Biomedical subjects

I L Opentanova

Publications and source records attributed to I L Opentanova.

5 recordsLinked to original sources

PubMed2001

Pentalyte does not decrease heparinoid release but does decrease circulating thrombotic mediator activity associated with aortic occlusion-reperfusion in rabbits.

Hemorrhage and thrombosis are associated with major vascular and trauma surgery. Release of heparinoids and thrombotic mediators may contribute to these complications and have been described in rabbits after aortic occlusion-reperfusion. We hypothesized that the resuscitative fluid used could reduce heparinoid and thrombotic mediator release after aortic occlusion-reperfusion in rabbits as assessed by thromboelastographic variables (R, reaction time; alpha, angle; and G, a measure of clot strength). Anesthetized rabbits were administered lactated Ringer's solution (n = 8) or PentaLyte (n = 8) at reperfusion after 30 min of ischemia. Blood was obtained before ischemia and after 30 min of reperfusion for thromboelastography under four conditions: 1) unmodified sample, 2) platelet inhibition, 3) heparinase, and 4) platelet inhibition and heparinase. During reperfusion, unmodified samples demonstrated a significant increase in R and decrease in alpha and G that was not affected by PentaLyte. In the presence of heparinase, no significant fluid-specific thromboelastographic differences were noted. However, thrombotic mediator release (discerned by a decrease in R and an increase in alpha) during reperfusion in samples with platelet inhibition and heparinase was significantly attenuated by PentaLyte. PentaLyte administration does not decrease heparinoid release but does decrease thrombotic mediator release after aortic occlusion-reperfusion.

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PubMed1999

Tissue factor expression in vital organs during murine traumatic shock: role of transcription factors AP-1 and NF-kappaB.

BACKGROUND: Tissue factor (TF) is a cell-surface glycoprotein responsible for initiating the extrinsic pathway of coagulation that has been shown to have a role in the pathophysiology of sepsis and reperfusion injury. The purpose of this study was to investigate TF expression in vital organs and to determine possible regulatory mechanisms of TF expression in the lung during traumatic shock in rats. METHODS: Noble-Collip drum trauma was induced in anesthetized Sprague-Dawley rats. Anesthetized rats without trauma served as controls. TF activity was measured in plasma and lung tissue. TF messenger RNA (mRNA) was measured in the lung, liver, and small intestine using ribonuclease protection assays. Electromobility shift assays were used to quantify binding of nuclear extracts from lung to TF-specific consensus domains for transcription factors NF-kappaB and AP-1. RESULTS: TF activity in plasma increased up to 14-fold and +232% in the lung (P < 0.001 for plasma and lung) 2 h after trauma. TF mRNA level was significantly increased in the lungs (P < 0.01), small intestine (P < 0.01), and liver (P < 0.05) 1 h after trauma compared to sham-operated control rats. TF mRNA expression continued to increase in the lungs and the liver (both, P < 0.001) 2 h after trauma TF sequence-specific complex binding to AP-1 and NF-kappaB domains was enhanced in the lungs of trauma rats (+395%, P < 0.001 and +168%, P < 0.001, respectively). CONCLUSIONS: These results suggest that TF may play an important role in the pathophysiology of severe trauma and that regulatory elements AP-1 and NF-kappaB may be involved in the regulation of TF mRNA expression in traumatic shock.

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PubMed1999

Endothelin-1, endothelin receptors and ecNOS gene transcription in vital organs during traumatic shock in rats.

Endothelin-1 (ET-1) is a vasoconstrictor peptide that may play an important role in the pathophysiology of severe trauma. We examined ET-1 gene expression in vital organs (i.e., heart, lungs, kidneys, liver and small intestine) during murine traumatic shock using ribonuclease protection assays. Our data show that ET-1 mRNA was significantly increased in the lungs two hours after trauma when compared with control anesthetized rats. There was also a significant increase in ET-1 transcripts occurring in the kidneys, heart and liver. During these experimental conditions, we also observed statistically significant increased endothelin type B (ET(B)) receptor mRNA expression in the lung, heart, liver, kidney and small intestine. Expression of endothelial constitutive nitric oxide synthase (ecNOS) gene, which is functionally coupled to ET(B) receptor, also was increased in vital organs during traumatic shock. Endothelin type A (ET(A)) receptor gene expression was slightly decreased in the lung, liver and small intestine. These results suggest that ET-1 and ET(B) mRNA expression are mainly increased in the lung and other vital organs and may play a functional role in the pathophysiology of murine traumatic shock.

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PubMed1981

[Effect of phospholipase A2 from the venoms of bee and Middle Asian cobra on choline uptake by synaptosomes].

The effect of purified phospholipase A2 from venom of the bee Apis mellifica and from venom of the cobra Naja naja oxiana on the Na+-dependent high affinity choline transport into the synaptosomes of rabbit corpus striatum (active uptake) was studied. Both phospholipases A2 were shown to inhibit the active choline uptake by the synaptosomes. The bee venom phospholipase at a concentration of 10(-8) M and the cobra venom phospholipase at a concentration of 10(-6) M produced a 50% inhibition of choline uptake. A relationship was found between the enzymatic activity of the phospholipases and their ability to block choline uptake by the synaptosomes. A removal of Ca-ions from the medium abolished the effects of both phospholipases. Replacement of Ca2+ by Sr2+ inhibited the effect of the cobra venom phospholipases but did not inhibit that of bee venom enzyme.

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PubMedDate not supplied

[Simultaneous extraction and fluorimetric determination of noradrenaline, dopamine, serotonin and 5-hydroxyindoleacetic acid in separate small brain segments].

Highly-sensitive and reproducible method is developed for simultaneous assay of noradrenaline, dopamine, serotonin and 5-hydroxyindolylacetic acid in small samples of brain tissue. The procedure comprised extraction of the substances with acidified butanol, reextraction of the compounds with phosphate buffer in presence of isooctane, separation of the amines form precursors and metabolites using ion exchange resin Amberlite CG-50 and of 5-hydroxyindolylacetic acid--on Sephadex G-10.

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