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Mesenteric Arterioles (mesenteric + arteriole)

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Medical Sciences	100%

Selected Abstracts

Inhibition of localized thrombosis in P2Y1 -deficient mice and rodents treated with MRS2179, a P2Y1 receptor antagonist

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 6 2003
N. Lenain
Summary., Previous studies in experimental models revealed a role for the P2Y1 platelet ADP receptor in systemic vascular thromboembolism models. In the present work, we used models of localized arterial and venous thrombosis to assess the role of the P2Y1 receptor in these processes. Arterial thrombosis was induced in one mesenteric arteriole of a mouse using FeCl3, while venous thrombosis was studied in a Wessler model adapted to rats. P2Y1 -deficient mice and mice treated with the P2Y1 antagonist MRS2179 displayed significantly less arterial thrombosis than their respective controls. Combination of P2Y1 deficiency with P2Y12 inhibition led to a significant additive effect. Venous thrombosis was slightly but significantly inhibited in MRS2179-treated rats. These results demonstrate a role for the P2Y1 receptor in both arterial and venous thrombosis, further establishing this receptor as a potential target for antithrombotic drugs. [source]

Anandamide mediates hyperdynamic circulation in cirrhotic rats via CB1 and VR1 receptors

BRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2006
L Moezi
Background and purpose: Hyperdynamic circulation and mesenteric hyperaemia are found in cirrhosis. To delineate the role of endocannabinoids in these changes, we examined the cardiovascular effects of anandamide, AM251 (CB1 antagonist), AM630 (CB2 antagonist) and capsazepine (VR1 antagonist), in a rat model of cirrhosis. Experimental approach: Cirrhosis was induced by bile duct ligation. Controls underwent sham operation. Four weeks later, diameters of mesenteric arteriole and venule (intravital microscopy), arterial pressure, cardiac output, systemic vascular resistance and superior mesenteric artery (SMA) flow were measured after anandamide, AM251 (with or without anandamide), AM630 and capsazepine administration. CB1, CB2 and VR1 receptor expression in SMA was assessed by western blot and RT-PCR. Key results: Anandamide increased mesenteric vessel diameter and flow, and cardiac output in cirrhotic rats, but did not affect controls. Anandamide induced a triphasic arterial pressure response in controls, but this pattern differed markedly in cirrhotic rats. Pre-administration of AM251 blocked the effects of anandamide. AM251 (without anandamide) increased arterial pressure and systemic vascular resistance, constricted mesenteric arterioles, decreased SMA flow and changed cardiac output in a time-dependent fashion in cirrhotic rats. Capsazepine decreased cardiac output and mesenteric arteriolar diameter and flow, and increased systemic vascular resistance in cirrhotic rats, but lacked effect in controls. Expression of CB1 and VR1 receptor proteins were increased in cirrhotic rats. AM630 did not affect any cardiovascular parameter in either group. Conclusions and implications: These data suggest that endocannabinoids contribute to hyperdynamic circulation and mesenteric hyperaemia in cirrhosis, via CB1 - and VR1-mediated mechanisms. British Journal of Pharmacology (2006) 149, 898,908. doi:10.1038/sj.bjp.0706928 [source]

A platelet tetraspanin superfamily member, CD151, is required for regulation of thrombus growth and stability in vivo

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 12 2009
E. ORLOWSKI
Summary.,Background:,This study was designed to determine the role of CD151 in platelet thrombus formation in vivo and define the contribution of platelet vs. endothelial CD151 in regulating platelet thrombus formation in vivo. Methods and Results: Using intravital microscopy and ferric chloride (FeCl3) injury of mesenteric arterioles, we found that thrombi formed in CD151+/, and CD151,/, mice were smaller and less stable, than those formed in CD151+/+ mice, with a tendency for embolization. Similarly, in Folt's FeCl3,induced carotid injury model, both CD151+/, and CD151,/, mice showed more prolonged times to 95% vessel occlusion than CD151+/+ mice. In addition, laser-induced injury of cremaster muscle arterioles showed that thrombi formed in CD151+/, and CD151,/, mice were smaller and less stable than those formed in CD151+/+ mice. Following platelet depletion/reconstitution with ex vivo -labeled donor platelets, platelet-depleted CD151+/+ mice that received reconstitution with CD151,/, platelets had smaller thrombi that were unstable and embolized. In contrast, platelet-depleted CD151,/, mice that received reconstitution with CD151+/+ platelets had normal thrombi that were stable. Conclusions: These data provide evidence that platelet CD151 is required for regulating thrombus formation in vivo. [source]

Both ADP and Thrombin Regulate Arteriolar Thrombus Stabilization and Embolization, but Are Not Involved in Initial Hemostasis as Induced by Micropuncture

MICROCIRCULATION, Issue 3 2007
Miriam A. Van Gestel
ABSTRACT Objective: Thrombosis and embolization are main causes of morbidity and mortality. Up to now, the relative importance of mediators involved is only partly known. It was the aim of this study to investigate the involvement of ADP and thrombin in subsequent phases of arteriolar hemostasis and thromboembolism in vivo. Methods: Rabbit mesenteric arterioles were punctured, which induced bleeding, hemostasis, and subsequent thromboembolism. This reaction as well as the activation state of platelets involved ([Ca2 +]i), was monitored in real time by intravital (fluorescence) microscopy. Results: Neither inhibition of thrombin formation or thrombin activity nor blockade of platelet ADP receptors P2Y1 and P2Y12 influenced the initial hemostatic reaction: in all experiments initial bleeding was stopped by a primary thrombus within 2,3 s. On the other hand, both thrombin inhibition and P2Y1 blockade increased rebleeding frequency, which indicates reduced thrombus stability in the long term. Finally, inhibition of either thrombin or ADP (via both receptors) reduced aggregate formation during the embolization phase by at least 90%. While most participating platelets exhibited a transient increase in [Ca2 +]i during embolization, an increased percentage of platelets showed no calcium response at all during P2Y1 blockade, which was accompanied by reduced platelet,platelet interaction strength. Conclusions: Whereas thrombin and ADP are not involved in the initial hemostatic reaction, both substances appear to be essential to prevent rebleedings in the long term. During subsequent embolization, ADP (via both receptors) and small amounts of thrombin are involved in platelet activation. [source]