ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1995.tb01552.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abstract.Although calcium salts are important components of gallstones, there are few data on the total and ionized calcium content of human bile. Therefore, in 14 fasting T‐tube patients studied 7–11 days after cholecystectomy, we measured bile flow, bile acid [BA], total [CaTOt] and free ionized [Ca++] calcium concentrations, in 20–30 min bile collections during acute BA pool depletion induced by 6–8 h of continuous bile drainage. During washout of the BA pool there were parallel falls in bile flow, BA output and total calcium output (correlation coefficients ranging from 0.59 to 0.99;P<0.02–0.001). In 12 of the 14 patients, [CaTOT] also fell (from 1.84 ± 0.29 to l.32 ± 0.34 mmol L‐1) in parallel with [BA] (from 34.0 ± 14.0 to 8.2 ± 8.0 mmol L‐1;r= 0.75–0.98;P<0.005). In contrast, biliary [Ca++] remained virtually unchanged. These data suggest that the BAs are linked to the bound, rather than to the free, ionized, fraction of biliary calcium, which is consistent within vivocalcium binding by BAs. A model is proposed in which BA‐induced biliary calcium secretion results from (i) bile acid‐induced water flow via solvent drag; and (ii) calcium binding in the bile canaliculus by bile acids, which induces paracellular diffusion of Ca++, thereby maintaining [Ca

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1995.tb01553.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abstract.Erythrocyte sodium‐lithium countertransport (SLC) is an obligatorily coupled equimolar exchange of intracellular sodium or lithium with extracellular sodium or lithium. SLC is partially inhibited by N‐ethylmaleimide (NEM) but only when a transported ion (sodium or lithium) is present in the extracellular medium. In essential hypertensive patients with a strong family history of hypertension the Km of SLC for extracellular sodium was lower and Vmax tended to be higher than in normal controls, but the ratio Vmax/ Km gave a much clearer distinction between the two groups. After NEM treatment, the remaining SLC activity in normal individuals had a lower Vmax and Km for sodium but Vmax/Km was not affected. In essential hypertensives the remaining SLC activity after NEM again had lowered Vmax and Km but in these patients the Vmax/Km was much lower than in untreated erythrocytes and was then the same as in normal controls. On the assumption that NEM reacts with a ‐SH group on a membrane protein that regulates SLC, and that the ratio Vmax/Km reflects a rate constant for binding extracellular sodium to the unloaded carrier, the results suggest that (a) essential hypertensives have an increased rate of sodium binding to the transporter and (b) this is due to abnormal behaviour of a membrane ‐S

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1995.tb01554.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abstract.The present study has evaluated the influence of high concentrations of cytochalasins B and E on the detergent‐resistant actin levels in fully spread platelets by PAGE gel electrophoresis, and the effects of the two inhibitors of new actin filament assembly on translocation of fibrinogen gold (Fgn/Au) labelled GPIIb‐IIIa receptors on the surface‐activated cells. Concentrations of 10‐ 4m and 10‐5m cytochalasin B and E reduced detergent‐resistant actin in fully spread platelets to levels present in resting discoid platelets in suspension. Despite reduction of actin filaments to levels in resting cells, cytochalasin B did not prevent translocation of Fgn/Au from platelet margins into channels of the open canalicular system (OCS). Similar concentrations of cytochalasin E completely blocked translocation of receptor‐ligand complexes and produced a patching phenomenon not observed in previous studies. Rinsing of the spread cells to remove cytochalasin, followed by incubation of the treated platelets in Hank's buffered salt solution (HBSS) restored levels of detergent‐resistant actin to those found in untreated, spread platelets. Resting grids of 105m cytochalasin E‐treated platelets on drops of HBSS for 15min restored their ability to clear FGN/Au linked to GPIIb‐IIIa from exposed surfaces to the OCS, but 10‐4m cytochalasin E‐treated cells remained anergic after incubation on drops of HBSS. Thus a fully assembled cytoplasmic actin filament cytoskeleton does not appear to be essential for translocating receptor‐ligand complexes on the platelet surface to the OCS, nor does its presence guarantee that the ability to clear GPIIb‐IIIa

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1995.tb01555.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abstract.Renal extraction and renal plasma clearance of atrial natriuretic peptide from pigs with complete unilateral ureteral obstruction (UUO) and from intact anaesthetized pigs were determined from arterio‐venous differences in plasma atrial natriuretic peptide and measured renal plasma flow. The effect of administration of either a cyclooxygenase inhibitor or an angiotensin converting enzyme inhibitor was examined during UUO. Renal extraction ratio and renal clearance rate of plasma atrial natriuretic peptide (ANP) in the intact pig was stable during the 15 h observation period. UUO resulted in a significant (P<0.05) temporary increase in renal extraction ratio and a significant (P<0.05) reduction in the renal clearance rate of atrial natriuretic peptide. During cyclooxygenase inhibition there was a significant increase in the renal extraction ratio of ANP. During angiotensin II converting enzyme inhibition, renal handling of atrial natriuretic peptide did not differ from that observed in control animals. The present data demonstrate that atrial natriuretic peptide is extracted by the obstructed kidney. Despite the significant reduction in renal blood flow during indo‐methacin administration, renal clearance of ANP was unaltered. The increase in ipsilateral renal extraction of atrial natriuretic peptide immediately after ureteral obstruction and indomethacin administration could be explained either by a direct influence of PGE2on the renal haemodynamics altering renal extraction of ANP, or by a compensatory mechanism attempting to preserve renal funct

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1995.tb01556.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abstract.In order to evaluate whether changes in plasma phospholipid composition are rapidly transmitted to the red blood cell membrane (RBCM) underin vivoconditions, the levels of major phospholipids in plasma, low density and high density lipoproteins (LDL and HDL) as well as in RBCM were determined before (pre), directly after (post) and 2 days after (48 h post) LDL apheresis in six patients with severe hypercholesterolaemia. LDL apheresis induced a 30–70% decrease in plasma and LDL cholesterol and total phospholipid levels within 2–3 h. Concomitantly, the percentages of plasma phosphatidylcholine (PC) and the PC/sphingomyelin (SM) ratio were increased compared to initial values. The percentage of plasma lyso PC (LPC) determined before apheresis in the patients was 30% lower with respect to the mean level of LPC in a normolipidaemic control. For LPC of LDL no differences were observed between normolipidaemia and hypercholesterolaemia. LDL apheresis induced a rise by about one third in the percentage of plasma LPC. At 48 h post, plasma LPC levels reapproached pre‐apher‐esis levels, while the percentages of PC and the PC/SM ratio remained elevated. The pattern of changes induced by apheresis in plasma PC, SM and LPC levels was mimicked by changes in RBCM phospholipids. Strong positive relationships were noted for PC, SM and PC/SM as determined at pre, post and 48 h post between plasma and RBCM. In summary, changes in plasma PC, LPC, and PC/SM ratios as induced by LDL apheresis are rapidly transmitted to the RBCM underin vivoconditions, most probably as a result of phospholipid transfer between both compartments. In addition, the percentages of LPC in plasma and LDL particles of patients with severe hypercholesterolaemia are certainly below the levels of LPC reported to mediate biological effects ofin vitrooxidi

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1995.tb01557.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abstract.In this study we examined whether the reduced fibrionolysis and increased platelet activity that are known to occur in hypertension are already present in borderline hypertension. Twelve patients with ‘borderline’ hypertension (diastolic blood pressure 90–95 mmHg) were found to have substantially reduced fibrinolytic activity, both at rest and during exercise, compared with 12 normotensive controls. Euglobulin clot lysis time (ECLT) was significantly higher in hypertensive subjects (218 min vs. 145 min;P<0.05), and this difference persisted during exercise. Resting tissue plasminogen activator activity (t‐PA) did not differ in the two groups, but the brisk increase in t‐PA in controls during exercise (0.64 rising to 1.4IU mL‐1;P<0.01) did not occur to the same extent in the borderline hypertensive subjects. Levels of the fast‐acting t‐PA inhibitor, normally referred to as PAI‐1, were considerably higher in hypertensives (9.22 vs. 4.41 IU mL‐1;P<0.02), and this difference persisted in the upright posture, indicating a decrease in fibrinolytic activity. Platelet aggregability induced by ADPin vitrowas not significantly higher in the hypertensive subjects, but indices of platelet activityin vivo(B‐TG and PF‐4 levels) revealed enhanced platelet function in the hypertensives. These results indicate that the indicators of altered haemostatic function known to occur in hypertension, namely diminished fibrinolytic activity and increased platelet function, are already detectable during the very earlie

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1995.tb01558.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abstract.We describe two siblings with fat malab‐sorption and jejunal chylomicron retention. Plasma lipoproteins were studied in the patients and their first‐degree relatives. The patients were a 14‐year‐old girl and her 8‐year‐old brother. Compared to healthy controls, they both had low fasting plasma concentrations of plasma total, HDL, and LDL cholesterol, as well as of apolipoproteins A‐I and B. No increase in plasma lipoprotein levels or detectable apo B‐48 was observed following an oral fat load. Histological studies of jejunal biopsy specimens obtained during fasting and 1 h postprandially showed severe steatosis, and an apparent block of chylomicron secretion from the endoplasmic reticulum into the Golgi apparatus was observed by electron microscopy. Liver biopsy specimens showed moderate steatosis and ultrastruc‐tural changes similar to those in the enterocytes. One healthy sister had a normal plasma lipoprotein pattern, and showed increased plasma triglyceride levels as well as the presence of apo B‐48 following an oral fat load. Both parents had normal plasma total cholesterol levels, but clearly reduced fasting concentrations of HDL cholesterol and apo A‐I. At least in this family, determination of plasma apo A‐I levels might thus prove useful in the identifi

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1995.tb01559.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Abstract.The effects of a continuous i.v. infusion of urodilatin at a dose of 30 ng kg‐1min‐1were studied in a patient with congestive heart failure. After 30 min, urodilatin had induced a marked stimulation of plasma cyclic GMP concentrations. In parallel haematocrit increased. No significant diuresis and no change of invasive haemodynamics was observed. After 2 h the patient developed a profuse perspiration. Eighty minutes later he suffered from dizziness due to hypotension (blood pressure 80/40 mmHg) and a sudden bradycardia (50bpm). Urodilatin was discontinued and symtoms were relieved by bed tilt and rapid infusion of isotonic saline solution. Mechanisms contributing to these adverse effects may be fluid extravasation to the third space and sympathoinhibitory effects known to occur with natriuretic peptide infus

ISSN:0014-2972    

DOI:10.1111/j.1365-2362.1995.tb01560.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY