Role of thromboxane in producing portal hypertension following trauma-hemorrhage.
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Thromboxane A2 (TXA2) and endothelin-1 (ET-1) have been proposed as the important vasoconstrictors that increase portal venous resistance in paracrine or autocrine fashion. We hypothesized that the hepatic damage following trauma-hemorrhage (T-H) is induced by the impaired hepatic circulation due to the increased production of vasoconstrictors such as ET-1 and TXA2 by the liver. To test this, male Sprague-Dawley rats (n = 6/group) were subjected to trauma (i.e., midline laparotomy) and hemorrhage (35-40 mmHg for 90 min followed by fluid resuscitation) or sham operation. At 2 or 5 h after the end of resuscitation, the liver was isolated and perfused and portal inflow pressure, bile flow, and release of ET-1 and thromboxane B2 (TXB2; a stable metabolite of TXA2) into the perfusate were measured. The level of portal pressure was higher at 5 h following T-H compared with 2 h after T-H and sham. The portal pressure was inversely correlated to the amount of bile production. Furthermore, the bile flow was significantly correlated to the hepatic damage as evidenced by release of lactate dehydrogenase into the perfusate. The level of ET-1 at 5 h following T-H in the perfusate after 30 min of recirculation did not show any difference from sham. However, the levels of TXB2 in the T-H group were significantly higher than those in sham at that interval. These results indicate that the increased release of TXA2 but not ET-1 following T-H might be responsible for producing the increased portal resistance, decreased bile production, and hepatic damage. (+info)
Effects of 18 days of bed rest on leg and arm venous properties.
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Venous function may be altered by bed rest deconditioning. Yet the contribution of altered venous compliance to the orthostatic intolerance observed after bed rest is uncertain. The purpose of this study was to assess the effect of 18 days of bed rest on leg and arm (respectively large and small change in gravitational gradients and use patterns) venous properties. We hypothesized that the magnitude of these venous changes would be related to orthostatic intolerance. Eleven healthy subjects (10 men, 1 woman) participated in the study. Before (pre) and after (post) 18 days of 6 degrees head-down tilt bed rest, strain gauge venous occlusion plethysmography was used to assess limb venous vascular characteristics. Leg venous compliance was significantly decreased after bed rest (pre: 0.048 +/- 0.007 ml x 100 ml(-1) x mmHg(-1), post: 0.033 +/- 0.007 ml x 100 ml(-1) x mmHg(-1); P < 0.01), whereas arm compliance did not change. Leg venous flow resistance increased significantly after bed rest (pre: 1.73 +/- 1.08 mmHg x ml(-1) x 100 ml x min, post: 3.10 +/- 1.00 mmHg x ml(-1) x 100 ml x min; P < 0.05). Maximal lower body negative pressure tolerance, which was expressed as cumulative stress index (pressure x time), decreased in all subjects after bed rest (pre: 932 mmHg x min, post: 747 mmHg x min). The decrease in orthostatic tolerance was not related to changes in leg venous compliance. In conclusion, this study demonstrates that after bed rest, leg venous compliance is reduced and leg venous outflow resistance is enhanced. However, these changes are not related to measures of orthostatic tolerance; therefore, alterations in venous compliance do not to play a major role in orthostatic intolerance after 18 days of head-down tilt bed rest. (+info)
Intrinsic autoregulation of cardiac output in rainbow trout (Oncorhynchus mykiss) at different heart rates.
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Intrinsic regulation of the heart in teleosts is partly driven by central venous pressure, which exerts a modulatory role on stroke volume according to the well-known Frank-Starling mechanism. Although this mechanism is well understood from heart perfusion studies, less is known about how this mechanism operates in vivo, where heart rate varies markedly. We used zatebradine, a bradycardic agent, to attain resting heart rates in surgically instrumented animals. A dose of zatebradine of 2.79+/-0.47 mg l(-1) decreased heart rate by half, from 44.4+/-4.19 beats min(-1) to 22.1+/-1.9 beats min(-1). Zatebradine had no significant effect on the peripheral vasculature and no inotropic effects, so was a suitable pharmacological agent with which to manipulate heart rate. When heart rate halved, cardiac output dropped to 87.5+/-4.6% of the control value, due to the concomitant increase in stroke volume to 165+/-13%. In vivo recordings of venous pressure at varying heart rates indicated that the partial compensation in cardiac output was possible through an increase in pressure in the sinus venosus, from -0.06+/-0.04 kPa at a control heart rate of 58.3+/-3.5 beats min(-1) (N=10) to 0.07+/-0.05 kPa after injection of zatebradine (4 mg kg(-1)). The operation of the so-called time-dependent autoregulatory mechanism was further demonstrated in perfused hearts. The positive pressures recorded in the sinus venosus at low heart rates coincident with non-invasive measurements in trout suggest that atrial filling in trout is more dependent on the build-up of pressure in the venous circulation (vis-a-tergo filling) than a suction mechanism during ventricular contraction (vis-a-fronte filling). (+info)
Can lymphatic drainage be measured non-invasively in human limbs, using plethysmography?
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There is always rapid volume restitution of the accumulated interstitial fluid after a VCP (venous congestion plethysmography) protocol. It has been suggested that backward extrapolation of the relationship between applied hydrostatic pressure and fluid filtration may give a measure of tissue J (vL) (lymph flow); if so, this could be of immense value in pathophysiological investigations. We hypothesized that the congestion pressure decrease following the VCP protocol might be the stimulus for activating the observed rapid interstitial fluid removal mechanism. We investigated this hypothesis by using a cumulative small step VCP protocol to a maximum arterial diastolic pressure, followed by a mirror image of step pressure decreases. The increases and decreases in cuff pressure produced capillary filtration capacities that were not significantly different from one another [(3.8+/-1.0) x 10(-3) and (3.7+/-1.2) x 10(-3) ml x 100 ml(-1) x min(-1) x mmHg(-1) respectively]. However, we did observe a significant 3-fold increase in estimated lymph flow between the up and 'mirror' down protocol. Moreover, the calculated supine control value, reflecting interstitial fluid removal ( J (vL)), of 0.03+/-0.03 ml x 100 ml(-1) x min(-1) was within the range of lymph flows in human limbs described by other workers, as was the 3-fold increase to 0.09+/-0.03 ml x 100 ml(-1) x min(-1) following the release of the venous congestion. These results support the notion that strain-gauge plethysmography might provide a non-invasive means of assessing peripheral lymph flow in human limbs. (+info)
Dopaminergic vasodilation in the choroidal circulation by d1/d5 receptor activation.
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PURPOSE: To test whether exogenous dopamine can cause choroidal vasodilation and to identify the mediating receptors in anesthetized rabbits. METHODS: Mean arterial pressure (MAP), intraocular pressure (IOP), and orbital venous pressure (OVP) were measured by direct cannulation of the central ear artery, the vitreous, and the orbital venous sinus, respectively. Laser Doppler flowmetry was used to measure choroidal blood flow (ChorBF) while MAP was manipulated mechanically with occluders on the aorta and vena cava, thus changing perfusion pressure (PP) over a wide range. In the first group of animals (n = 11), pressure-flow (PF) relationships were performed at control and in response to 40 micro g/kg per minute intravenous (IV) dopamine (D40) and D40+SCH-23390 (0.5 mg/kg, bolus injection IV). In the second group of animals (n = 6), PF relationships were recorded at control and during infusion of SKF-38393 (80 micro g/kg per minute). RESULTS: D40 lowered IOP and caused an upward shift in the choroidal PF relationship, which was blocked by the D1/D5 antagonist SCH-23390 suggesting the involvement of the dopamine D1/D5 receptors. Stimulation of the D1/D5 receptors by infusion of the selective agonist SKF-38393 also lowered IOP and caused an upward shift in the PF relationship. Dopamine and SKF-38393 tended to decrease OVP, but the effect was not significant. CONCLUSIONS: Dopamine can cause choroidal vasodilation in anesthetized rabbits. Because SCH-23390 was able to block the response and SKF-38393 caused a similar vasodilation, we conclude that the vasodilation is caused by a D1/D5-receptor-mediated mechanism. (+info)
Elevated circulating adiponectin levels in liver cirrhosis are associated with reduced liver function and altered hepatic hemodynamics.
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Adiponectin is a novel adipocytokine negatively correlated with parameters of the metabolic syndrome, such as body mass index (BMI), body fat mass (BFM), and circulating insulin levels. Furthermore, metabolic actions directly on the liver have been described. The aim of the present study was to characterize circulating adiponectin levels, hepatic turnover, and the association of adiponectin with key parameters of hepatic as well as systemic metabolism in cirrhosis, a catabolic disease. Circulating adiponectin levels and hepatic turnover were investigated in 20 patients with advanced cirrhosis. Hepatic hemodynamics [portal pressure, liver blood flow, hepatic vascular resistance, indocyanine green (ICG) half-life], body composition, resting energy expenditure, hepatic free fatty acids (FFA) and glucose turnover, and circulating levels of hormones (catecholamines, insulin, glucagon) and proinflammatory cytokines (IL-1beta, TNF-alpha, IL-6) were also assessed. Circulating adiponectin increased dependently on the clinical stage in cirrhosis compared with controls (15.2 +/- 1.7 vs. 8.2 +/- 1.1 microg/ml, respectively, P < 0.01), whereas hepatic extraction decreased. Adiponectin was negatively correlated with parameters of hepatic protein synthesis (prothrombin time: r = -0.62, P = 0.003; albumin: r = -0.72, P < 0.001) but not with transaminases or parameters of lipid metabolism. In addition, circulating adiponectin increased with portal pressure (r = 0.67, P = 0.003), hepatic vascular resistance (r = 0.60, P = 0.008), and effective hepatic blood flow (ICG half-life: r = 0.69, P = 0.001). Adiponectin in cirrhosis was not correlated with BMI, BFM, parameters of energy metabolism, insulin levels, hepatic FFA and glucose turnover, and circulating proinflammatory cytokines. These results demonstrate that 1) adiponectin plasma levels in cirrhosis are significantly elevated, 2) the liver is a major source of adiponectin extraction, and 3) adiponectin levels in cirrhosis do not correlate with parameters of body composition or metabolism but exclusively with reduced liver function and altered hepatic hemodynamics. (+info)
Endovascular treatment of central venous stenoses in patients with dialysis shunts.
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OBJECTIVE: Evaluation of long-term results of percutaneous treatment of central vein stenoses or occlusions in patients with haemodialysis shunt. MATERIALS AND METHODS: In 26 patients with haemodialysis shunts and confirmed central vein stenosis or occlusion, 28 primary percutaneous transluminal angioplasties (PTA) and 5 repeated PTAs (re-PTA) were performed; in three patients a stent was implanted - primary in one patient and due to early restenosis after PTA in two patients. To maintain stent patency, 10 re-PTA were performed. RESULTS: The technical success rate of primary interventions was 96 % (100 % in stenoses and 50 % in occlusions). Primary post-PTA patency rate was 70 % at 3 months, 60 % at 6 months and 30 % at 12 months. CONCLUSION: PTA with possible stent implantation is a first-choice method in the treatment of stenoses and occlusions of the central venous system. Despite the relatively frequent re-interventions, endovascular treatment is capable to preserve long-term function of the dialysis shunt. (+info)
Splenorenal reflex modulates renal blood flow in the rat.
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We have previously shown that the splenorenal reflex controls renin release through splenic afferent and renal sympathetic nerves. We proposed that this reflex would also affect renal blood flow (RBF). RBF was measured in male Long Evans rats using transit-time flow probes. There were no significant differences between any of the experimental groups with respect to baseline values of RBF (8.9 +/- 0.4 ml min(-1), n= 25) or mean arterial pressure (MAP, 98.7 +/- 2.5 mmHg, n= 25). Splenic venous pressure was selectively raised (from 7.9 +/- 0.6 to 21.6 +/- 0.3 mmHg, n= 25) in anaesthetized rats by partial ligation of the splenic vein. This caused an immediate fall in RBF (-2.1 +/- 0.2 ml min(-1), n= 7) and in MAP (-12.4 +/- 2.8 mmHg, n= 7). The fall in RBF, but not the fall in blood pressure, was attenuated by renal denervation (DeltaRBF: - 0.7 +/- 0.1 ml min(-1), n= 6), splenic denervation (DeltaRBF: -0.8 +/- 0.1 ml min(-1), n= 6) and close renal arterial injection of the alpha1-adrenergic blocker phenoxybenzamine (12.5 microg; DeltaRBF: -0.8 +/- 0.1 ml min(-1), n= 6). Renal conductance fell only in the intact control group, i.e. the residual fall in RBF in the denervated and phenoxybenzamine-treated animals could be attributed to the fall in MAP. We also showed that splenic vein occlusion increased both splenic afferent (from 3.0 +/- 0.3 to 6.6 +/- 0.6 spikes s(-1), n= 5) and renal efferent (from 24.8 +/- 2.0 to 50.2 +/- 4.9 spikes s(-1), n= 9) nerve activity. We conclude that obstruction to splenic venous outflow, such as would occur in portal hypertension, initiates increased splenic afferent nerve activity and renal vasoconstriction through the splenorenal reflex, as well as a fall in blood pressure. We propose that this contributes to the renal and cardiovascular dysfunction observed in portal hypertension. (+info)