Flow Decreased (flow + decreased)

Distribution by Scientific Domains

Kinds of Flow Decreased

  • blood flow decreased

  • Selected Abstracts

    Intra-articular stabilisation of the equine cricoarytenoid joint

    Summary Reasons for performing study: The success of laryngoplasty is limited by abduction loss in the early post operative period. Objective: To determine the efficacy of polymethylmethacrylate (PMMA) in stabilising the cricoarytenoid joint (CAJ) and reducing the force on the laryngoplasty suture. Hypothesis: Injection into the cricoarytenoid joint resists the forces produced by physiological laryngeal air flows and pressures thereby reducing the force experienced by the laryngoplasty suture. Methods: Ten cadaver larynges were collected at necropsy and PMMA was injected into one CAJ at selected random. Each larynx was subjected to physiological conditions with with constant (static) or cycling (dynamic) flow. The specimens were tested sequentially in each of 4 conditions: 1) bilateral full abduction (Control 1); 2) transection of the suture on the side without PMMA; 3) bilateral abduction achieved by replacing the suture (Control 2); and 4) cutting the suture on the PMMA side. Tracheal pressure and flow and pressure in the flow chamber were recorded using pressure and flow transducers. The strain experienced by each suture during bilateral abduction (Controls 1 and 2) was measured. Statistical comparison of the 4 conditions was performed using a mixed effect model with Tukey's post hoc test for multiple comparisons. The strain gauge data were analysed by paired comparison of the regression slopes. Results: In the static and dynamic states, tracheal pressure increased and tracheal flow decreased when the suture on the non-cement side was cut (P<0.05). There was no significant difference in any outcome measure between PMMA injected into the CAJ and bilaterally abducted specimens (Controls 1 and 2) for either condition. The rate of increase in strain with increasing translaryngeal pressure was significantly less on the suture with PMMA placed in the CAJ (P = 0.03). Conclusions: These data provide strong evidence that injecting PMMA into the CAJ resists the collapsing effect of physiological airflows and pressures in vitro and reduces the force experienced by the laryngoplasty suture during maximal abduction. Potential relevance: Augmentation of prosthetic laryngoplasty with this technique may reduce arytenoid abduction loss in the early post operative period. [source]

    Tumoricidal activity of high-dose tumor necrosis factor-, is mediated by macrophage-derived nitric oxide burst and permanent blood flow shutdown

    Chandrakala Menon
    Abstract This study investigates the role of tumor nitric oxide (NO) and vascular regulation in tumor ulceration following high-dose tumor necrosis factor-, (TNF) treatment. Using TNF-responsive (MethA) and nonresponsive (LL2) mouse tumors, tumor NO concentration was measured with an electrochemical sensor and tumor blood flow by Doppler ultrasound. Mice were also pretreated with a selective inducible nitric oxide synthase (iNOS) inhibitor, 1400 W. Tumors harvested from TNF-treated mice were cryosectioned and immunostained for murine macrophages, or/and iNOS. MethA tumor-bearing mice were depleted of macrophages. Pre- and post-TNF tumor NO levels were measured continuously, and mice were followed for gross tumor response. In MethA tumors, TNF caused a 96% response rate, and tumor NO concentration doubled. Tumor blood flow decreased to 3% of baseline by 4 hr and was sustained at 24 hr and 10 days post-TNF. Selective NO inhibition with 1400 W blocked NO rise and decreased response rate to 38%. MethA tumors showed tumor infiltration by macrophages post-TNF and the pattern of macrophage immunostaining overlapped with iNOS immunostaining. Depletion of macrophages inhibited tumor NO increase and response to TNF. LL2 tumors had a 0% response rate to TNF and exhibited no change in NO concentration. Blood flow decreased to 2% of baseline by 4 hr, recovered to 56% by 24 hr and increased to 232% by 10 days. LL2 tumors showed no infiltration by macrophages post-TNF. We conclude that TNF causes tumor infiltrating, macrophage-derived iNOS-mediated tumor NO rise and sustained tumor blood flow shutdown, resulting in tumor ulceration in the responsive tumor. 2008 Wiley-Liss, Inc. [source]

    Hepatic effects of an open lung strategy and cardiac output restoration in an experimental lung injury

    Background: Ventilation with high positive end-expiratory pressure (PEEP) can lead to liver dysfunction. We hypothesized that an open lung concept (OLC) using high PEEP impairs liver function and integrity dependent on the stabilization of cardiac output. Methods: Juvenile female Pietrain pigs instrumented with flow probes around the common hepatic artery and portal vein, pulmonary and hepatic vein catheters underwent a lavage-induced lung injury. Ventilation was continued with a conventional approach (CON) using pre-defined combinations of PEEP and inspiratory oxygen fraction or with an OLC using PEEP set above the lower inflection point of the lung. Volume replacement with colloids was guided to maintain cardiac output in the CON(V+) and OLC(V+) groups or acceptable blood pressure and heart rate in the OLC(V,) group. Indocyanine green plasma disappearance rate (ICG-PDR), blood gases, liver-specific serum enzymes, bilirubin, hyaluronic acid and lactate were tested. Finally, liver tissue was examined for neutrophil accumulation, TUNEL staining, caspase-3 activity and heat shock protein 70 mRNA expression. Results: Hepatic venous oxygen saturation was reduced to 18 16% in the OLC(V,) group, while portal venous blood flow decreased by 45%. ICG-PDR was not reduced and serum enzymes, bilirubin and lactate were not elevated. Liver cell apoptosis was negligible. Liver sinusoids in the OLC(V+) and OLC(V,) groups showed about two- and fourfold more granulocytes than the CON(V+) group. Heat shock protein 70 tended to be higher in the OLC(V,) group. Conclusions: Open lung ventilation elicited neutrophil infiltration, but no liver dysfunction even without the stabilization of cardiac output. [source]

    Recombinant activated factor VII efficacy and safety in a model of bleeding and thrombosis in hypothermic rabbits: a blind study

    Summary.,Background:,Recombinant activated factor VII (rFVIIa) is increasingly used to secure hemostasis in hemorrhagic situations in trauma and surgical patients. Hypothermia is often observed in these clinical settings. Objective:,To study the efficacy and safety of rFVIIa in hypothermia in a rabbit model of bleeding and thrombosis. Methods:,Sixty-nine rabbits were anesthetized, ventilated and monitored for blood pressure, temperature and carotid flow. The Folts model was used: a stenosis (75%) and an injury were carried out on the carotid artery, inducing thrombosis. Blood flow decreased as thrombus size increased until the pressure gradient was such that the thrombus was released and local arterial blood flow was suddenly restored. This is known as a cyclic flow reduction (CFR). After counting baseline CFRs during a 20-min period (P1), rabbits were randomized blindly to one of four groups: normothermic (NT) placebo or rFVIIa (150 ,g kg,1), hypothermic (HT) (34 C) placebo or rFVIIa. Then CFRs were recorded over a second period (P2). At the end of the experiment, a hepato-splenic section was performed and the amount of blood loss was recorded. After each period, the following were measured: ear immersion bleeding time (BT), hemoglobin, platelet count, prothrombin time (PT), activated partial thromboplastin time (aPTT) and fibrinogen. Results:,Hypothermia increased BT and blood loss. These effects were reversed by rFVIIa. In NT rabbits, rFVIIa shortened BT but did not reduce blood loss. rFVIIa-treated rabbits bled similarly regardless of temperature. The incidence of CFRs was higher in treated than placebo animals regardless of temperature. rFVIIa decreased PT and aPTT without modifying platelet count or fibrinogen level. Conclusion:,Hemostatic efficacy of rFVIIa was maintained in hypothermia. However, the number of CFRs was higher in the rFVIIa-treated group than in the placebo groups, whether for NT or HT rabbits. [source]

    Effects of atrial natriuretic peptide on the extrasplenic microvasculature and lymphatics in the rat in vivo

    Zo L. S. Brookes
    We developed a novel model using fluorescent intravital microscopy to study the effect of atrial natriuretic peptide (ANP) on the extrasplenic microcirculation. Continuous infusion of ANP into the splenic artery (10 ng min,1 for 60 min) of male Long,Evans rats (220,250 g, n= 24) induced constriction of the splenic arterioles after 15 min (,7.2 6.6% from baseline diameter of 96 18.3 ,m, mean s.e.m.) and venules (,14.4 4.0% from 249 25.8 ,m; P < 0.05). At the same time flow did not change in the arterioles (from 1.58 0.34 to 1.27 0.27 ml min,1), although it decreased in venules (from 1.67 0.23 to 1.15 0.20 ml min,1) and increased in the lymphatics (from 0.007 0.001 to 0.034 0.008 ml min,1; P < 0.05). There was no significant change in mean arterial pressure (from 118 5 to 112 5 mmHg). After continuous ANP infusion for 60 min, the arterioles were dilated (108 16 ,m, P < 0.05) but the venules remained constricted (223 24 ,m). Blood flow decreased in both arterioles (0.76 0.12 ml min,1) and venules (1.03 0.18 ml min,1; P < 0.05), but was now unchanged from baseline in the lymphatics (0.01 0.001 ml min,1). This was accompanied by a significant decrease in MAP (104 5 mmHg; P < 0.05). At 60 min, there was macromolecular leak from the lymphatics, as indicated by increased interstitial fluorescein isothiocyanate,bovine serum albumin fluorescence (grey level: 0 = black; 255 = white; from 55.8 7.6 to 71.8 5.9, P < 0.05). This study confirms our previous proposition that, in the extrasplenic microcirculation, ANP causes greater increases in post- than precapillary resistance, thus increasing intrasplenic capillary hydrostatic pressure (Pc) and fluid efflux into the lymphatic system. Longer-term infusion of ANP also increases Pc, but this is accompanied by increased ,permeability' of the extrasplenic lymphatics, such that fluid is lost to perivascular third spaces. [source]


    M Sertac Yilmaz
    SUMMARY 1The aim of the present study was to investigate the effect of the intracerebroventricular (i.c.v.) or intravenous (i.v.) administration of cytidine 5-diphosphocholine (CDP-choline) on superior mesenteric artery (SMA) and renal artery (RA) blood flow, along with the cardiovascular parameters and survival time of anaesthetized rats under conditions of haemorrhagic shock. 2Rats were anaesthetized with urethane (1.25 g/kg, i.p.) and acute haemorrhage was mimicked by the withdrawal of a total volume of 2,2.1 mL blood/100 g bodyweight over a period of 20 min. The CDP-choline was injected i.c.v. (1.0, 1.5 and 2.0 mmol) or i.v. (250 mg/kg) after the end of haemorrhage. Blood pressure, heart rate, SMA and RA flow values and the survival time of rats were recorded. Changes in blood flow were estimated by laser-Doppler flowmetry. 3The haemorrhage procedure decreased the blood pressures of rats by 60% and limited their survival time to 22 2 min. Both SMA and RA flow decreased to approximately 25% of initial values at the end of the haemorrhage procedure. 4The i.c.v. administration of CDP-choline (1.0, 1.5 and 2.0 mmol) increased blood pressure and partially reversed the hypotension in a dose- and time-dependent manner. At 1.5 and 2.0 mmol, i.c.v., CDP-choline completely restored the decreased flow of the RA and transiently reversed hypoperfusion of the SMA. It also produced an almost fourfold increase in the survival time of rats. 5The i.v. administration of CDP-choline (250 mg/kg) also completely, but transiently, restored SMA and RA flow, whereas it increased blood pressure by only 40% compared with control values. The survival time of rats in the i.v. CDP-choline group was doubled that of control. 6These results indicate that both centrally and peripherally injected CDP-choline can restore SMA and RA flow, together with a partial reversal of hypotension and an increase in the survival time of rats. [source]