Role of matrix metalloproteinases in blood flow-induced arterial enlargement: interaction with NO.
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Tears in the internal elastic lamina (IEL) can be observed after chronic increases in arterial blood flow, suggesting a potential role for matrix metalloproteinases (MMPs) in flow-induced vascular remodeling. We undertook to study this phenomenon by constructing an arteriovenous fistula (AVF) between the left common carotid artery (CCA) and the external jugular vein in rabbits. The diameter of the flow-loaded left CCA increased by 13.6+/-1.8% by day 3 after construction of the AVF compared with the right CCA (n=4, P:<0.01) and by 40.7+/-7.5% by day-15 (n=10, P:<0.0001). Increased CCA diameter also coincided with IEL fragmentation. Three days after construction of the AVF, gelatin zymography of protein extracts from left CCAs of untreated rabbits showed a significant increase in the 62-kDa (active MMP-2) activity and the appearance of a lytic band at 92 kDa (pro-MMP-9). In further experiments, MMP activity was inhibited by treatment with doxycycline (DOX) or BB-94, a specific MMP inhibitor. The increase in the 62-kDa gelatinolytic band was abolished in DOX- and BB-94-treated rabbits. The 92-kDa gelatinolytic band was also reduced in DOX-treated animals. Furthermore, both increased left CCA diameter and IEL fragmentation were abolished in DOX- and BB-94-treated rabbits. To evaluate whether nitric oxide was involved in blood flow-induced MMP activation, the rabbits were treated with N:(G)-nitro-L-arginine methyl ester to inhibit nitric oxide synthesis. MMP activities were significantly decreased in the left CCAs of N:(G)-nitro-L-arginine methyl ester-treated animals. Hence, blood flow-induced MMP activation is critical in flow-induced vascular enlargement and IEL fragmentation, and blood flow-induced nitric oxide participates in MMP activation. (+info)
Intrarenal expression and distribution of cyclooxygenase isoforms in rats with experimental heart failure.
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The generation of PGs from arachidonic acid is mediated by cyclooxygenase (COX), which consists of a constitutive (COX-1) and an inducible (COX-2) isoform. The present study evaluated the relative expression and immunoreactive levels of COX-1 and COX-2, by means of RT-PCR, Western blot analysis, and immunohistochemistry, in the renal cortex and medulla of rats with congestive heart failure (CHF), induced by the placement of an aortocaval fistula. In addition, we examined the effects of a COX-1 inhibitor (piroxicam), COX-2 inhibitor (nimesulide), and nonselective COX inhibitor (indomethacin) at a dose of 5 mg/kg, on intrarenal blood flow by laser Doppler flowmetry. COX-1 and COX-2 mRNAs were abundantly expressed in the renal medulla of control and CHF rats and only minimally in the cortex. Moreover, both RT-PCR (32-36 cycles) and Western blot techniques revealed upregulation of medullary COX-2, but not of COX-1, in rats with advanced heart failure. In line with these findings, all three tested COX inhibitors provoked significant and sustained decreases (Delta approximately -20%) in medullary blood flow (MBF), which were similar in magnitude and duration in control animals. However, in CHF rats, indomethacin produced a greater reduction in MBF than that obtained with either piroxicam or nimesulide. Taken together, these results indicate that 1) both COX-1 and COX-2 are predominantly expressed in the renal medulla and 2) experimental CHF is associated with selective overexpression of COX-2. The latter may represent a mechanism aimed at defending MBF in the face of a decrease in renal perfusion pressure during the development of CHF. (+info)
Hemodialysis arteriovenous access: detection of stenosis and response to treatment by vascular access blood flow.
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BACKGROUND: Hemodialysis access to the circulation is best provided by native and synthetic arteriovenous fistulae (AVF and AVG). Thromboses caused by venous outflow stenoses prevent the long-term use of AV access. This pilot study was performed to evaluate the ability of ultrasound dilution-derived access blood flows to detect AV access stenosis and to evaluate the response to treatment. METHODS: This pilot study was a single-center, prospective observational intervention trial. The monitoring technique used was ultrasound dilution access blood flow measurements performed monthly and after any intervention. Screening criteria for interventions were decrements in access flow of 20% when the flow value fell under 1000 mL/min or absolute flow of <600 mL/min. The primary intervention when flow criteria were met was biplanar venography of the access with percutaneous transluminal angioplasty (PTA) of detected stenoses. Stenoses unresponsive to PTA were sent for surgical revision. Access thrombosis was considered a study ending event. RESULTS: Baseline access flow at study entry for AVF was 919 and 1237 mL/min for AVG. Sequential measurement of AV access flow detected AV access stenosis. PTA and surgical revision significantly restored AV access flow back toward the baseline flow measurement. Failure to restore access flow by at least 20% following intervention occurred in 14% of AVF and 21% of AVG PTA attempts. Transluminal angioplasty, once successfully performed, was required at a mean of 5.8-month intervals in order to maintain AVG flow. In contrast, AVF flow was restored for a much longer period of time following angioplasty (11.4 month follow-up at the time of study end). Compared with historic controls, which used venous dialysis pressure as the primary monitoring technique, the overall (AVF-AVG) thrombosis rates improved from 25 to 16% per patient year, and AVF thrombosis rates improved from 16 to 7% per patient year. When flow was not successfully restored, thrombosis ensued. Eight of 10 thrombosis episodes were predicted based on inability to improve access flow either as a result of stenosis treatment failure or unsuccessful referral for treatment. CONCLUSION: Sequential measurement of AV access flow is an acceptable means of both monitoring for the development of access stenoses and assessing response to therapy. PTAs of AVF are more durable than PTAs of AV grafts. (+info)
Absence of the brachial artery: report of a rare human variation and review of upper extremity arterial anomalies.
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Variations in the arterial anatomy of the upper extremities, although uncommon, occur in up to one in five patients. Most of these variants occur in either the radial or ulnar artery; brachial artery variations are less common. The case we report is a rare anomaly consisting of brachial artery agenesis or regression. The brachial artery was absent from its origin but reconstituted as a normal-appearing vessel 3 cm above the antecubital fossa. The profunda brachii artery and the superior and inferior ulnar collateral arteries were also absent in this patient. The axillary artery served as the main collateral to the forearm. This constellation of anomalies has not been previously described or explained by developmental models in humans and other primates. We speculate that failure of development or arrest of specific vascular anlage in the upper extremity occurs at particular embryological stages because of unknown factors. (+info)
Nondialysis uses for vascular access procedures.
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Chemotherapeutic agents, blood products and hyperalimentation solutions have been administered and recurrent diabetic ketoacidosis has been treated via vascular access procedures in 13 patients during the period from 1972 through 1977. Bovine heterograft, saphenous vein graft and the direct arteriovenous fistulae have been successfully utilized in the construction of arteriovenous fistulae in patients requiring vascular access for nonhemodialysis purposes. Operative techniques and therapeutic usefulness are discussed. (+info)
Hepatic arteriolo-portal venular shunting guarantees maintenance of nutritional microvascular supply in hepatic arterial buffer response of rat livers.
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To elucidate the hepatic microvascular response upon the hepatic arterial buffer response (HABR), we analysed blood flow (ultrasonic flowprobes) of the hepatic artery (HA) and portal vein (PV), microcirculation (intravital microscopy), and tissue oxygenation (polarography) in anaesthetized Sprague-Dawley rats and re-evaluated the role of adenosine in mediating the HABR by using 8-phenyltheophylline as a competitive antagonist. 2. Upon restriction of PV blood flow to 11 +/- 3 % of baseline values, HA blood flow increased by a factor of 1.77 (P < 0.05), thus confirming HABR. Strikingly, red blood cell velocity and volumetric blood flow in terminal hepatic arterioles (THAs) did not increase but were even found to be slightly decreased, by 8 and 13 %, respectively. In contrast, red blood cell velocity and volumetric blood flow in terminal portal venules (TPVs) decreased to only 66 % (P < 0.05), indicating upstream hepatic arteriolo-portal venular shunting. As a consequence, red blood cell velocity and volumetric blood flow in sinusoids were found to be reduced to only 66-68 % compared with baseline (P < 0.05). Diameters of neither of those microvessels changed, thus excluding THA-, TPV-, and sinusoid-associated mechanisms of vasomotor control in HABR. 3. Tissue PO2 and hepatocellular NADH fluorescence remained unchanged, indicating HABR-mediated maintenance of adequate oxygen delivery, despite the marked reduction of total liver blood flow. Further, hepatic arteriolo-portal venular shunting guaranteed homogeneity of nutritive blood flow upon HABR, as given by an unchanged intra-acinar coefficient of variance of sinusoidal perfusion. 4. Pretreatment of animals with the adenosine antagonist 8-phenyltheophylline completely blocked the hepatic arterial buffer response with the consequence of decreased tissue oxygenation and increased heterogeneity of sinusoidal perfusion. 5. In conclusion, hepatic microhaemodynamics, in particular unchanged diameters of THAs, TPVs and sinusoids, during HABR indicate that reduction in resistance to HA flow is located upstream and functions via hepatic arteriolo-portal venular shunts resulting in equal distribution of microvascular blood flow and oxygen delivery under conditions of restricted PV blood supply. (+info)
Ultrasound guided puncture of the brachial artery for haemodialysis fistula angiography.
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BACKGROUND: Arterio-venous (a-v) fistulae of haemodialysis patients frequently require function assessment by angiography. The purpose of the present study was to determine the efficacy and safety of ultrasound-guided transbrachial catheterization when a-v fistulae were evaluated. METHODS: Between July 1996 and December 1997, 208 dialysis patients, whose a-v fistulae (arterial inflow < 50 ml/min or venous pressure > 150 mm Hg in three consecutive HD sessions) were at the wrist or elbow, underwent transbrachial angiography using an ultrasound-guided 20-gauge IA needle to evaluate fistula function. Procedure-related symptoms or complications were noted in 28 patients and these were analysed. RESULTS: No apparent cases of vessel spasm or thrombosis were noted. Reported symptoms in 28 patients (13.5%) included local arm pain (3.3%), transient paresthesia (0.9%), mild ecchymosis (10.6%) and haematoma (0.9%). All complications were minor and none required surgical intervention. CONCLUSION: Ultrasound-guided puncture of the brachial artery is a safe, reliable and effective procedure in skilled hands and should be the preferred means of catheterization whenever haemodialysis angiography is performed. (+info)
Intravascular ultrasound imaging before and after angioplasty for stenosis of arteriovenous fistulae in haemodialysis patients.
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BACKGROUND: Complications of haemodialysis vascular access have emerged as a major cause of patient morbidity. Intravascular ultrasound imaging is a new technical modality providing visualization of the vessel lumen and wall structure in a cross-sectional fashion. Percutaneous transluminal angioplasty has long been used in the treatment of stenoses of arteriovenous fistulae. However, there is no detailed quantitative information on the stenotic lesion and the morphological change by angioplasty. METHODS: Intravascular ultrasound studies were performed in 40 haemodialysis patients with 63 stenoses in arteriovenous fistulae who had percutaneous transluminal angioplasty. The patients were qualitatively and quantitatively evaluated for echogenic patterns and morphological changes before and after angioplasty. RESULTS: Morphological plaque features in stenotic lesions were classified as 37 soft (58%), five hard (8%), 20 mixed (32%), and one calcified sites. Plaque fractures after angioplasty were detected in 45/63 (71%) instances. The lumen cross-sectional area was found to be dilated approximately threefold (from 3.8+/-2.4 to 11.1+/-4.5 mm(2)) and the external elastic membrane cross-sectional area was dilated approximately twofold (from 11.1+/-5.3 to 19.8+/-8.1 mm(2)) after angioplasty. CONCLUSION: These results indicate that intravascular ultrasound allows both qualitative and quantitative assessments of arteriovenous fistulae in haemodialysis patients. The results further suggest that the mechanism of expansion of arteriovenous fistulae stenoses by percutaneous transluminal angioplasty involves stretching of the vessel wall as well as plaque fractures. (+info)