist) had no efffect in control, but inhibited myogenic tone in db/db mice. Endothelium-dependent vasodilation induced by acetylcholine and bradykinin, was depressed in db/db mice and potentiated by SQ29548 and LY333531 (protein kinase C(beta) inhibitor). Messenger RNA expression levels for PKC(beta) were over-expressed 2.5-fold in db/db relative to those in control mice. However, expression levels of mRNA for eNOS, PKC(alpha), and PKC(xi) were similar in the db/db and control mice. Collectively, these results suggest that the greater myogenic tone in resistance arteries from diabetic mice may be attributable, to greater amounts of one or more vasoconstricting prostanoids. Our data indicate that in diabetic mice, basal and agonist-stimulated NO releases are depressed and NO-mediated vasorelaxation in these mice may be countered by an endogenous vasoconstrictive prostanoid. This prostanoid-induced vasoconstriction is mediated by a PKC(beta)-dependent mechanism. Therefore, heightened activation of PKC(beta) and release of a vasoconstrictor prostanoid could play a role in endothelial dysfunction associated with type II diabetes.
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PMID:Influence of type II diabetes on arterial tone and endothelial function in murine mesenteric resistance arteries. 1174 Jan 57

The influence of diabetes on the response of isolated rabbit renal arteries to 5-hydroxytryptamine (5-HT) was examined. 5-HT induced a concentration-related contraction that was higher in arteries from diabetic rabbits than in arteries from control rabbits. Endothelium removal did not significantly modify 5-HT contractions in arteries from control rabbits but enhanced the response to 5-HT in arteries from diabetic rabbits. Incubation with N(G)-nitro-L-arginine (L-NA) enhanced contractions to 5-HT in arteries from control and diabetic rabbits. In arteries with endothelium, this L-NA enhancement was lower in diabetic rabbits than in control rabbits. In arteries without endothelium, incubation with L-NA enhanced the maximal contractions to 5-HT in control rabbits but did not in diabetic rabbits. Indomethacin inhibited 5-HT-induced contraction of arteries from control rabbits and enhanced the maximal contraction to 5-HT of arteries from diabetic rabbits. In summary, diabetes enhances contractile response of rabbit renal artery to 5-HT. In control animals, this response is regulated by both endothelial and non-endothelial (neuronal) nitric oxide (NO) and by a vasoconstrictor prostanoid. Diabetes impairs the release of non-endothelial NO and the vasoconstrictor prostanoid.
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PMID:Experimental diabetes induces hyperreactivity of rabbit renal artery to 5-hydroxytryptamine. 1193 1

Thirty-five plant species were selected from the published literature as traditionally used by the Indigenous Peoples of the boreal forest in Canada for three or more symptoms of diabetes or its complications. Antioxidant activities in methanolic extracts support the contribution of these traditional medicines in a lifestyle historically low in the incidence of diabetes. In a DPPH assay of free radical scavenging activity 89% of the methanol extracts had activity significantly greater than common modern dietary components, 14% were statistically equal to ascorbic acid and 23% had activities similar to green tea and a Trolox positive control. Superoxides produced with an NBT/xanthine oxidase assay found scavenging was significantly higher in 29% of the species as compared with the modern dietary components and Trolox. The methanol extracts of Rhus hirta, Quercus alba and Cornus stolonifera performed similarly to green tea's in this assay. Assessment of peroxyl radical scavenging using a DCF/AAPH assay showed 60% of the plant extracts statistically similar to Trolox while R. hirta and Solidago canadensis extracts were greater than green tea, ascorbic acid and Trolox. The majority of the species (63 and 97%, respectively) had scavenging activities similar to ascorbic acid in the superoxide and peroxyl radical scavenging assays.
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PMID:Antioxidant activity in medicinal plants associated with the symptoms of diabetes mellitus used by the indigenous peoples of the North American boreal forest. 1224 96

Numerous reports have demonstrated that oxidative stress induced by diabetes plays an important role in the development and progression of diabetic vascular complications including nephropathy. Indeed, there is emerging evidence that the formation of reactive oxygen species (ROS) is a direct consequence of hyperglycemia. Biomarkers for oxidative damage to DNA, lipids, and proteins are also supporting the concept of increased oxidative stress in diabetes and diabetic nephropathy. However, there is an unanswered question: When does oxidative stress as a pathogenetic event occur in the process of diabetic nephropathy? To answer this question, glomerular ROS was imaged with the use of 2', 7'-dichlorofluorescein diacetate (DCFH-DA). The image of DCF fluorescence was strong in glomeruli from diabetic rats as compared with that of glomeruli from nondiabetic control rats. mRNA expression of antioxidant enzymes such as catalase, glutathione peroxidase, Cu/Zn superoxide dismutase, and heme oxygenase-1 (HO-1) was also determined because oxidative stress definitely refers to the situation of an imbalance between the production of ROS and antioxidant defense. The mRNA expression of catalase, glutathione peroxidase, and Cu/Zn superoxide dismutase 2 wk after the induction of diabetes was not significantly different from that in control rats. Alternatively, mRNA and protein expression of HO-1 was strongly induced by 16-fold in diabetic glomeruli after the induction of diabetes. Antioxidant treatment with either vitamin E or probucol almost completely normalized HO-1 overexpression in diabetic glomeruli, supporting the existence of oxidative stress in the glomeruli of early diabetes. Furthermore, It has reported that antioxidant treatment with vitamin E, probucol, alpha-lipoic acid, or taurine normalized diabetes-induced not only renal dysfunction such as albuminuria and glomerular hypertension but also glomerular pathologies. In summary, oxidative stress by diabetes could play a crucial role in the development and progression of diabetic nephropathy, and antioxidant treatment could be a potential therapeutic procedure for diabetic nephropathy.
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PMID:Effects of antioxidants in diabetes-induced oxidative stress in the glomeruli of diabetic rats. 1287 41

The influence of diabetes on regulatory mechanisms and specific receptors implicated in the contractile response of isolated rabbit carotid arteries to endothelin-1 was examined. Endothelin-1 induced a concentration-dependent contraction that was greater in arteries from diabetic rabbits than in arteries from control rabbits. Endothelium removal or N(G)-nitro-L-arginine enhanced contractions in response to endothelin-1 only in control arteries, without modifying the endothelin-1 response in diabetic arteries. Indomethacin, furegrelate (thromboxane A(2) inhibitor), or cyclo-(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123; endothelin ET(A) receptor antagonist) inhibited the contractions in response to endothelin-1, the inhibition being greater in diabetic arteries than in control arteries. 2,6-Dimethylpiperidinecarbonyl-gamma-methyl-Leu-N(in)-(methoxycarbonyl)-D-Trp-D-Nle (BQ-788; endothelin ET(B) receptor antagonist) enhanced the contraction elicited by endothelin-1 in control arteries and displaced to the right the contractile curve for endothelin-1 in diabetic arteries. In summary, diabetes induces hyperreactivity of the rabbit carotid artery to endothelin-1 by a mechanism that at least includes: (1) enhanced activity of muscular endothelin ET(A) receptors; (2) impairment of endothelin ET(B) receptor-mediated nitric oxide (NO) release; and (3) enhancement of the production of thromboxane A(2).
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PMID:Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1. 1475 7

Streptozotocin (STZ) is widely used for the induction of diabetes in animals by causing destruction of pancreatic beta cells. This experiment was designed to elucidate the sequential process of beta-cell destruction in rats with a single high-dose injection of STZ. At 0, 2, 5, 8 and 24 h after injection, rats were perfused with Krebs-Ringer buffer with dichlorofluorescein diacetate (DCF-DA), a marker for free radicals, and the pancreata were pathologically analyzed. Injection of STZ rapidly elicited an increase in fluorescence of DCF-DA in beta cells at 2 h after the injection. The fluorescence was diminished by carboxy-PTIO, a specific scavenger of nitric oxide (NO), but not by L-NAME, an inhibitor of NO synthase. During this process, an inducible form of NO synthase was not detected. Thereafter, upregulated expression of poly(ADP ribose) polymerase (PARP) and massive beta-cell death were detected at 5-8 h after injection. Migration of macrophages into the islet was conspicuous at 24 h, clearing up the debris of destroyed beta cells. Nicotinamide, a PARP inhibitor, significantly inhibited beta-cell death without apparent suppression of NO generation at 2 h. The current study documented serial processes of STZ-induced beta-cell death, starting with NO generation and PARP activation followed by a clearance with macrophages, where the activation of PARP plays a central role in beta-cell death.
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PMID:Nitric oxide generation and poly(ADP ribose) polymerase activation precede beta-cell death in rats with a single high-dose injection of streptozotocin. 1476 14

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