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      Prostacyclin Reduces Microvascular Fluid Conductivity in Cat Skeletal Muscle through Opening of ATP-Dependent Potassium Channels


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          Prostacyclin is suggested to reduce microvascular permeability, but the cellular mechanisms mediating this response in the microvascular endothelial cells are still unknown. Considering that prostacyclin relaxes vascular smooth muscle cells via opening of ATP-dependent potassium channels, and opening of ATP-dependent potassium channels in the endothelial cells is suggested to influence microvascular permeability, this study was designed to test (1) if ATP-dependent potassium channels are involved in the regulation of microvascular hydraulic permeability, (2) if the permeability-reducing effect of prostacyclin is mediated through opening of ATP-dependent potassium channels, and (3) if cAMP is involved in this process. An autoperfused cat calf hindlimb was used as experimental model, and microvascular hydraulic permeability (conductivity) was estimated by a capillary filtration coefficient (CFC) technique. The potassium channel opener PCO-400 (0.5 μg·min<sup>–1</sup> per 100 g muscle, intra-arterially), prostacyclin (1 ng·min<sup>–1</sup> per kg body weight, intravenously) and the cAMP analogue dibutyryl-cAMP (24 μg·min<sup>–1</sup> per 100 g muscle, intra-arterially), decreased CFC to 77, 72 and 69% compared to control, respectively (p < 0.01). The decrease in CFC obtained by these substances was completely restituted after the start of a simultaneous infusion of the ATP-dependent potassium channel blocker glibenclamide (6 μg·min<sup>–1</sup> per 100 g muscle, intra-arterially; p < 0.01). Infusion of glibenclamide alone increased CFC to 107% of control (p < 0.05). In conclusion, the ATP-dependent potassium channels contribute to the regulation of microvascular hydraulic conductivity, and the prostacyclin permeability-reducing effect may act through this mechanism via increase in intracellular cAMP.

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          One-stage coronary angiography and angioplasty.

          The combination of diagnostic angiography and angioplasty as a single procedure is becoming common practice in many institutions, but the feasibility and safety of this strategy have not been reported. This report describes 2,069 patients who underwent coronary angioplasty over a 3-year period at an institution where combined angiography and angioplasty is the norm. All patients were prepared before angiography for potential immediate angioplasty. In 1,719 patients, angioplasty was performed immediately after the diagnostic angiogram, while separate procedures were performed in 350 patients. Of those 350 patients, 254 were referred for angioplasty after diagnostic angiography at other hospitals. One thousand one hundred ninety-seven patients were admitted electively for treatment of stable angina pectoris, and 872 underwent procedures during hospitalization for unstable angina or acute myocardial infarction. One thousand nine hundred seven patients (92.2%) had successful angioplasties; in 130 patients (6.3%) the lesion could not be dilated, but no complication occurred, and in 32 patients (1.5%) angioplasty ended with a major complication (0.8% death, 1.0% Q-wave myocardial infarction, 0.5% emergency coronary artery bypass surgery). There was no difference between the combined and staged groups with regard to success, major and minor complication rates or in length of hospitalization after angioplasty. We conclude that routine combined strategy for angiography and angioplasty is feasible, safe, easier for the patient, and more cost-effective than 2 separate procedures.
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            Modification of postischemic increase of leukocyte adhesion and vascular permeability in the hamster by Iloprost.

            This study of the postischemic events in the hamster cheek pouch showed that there is an increase in number of leukocytes adhering to the venular endothelium after reperfusion. It also showed that the stable prostacyclin analogue Iloprost could counteract both the postischemic increase in leukocyte adhesion and the postischemic increase in vascular permeability to macromolecules. The hamsters were anesthetized and the cheek pouch was everted and prepared for intravital microscopy. Temporary ischemia (30 min) was obtained using an expandable cuff placed around the proximal part of the cheek pouch. Fluorescein labelled dextran (FITC-dextran, Mw 150,000) was used as a tracer of macromolecular leakage from the postcapillary venules. Iloprost, given either topically (0.1 nM) or as an intravenous infusion (40 ng/kg/min), reduced the postischemic permeability increase (P less than 0.05) but did not affect the hemodynamics or the permeability response induced by histamine. It is proposed that these effects could be due to inhibition of leukocyte activation by Iloprost, indicating that these cells could play a role in the permeability increase during reperfusion after ischemia.
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              Role of Prostacyclin and Nitric Oxide in Regulation of Basal Microvascular Hydraulic Permeability in Cat Skeletal Muscle

              The effects of prostacyclin, nitric oxide (NO) and β 2 -receptor stimulation on capillary filtration coefficient (CFC) and vascular tone were analyzed in an autoperfused cat skeletal muscle in vivo preparation, to evaluate if these substances are involved in regulation of basal microvascular hydraulic permeability. CFC was increased from control (100%) to 124% with the prostacyclin-synthase inhibitor tranylcypromine and restored by simultaneous infusion of prostacyclin at 0.1 ng·kg –1 · min –1 , with further reduction to 76% at 1 ng· kg –1 ·min –1 . Prostacyclin at these doses did not influence vascular tone. NO inhibition by L-NAME increased CFC to 116% of control, with a vascular resistance increase of 45%. CFC was restored by simultaneous infusion of the NO precursor L -arginine. L -arginine given alone reduced CFC to 86% of control. Tranylcypromine and L-NAME given together increased CFC to 141% of control and CFC was reduced to 86% by prostacyclin at 1 ng·kg –1 ·min –1 with no significant further reduction by adding L -arginine. Adrenaline alone, in a vasodilating dose verifying β 2 stimulation, or when followed by simultaneous β-blockade with propranolol, did not influence CFC. We conclude that NO and especially prostacyclin are involved in bi-directional regulation of basal microvascular hydraulic permeability and can account for up to 30–40% increase or decrease from a basal value. Physiological β 2 stimulation has no effect on basal hydraulic permeability. The permeability-reducing effects of prostacyclin and NO are additive. NO, but not prostacyclin, is involved in regulation of basal vascular tone.

                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                December 1999
                24 December 1999
                : 36
                : 6
                : 516-523
                Departments of aPhysiology, and bAnaesthesia and Intensive Care, University of Lund, Sweden
                25695 J Vasc Res 1999;36:516–523
                © 1999 S. Karger AG, Basel

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                Page count
                Figures: 6, References: 30, Pages: 8
                Research Paper


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