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Arteriovenous Difference (arteriovenous + difference)
Selected AbstractsThe noradrenaline plasma concentration and its gradient across the lungEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2000Marenzi Background We investigated the lung contribution to circulating noradrenaline (NA) homeostasis. Evaluation of the transpulmonary NA gradient, related to the NA amount entering the lungs, is potentially important, mainly regarding clinical conditions, such as congestive heart failure (CHF), that are associated with excessive circulating NA. Materials and methods 15 moderate (group 1) and 15 severe (group 2) CHF patients, and 10 normal individuals had determination of NA transpulmonary gradient in the baseline and during rise (exercise, in normals and group 1) or fall (withdrawal from plasma by ultrafiltration, in group 2) of plasma NA. Results NA gradient (pg mL,1) at rest was 30 ± 3 in normals, 21 ± 6 in group 1 and 5 ± 8 in group 2. Increase of NA concentration in the mixed venous blood with exercise was paralleled by depression of the transpulmonary gradient. Pulmonary arteriovenous difference disappeared when NA entering the lungs averaged 1300 pg mL,1. In group 2, ultrafiltration lowered NA in the mixed venous blood from 1225 ± 213 to 718 ± 182, which caused transpulmonary gradient to increase from 5 ± 8 to 22 ± 9. Conclusions Transpulmonary gradient of NA diminishes when NA entering the lungs increases, and 1300 pg mL,1 in the pulmonary artery is, both in patients and normal subjects, the level at which gradient disappears; which likely reflects cessation of NA uptake or achievement of a balance between lung uptake and production. This may have physiological and pathological implications. [source] The role of arginine vasopressin in human labour: functional studies, fetal production and localisation of V1a receptor mRNABJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 1 2002S. Thornton Objective To investigate labour-associated changes in: 1. the myometrial contractile response to arginine vasopressin compared with oxytocin in vitro 2. fetal production of arginine vasopressin and 3. myometrial vasopressin V1a receptor mRNA. Design The contractile response to vasopressin (compared with oxytocin) was investigated in paired myometrial strips in vitro. Blood was taken from the umbilical artery and vein at delivery and arginine vasopressin measured by radio-immunoassay. V1a receptor mRNA was determined by in situ hybridisation. Results Myometrium was more sensitive to arginine vasopressin than oxytocin (P <0.05 for frequency, amplitude and activity integral in paired strips) after, but not before labour. There was a marked umbilical arteriovenous difference in arginine vasopressin concentration at delivery suggesting fetal production which was not influenced by labour. Myometrial vasopressin V1a receptor mRNA was not increased after the onset of labour. Conclusions The human uterus is extremely sensitive to arginine vasopressin in vitro. Arginine vasopressin is produced by the fetus but fetal formation is not increased during labour. [source] Noninvasive oximetry and glaucomaACTA OPHTHALMOLOGICA, Issue 2009OB OLAFSDOTTIR Purpose To investigate retinal vessel oxygen saturation in relation to glaucomatous visual field damage. Specifically, we examined whether oxygen saturation in retinal blood vessels differs between regions corresponding to glaucomatous visual field defects compared to regions without visual field defects. Methods A spectrophotometric retinal oximeter (Oxymap ehf, Reykjavík, Iceland) was used to measure oxygen saturation in retinal arterioles and venules. The oximeter consists of a fundus camera, beam splitter, light filters and software that evaluate the oxygen saturation. The glaucomatous defect was estimated from a visual field test using the Octopus 1-2-3 perimeter. One eye in 13 individuals with open angle glaucoma with or without pseudoexfoliation syndrome was examined. Results In retinal areas with no visual field defect, the mean oxygen saturation in arterioles was 102±6% and 65±9%, (mean±SD) in venules. The arteriovenous difference was 37±10%. In retinal areas corresponding to visual field defects, the mean oxygen saturation in arterioles was significantly lower; 98±5% (p=0.04, paired t-test, n=13). The venules were at 68±7% (p=0.3) and the arteriovenous difference was also significantly lower; 30±10% (p=0.04). Conclusion Arteriolar oxygen saturation and arteriovenous difference is statistically lower in areas with visual field defects compared to areas without visual field defects. This data suggests that visual field defects are associated with a reduction in retinal oxygen delivery and metabolism. [source] Elective coronary angioplasty with 60 s balloon inflation does not cause peroxidative injuryEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2002K. Cedro Abstract Background The aim of this study was to evaluate the ongoing controversial issue of whether ischemia/reperfusion during elective coronary angioplasty evokes myocardial peroxidative injury. Design We measured indicators of free radical damage to lipids (free malondialdehyde) and proteins (sulphydryl groups) in coronary sinus blood in 19 patients with stable angina who were undergoing elective angioplasty for isolated stenosis of the proximal left anterior descending coronary artery. Ischemia induced by 60 s balloon inflations was confirmed by lactate washout into coronary sinus after deflation, with immediate and 1 min samples. Peroxidative injury was assessed from washout of (a) malondialdehyde measured directly by high performance liquid chromatography and (b) reduced sulphydryl groups, inverse marker of protein oxidative stress. Results Mean lactate concentration immediately after each deflation increased by 120,150% of the initial value, confirming ischemia and showing that blood originated largely from the ischemic region. Lack of myocardial production of malondialdehyde was confirmed by (a) no arteriovenous differences in individual basal concentrations (aortic, range 0·33,12·03 nmol mL,1, mean 7·82; coronary sinus blood, range 0·52,15·82 nmol mL,1, mean 8·18), and (b) after deflations, mean concentrations were not significantly different from preocclusion value. There was no decrease in concentration of sulphydryl groups throughout angioplasty. Conclusion Elective coronary angioplasty with 60 s balloon inflations is a safe procedure that does not induce peroxidative myocardial injury as assessed by methods used in the present study. [source] Interorgan ammonia and amino acid metabolism in metabolically stable patients with cirrhosis and a TIPSSHEPATOLOGY, Issue 5 2002Steven W. M. Olde Damink Ammonia is central to the pathogenesis of hepatic encephalopathy. This study was designed to determine the quantitative dynamics of ammonia metabolism in patients with cirrhosis and previous treatment with a transjugular intrahepatic portosystemic stent shunt (TIPSS). We studied 24 patients with cirrhosis who underwent TIPSS portography. Blood was sampled and blood flows were measured across portal drained viscera, leg, kidney, and liver, and arteriovenous differences across the spleen and the inferior and superior mesenteric veins. The highest amount of ammonia was produced by the portal drained viscera. The kidneys also produced ammonia in amounts that equaled total hepatosplanchnic area production. Skeletal muscle removed more ammonia than the cirrhotic liver. The amount of nitrogen that was taken up by muscle in the form of ammonia was less than the glutamine that was released. The portal drained viscera consumed glutamine and produced ammonia, alanine, and citrulline. Urea was released in the splenic and superior mesenteric vein, contributing to whole-body ureagenesis in these cirrhotic patients. In conclusion, hyperammonemia in metabolically stable, overnight-fasted patients with cirrhosis of the liver and a TIPSS results from portosystemic shunting and renal ammonia production. Skeletal muscle removes more ammonia from the circulation than the cirrhotic liver. Muscle releases excessive amounts of the nontoxic nitrogen carrier glutamine, which can lead to ammonia production in the portal drained viscera (PDV) and kidneys. Urinary ammonia excretion and urea synthesis appear to be the only way to remove ammonia from the body. [source] | ||||||||||