Suloctidil Does not Inhibit Vascular Prostacyclin Activity in Rats

1979 ◽  
Author(s):  
S. Villa ◽  
A.E. Cavenaghi ◽  
G. de Gaetano
Keyword(s):  
Platelet Aggregation ◽  
Inferior Vena ◽  
Vena Cava ◽  
Vascular Wall ◽  
Acute Effect ◽  
Human Beings ◽  
Inhibitory Potency ◽  
Antithrombotic Activity ◽  
Antiplatelet Aggregation

Suloctidil [1-(4-isopropyl-thiophenyl)-2-n-octylaminopropanol, Continental Pharma, Belgium] is a drug which inhibits platelet aggregation in human beings and possesses antiplatelet aggregation and antithrombotic properties in several animal models. In the present study, the acute effect of suloctidil on vascular prostacyclin activity was evaluated in rats.. Male CD rats (250-300 g) were given the drug (200-400 mg/kg b.w.) orally 1 h before testing. Prostacyclin activity was measured as the plotelet aggregation inhibitory potency of supernatant buffer following 4 min incubation with rings of either abdominal aorta or inferior vena cava. Treatment with suloctidil did not induce any significant modification of prostacyclin activity. In contrast, in vivo platelet aggregation induced by i.v. infusion of ADP (1 mg/kg) or collagen (2.6 mg/kg) was significantly (p < 0.001) inhibited. It is su.ggested that suloctidil may interfere with platelet function without affecting the potential antithrombotic activity of the vascular wall.

scholarly journals 5-HT causes splanchnic venodilation

2017 ◽  
Vol 313 (3) ◽  
pp. H676-H686 ◽  
Author(s):  
Bridget M. Seitz ◽  
Hakan S. Orer ◽  
Teresa Krieger-Burke ◽  
Emma S. Darios ◽  
Janice M. Thompson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Inferior Vena Cava ◽  
Portal Vein ◽  
Superior Mesenteric Vein ◽  
Inferior Vena ◽  
Vena Cava ◽  
Receptor Protein ◽  
Mesenteric Vein

Serotonin [5-hydroxytryptamine (5-HT)] causes relaxation of the isolated superior mesenteric vein, a splanchnic blood vessel, through activation of the 5-HT7 receptor. As part of studies designed to identify the mechanism(s) through which chronic (≥24 h) infusion of 5-HT lowers blood pressure, we tested the hypothesis that 5-HT causes in vitro and in vivo splanchnic venodilation that is 5-HT7 receptor dependent. In tissue baths for measurement of isometric contraction, the portal vein and abdominal inferior vena cava relaxed to 5-HT and the 5-HT1/7 receptor agonist 5-carboxamidotryptamine; relaxation was abolished by the 5-HT7 receptor antagonist SB-269970. Western blot analyses showed that the abdominal inferior vena cava and portal vein express 5-HT7 receptor protein. In contrast, the thoracic vena cava, outside the splanchnic circulation, did not relax to serotonergic agonists and exhibited minimal expression of the 5-HT7 receptor. Male Sprague-Dawley rats with chronically implanted radiotelemetry transmitters underwent repeated ultrasound imaging of abdominal vessels. After baseline imaging, minipumps containing vehicle (saline) or 5-HT (25 μg·kg−1·min−1) were implanted. Twenty-four hours later, venous diameters were increased in rats with 5-HT-infusion (percent increase from baseline: superior mesenteric vein, 17.5 ± 1.9; portal vein, 17.7 ± 1.8; and abdominal inferior vena cava, 46.9 ± 8.0) while arterial pressure was decreased (~13 mmHg). Measures returned to baseline after infusion termination. In a separate group of animals, treatment with SB-269970 (3 mg/kg iv) prevented the splanchnic venodilation and fall in blood pressure during 24 h of 5-HT infusion. Thus, 5-HT causes 5-HT7 receptor-dependent splanchnic venous dilation associated with a fall in blood pressure. NEW & NOTEWORTHY This research is noteworthy because it combines and links, through the 5-HT7 receptor, an in vitro observation (venorelaxation) with in vivo events (venodilation and fall in blood pressure). This supports the idea that splanchnic venodilation plays a role in blood pressure regulation.

scholarly journals In vivo magnetic particle imaging: angiography of inferior vena cava and aorta in rats using newly developed multicore particles

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Azadeh Mohtashamdolatshahi ◽  
Harald Kratz ◽  
Olaf Kosch ◽  
Ralf Hauptmann ◽  
Nicola Stolzenburg ◽  
...  
Keyword(s):  
Image Quality ◽  
Inferior Vena Cava ◽  
Temporal Resolution ◽  
Magnetic Particle ◽  
Inferior Vena ◽  
Vena Cava ◽  
High Temporal Resolution ◽  
Magnetic Particle Imaging ◽  
Particle Imaging

Abstract Magnetic Particle Imaging (MPI) is a new imaging modality, which maps the distribution of magnetic nanoparticles (MNP) in 3D with high temporal resolution. It thus may be suited for cardiovascular imaging. Its sensitivity and spatial resolution critically depend on the magnetic properties of MNP. Therefore, we used novel multicore nanoparticles (MCP 3) for in-vivo MPI in rats and analyzed dose requirements, sensitivity and detail resolution. 8 rats were examined using a preclinical MPI scanner (Bruker Biospin GmbH, Germany) equipped with a separate receive coil. MCP 3 and Resovist were administered intravenously (i.v.) into the rats’ tail veins at doses of 0.1, 0.05 and 0.025 mmol Fe/kg followed by serial MPI acquisition with a temporal resolution of 46 volumes per second. Based on a qualitative visual scoring system MCP 3–MPI images showed a significantly (P ≤ 0.05) higher image quality than Resovist-MPI images. Morphological features such as vessel lumen diameters (DL) of the inferior vena cava (IVC) and abdominal aorta (AA) could be assessed along a 2-cm segment in mesenteric area only after administration of MCP 3 at dosages of 0.1, 0.05 mmol Fe/kg. The mean DL ± SD estimated was 2.7 ± 0.6 mm for IVC and 2.4 ± 0.7 mm for AA. Evaluation of DL of the IVC and AA was not possible in Resovist-MPI images. Our results show, that MCP 3 provide better image quality at a lower dosage than Resovist. MCP 3-MPI with a clinically acceptable dose of 0.05 mmol Fe/kg increased the visibility of vessel lumens compared to Resovist-based MPI towards possible detection of vascular abnormalities such as stenosis or aneurysms, in vivo.

Abstract 32: Ly6C Lo Monocyte/Macrophages Are Essential for Thrombus Resolution in a Murine Model of Venous Thrombosis

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Andrew S Kimball ◽  
Cathy Luke ◽  
Qing Cai ◽  
Andrea Obi ◽  
Farouc Jaffer ◽  
...  
Keyword(s):  
Venous Thrombosis ◽  
Murine Model ◽  
Inferior Vena ◽  
Tissue Injury ◽  
Vena Cava ◽  
Venous Reflux ◽  
Western Immunoblotting ◽  
Vein Wall ◽  
Wall Injury

Venous thrombosis (VT) results in vein wall injury by promoting inflammation and fibrosis leading to venous reflux, swelling, pain, and potentially, recurrent thrombosis. While prior work has shown that infiltrating leukocytes are important for VT resolution, as of yet, the precise roles of different leukocyte subsets are not well understood. Monocyte/macrophages (Mo/MΦs) are essential for the repair and resolution of tissue injury in other models, and come in inflammatory (Ly6C Hi ) or pro-resolution (Ly6C Lo ) subtypes. We hypothesized that infiltrating Mo/MΦs would be critical to VT resolution. In order to study this in vivo , we utilized a conditional macrophage depletion technique, using CD11b-DTR mice, to examine the effects of Mo/MΦs in a murine model of stasis VT by inferior vena cava ligation. Administration of 10ng/g diphtheria toxoid (DTx) every 48 hours by intra-peritoneal injection in CD11b-DTR mice resulted in an 89% and 55% decrease in circulating monocytes at 24hrs and 48hrs, respectively. When compared to saline controls, DTx injection had no effects on thrombogenic response or IVC thrombus cell populations in C57BL/6 control mice. At 8 days’ post-ligation, DTx treated CD11b-DTR mice had preferentially decreased vein wall-thrombus Ly6C Lo Mo/MΦs as compared with controls. DTx treated mice had significantly larger thrombi (1.7-fold) and less TGF-β, FSP-1, and plasminogen by western immunoblotting (all P-values ≤ 0.01). Consistent with a reduction in Ly6C Lo Mo/MΦs was a significant decrease in cellular TGF-β by intra-cellular flow cytometry. These findings suggest that Ly6C Lo Mo/MΦs are essential for normal VT resolution and may promote thrombus resolution via a plasminogen-mediated mechanism.

EFFECTS OF OESTRADIOL ON WATER UPTAKE AND α-AMINOISOBUTYRIC ACID ACCUMULATION BY UTERI OF HEPATECTOMIZED RATS

1963 ◽  
Vol 28 (1) ◽  
pp. 73-78 ◽  
Author(s):  
J. R. DANIELS ◽  
S. M. KALMAN
Keyword(s):  
Inferior Vena ◽  
Vena Cava ◽  
Early Response ◽  
Isobutyric Acid ◽  
Acid Accumulation ◽  
One Step ◽  
Long Evans ◽  
Amino Isobutyric Acid

SUMMARY Adult Long Evans rats were ovariectomized and, one month later, were subjected to partial hepatectomy. Immature Long Evans rats were either partially hepatectomized in one step, or complete hepatectomy was accomplished by a two-stage operation which included ligation of the inferior vena cava followed by a partial evisceration. The response of these animals to injected oestradiol was compared with that of sham-operated controls by observing uptake of water by the uterus in vivo, and also by estimating the ability of surviving uterine fragments to accumulate radioactive α-amino-isobutyric acid in vitro. It was found that partial or complete hepatectomy did not abolish the response of the uterus to oestradiol. These results seem to exclude an essential role for the liver in the early response of a target organ to an oestrogenic hormone.

Compartment analysis of the radiorenogram and distribution of Hippuran I131 in dogs

1963 ◽  
Vol 204 (6) ◽  
pp. 1059-1064 ◽  
Author(s):  
M. Donald Blaufox ◽  
Alan L. Orvis ◽  
Charles A. Owen
Keyword(s):  
Inferior Vena Cava ◽  
Plasma Volume ◽  
Biliary Excretion ◽  
Inferior Vena ◽  
Vena Cava ◽  
Plasma Samples ◽  
Compartment Analysis ◽  
Arterial Plasma ◽  
Blood Radioactivity

Radioiodinated Hippuran was injected into the inferior vena cava of three unilaterally and three bilaterally nephrectomized dogs. Radioactivity was recorded over the precordium and remaining kidney in the former group and the precordium and renal fossa in the latter. The disappearance of I131 from plasma was analyzed and interpreted by two-compartment and three-compartment systems. Theoretical curves for cardiac and renal areas (constructed from analysis of arterial plasma samples) agreed well with curves from in vivo counting. Analyzed by either model, the first compartment exceeded the plasma volume severalfold, part seeming to be in the kidney. Extravascular compartments, impossible to sample, were not identified. About 15% of whole-blood radioactivity was in erythrocytes. Biliary excretion of Hippuran I131 was insignificant unless nephrectomy was bilateral; then up to 60% was excreted in the bile in 24 hr. Protein binding could not be demonstrated. Radiorenograms converted to fairly accurate rate constants may prove more useful than descriptive methods currently employed. Understanding the distribution and excretion of Hippuran appears helpful to accurate interpretation of the radiorenogram.

The Interaction Of Platelet Active Drugs With Prostacyclin In Vitro And Against Biolaser Induced Intravascular Thrombosis

1981 ◽  
Author(s):  
J S Fleming ◽  
B T Cornish ◽  
J O Buchanan ◽  
J P Buyniski
Keyword(s):  
Platelet Aggregation ◽  
Arachidonic Acid Metabolism ◽  
In Vivo Model ◽  
Additive Interaction ◽  
Antithrombotic Activity ◽  
Intravascular Thrombosis ◽  
Low Levels ◽  
Induced Aggregation

Prostacyclin and thromboxane A2, two of the physiologically most important end products of arachidonic acid metabolism, represent a basic control system which modulates platelet function. Decreased vascular prostacyclin is believed to play a role in the increased thrombotic tendency associated with various clinical diseases including diabetes and atherosclerosis. Compounds which either enhance the formation or release of prostacyclin or potentiate the activity of low levels of prostacyclin may be therapeutically useful in ameliorating this associated pathology. We have studied various inhibitors of platelet aggregation for their ability to potentiate the activity of low levels of prostacyclin both in vitro and in an in vivo model of experimental thrombosis. Anagrelide, aspirin, dipyridamole, sulfinpyrazone and ticlopidine all demonstrated interaction with prostacyclin in vitro against collagen-induced platelet aggregation. More limited interactions were observed against ADP-induced aggregation. Using isobolographic analysis most combinations demonstrated additive interaction. However, pronounced supra-additive interaction was observed vs. both aggregating agents in the case of prostacyclin (0.1-1 ng/ml) - anagrelide (8-90 ng/ml) combinations. Dramatic enhancement of the effects of prostacyclin on biolaser-induced thrombosis was also seen in anagrelide (0.5 mg/kg po) pretreated animals. Other inhibitors of platelet aggregation used in combination with prostacyclin produced less spectacular results. These findings suggest that aside from inherent antiaggregatory and antithrombotic activity, certain platelet active drugs may produce equally important effects by virtue of their ability to interact with prostacyclin in a clinically beneficial manner.

Macrovascular thrombosis is driven by tissue factor derived primarily from the blood vessel wall

Blood ◽  
2005 ◽  
Vol 105 (1) ◽  
pp. 192-198 ◽  
Author(s):  
Sharlene M. Day ◽  
Jennifer L. Reeve ◽  
Brian Pedersen ◽  
Diana M Farris ◽  
Daniel D. Myers ◽  
...  
Keyword(s):  
Blood Vessel ◽  
Tissue Factor ◽  
Vessel Wall ◽  
Thrombus Formation ◽  
Vena Cava ◽  
Vascular Wall ◽  
Blood Vessel Wall ◽  
Wild Type

Abstract Leukocytes and leukocyte-derived microparticles contain low levels of tissue factor (TF) and incorporate into forming thrombi. Although this circulating pool of TF has been proposed to play a key role in thrombosis, its functional significance relative to that of vascular wall TF is poorly defined. We tested the hypothesis that leukocyte-derived TF contributes to thrombus formation in vivo. Compared to wild-type mice, mice with severe TF deficiency (ie, TF–/–, hTF-Tg+, or “low-TF”) demonstrated markedly impaired thrombus formation after carotid artery injury or inferior vena cava ligation. A bone marrow transplantation strategy was used to modulate levels of leukocyte-derived TF. Transplantation of low-TF marrow into wild-type mice did not suppress arterial or venous thrombus formation. Similarly, transplantation of wild-type marrow into low-TF mice did not accelerate thrombosis. In vitro analyses revealed that TF activity in the blood was very low and was markedly exceeded by that present in the vessel wall. Therefore, our results suggest that thrombus formation in the arterial and venous macrovasculature is driven primarily by TF derived from the blood vessel wall as opposed to leukocytes.

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