[Kidney failure in an elderly woman].
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Aged↗
Biomedical subjects
K Metsärinne
Publications and source records attributed to K Metsärinne.
Effect of oxygen on pulmonary hemodynamics and incidence of atrial fibrillation after noncardiac thoracotomy.
OBJECTIVE: The mechanism of postthoracotomy atrial fibrillation (AF) could be related to right ventricular (RV) strain. The effect of oxygen on the occurrence of postoperative AF and on RV function was studied. DESIGN: A prospective, randomized study. SETTING: A university hospital. PARTICIPANTS: Twenty-four noncardiac thoracotomy patients. INTERVENTIONS: At the end of the postoperative anesthesia care unit period, the patients were randomly allocated to receive 35% oxygen until either the third (P = prolonged group) or the first postoperative morning (S = short group). MEASUREMENTS AND MAIN RESULTS: Measurement of hemodynamic variables using a thermodilution pulmonary artery catheter, oxygenation, concentration of plasma atrial natriuretic peptide (ANP) and Holter monitoring were started preoperatively and continued for the 3 postoperative days (PODs). Systolic RV pressure (systolic RVP) and pulmonary vascular resistance (PVR) increased postoperatively only in group S. Major changes in RV performance were not seen with echocardiography or the thermodilution method in any patient. Silent episodes of AF occurred in three patients (25%) in group P and in one patient (8%) in group S (not significant [NS]) without deviations in plasma ANP concentration. On each of the 3 PODs, all patients were exposed to 60% oxygen for 15 minutes. Systolic RVP decreased significantly during the exposure to 60% oxygen only in group S, but not in patients developing AF. Predictive factors for AF were a high preoperative PVR, intraoperative bleeding necessitating volume loading, and elevated systolic RVP immediately after thoracotomy. CONCLUSION: Short episodes of AF occurred irrespective of the length of oxygen therapy. Occurrence of AF could not be explained by changes in RV function.
Atrial Fibrillation↗
Carvedilol and its metabolites suppress endothelin-1 production in human endothelial cell culture.
Carvedilol (0.25-25 microM), an antihypertensive drug is shown here to reduce endothelin-1 (ET-1) production in cultured human umbilical cord endothelial cells. Two of its metabolites, M14 and M21 (2.5-25 microM) also suppressed ET-1 production, less potently, however, than carvedilol. Carvedilol is a multiple-acting compound with non-selective beta-adrenoceptor and selective alpha 1-adrenoceptor blocking activity, calcium channel blocking and anti-oxidant activity. To study whether these activities were related to suppressed ET-1 production, endothelial cells were treated with a beta 1-blocker, metoprolol (1-10 microM), a non-selective beta-blocker, propanolol (1-10 microM), an alpha 1-blocker, prazosin (1-10 microM), a calcium channel antagonist, nicardipine (1-10 microM), or with the antioxidative compounds probucol (1-100 microM) and ascorbic acid (1-100 microM). None of these compounds modified ET-1 production. The inhibitory effects of carvedilol, M14 or M21 on ET-1 production were not reversed by N Nitro-L-arginine methyl ester (L-NAME) (1.9 mM), or by indomethacin (1.5 microM), suggesting that mechanisms other than the stimulation of nitric oxide or prostacyclin production were involved.
Adrenergic alpha-Antagonists↗
Degradation of endothelin-1 by extracts of rat lung, kidney, and liver.
Degradation of 125I-labeled endothelin-1 (125I-ET-1) when incubated 120 min at 37 degrees C with rat lung, kidney and liver plasma membrane extracts was examined using HPLC. Lung and kidney extracts showed degrading enzyme activity, but none was found in liver extract. EDTA almost abolished degradation of 125I-ET-1 in lung and kidney extracts. Phosphoramidon and SCH 39370, both inhibitors of neutral endopeptidase 24.11 (NEP), markedly inhibited degradation of 125I-ET-I in lung extract and clearly less in kidney extract. Soybean trypsin inhibitor (STI) and elastase inhibitor partly inhibited degradation in lungs and in kidney extract. Leupeptin had no inhibitory effect neither in lung nor in kidney extract. Our results suggest: (1) at least two types of enzymes degrade ET-1 in lung and kidney extracts, namely metallo-proteinases and serine proteinases. (2) The ET-1 degrading effect appears to be different in lungs and kidneys, metallo-proteinases being more important in pulmonary than in renal degradation of ET-1.
Animals↗
Effects of prolonged tourniquet ischaemia and short-term venous stasis on plasma endothelin-1 levels in man.
In vitro studies have indicated increased endothelial release of endothelin during tissue and cellular hypoxia. Therefore, we studied the effect of tourniquet ischaemia and venous stasis on plasma endothelin-1 (ET-1) levels in humans in vivo. The effect of hypoxia on plasma ET-1 levels in 16 patients subjected to an orthopaedic operation and six healthy volunteers was studied by (a) tourniquet ischaemia, in which a limb is totally emptied of blood and kept ischaemic by means of a pneumatic tourniquet, and (b) venous stasis in an upper arm. The mean (SEM) basal plasma ET-1 concentration in the patients subjected to tourniquet ischaemia of a lower limb was 4.1 (1.0) pg ml-1. No significant change in plasma ET-1 levels during or after tourniquet ischaemia was found. The mean (SEM) plasma ET-1 concentration in six healthy subjects prior to venous occlusion in the right upper arm was 3.3 (0.7) and 2.7 (0.3) pg ml-1 in the right and left arm, respectively. A significant increase in plasma ET-1 concentration after 20 min was observed in the arm subjected to venous stasis, but not in the other, control, arm. Mean arterial blood pressure did not change significantly. Local tissue hypoxia may not be an important stimulus for ET-1 release in humans in vivo, whereas short-term venous occlusion in an upper arm leads to local release of ET-1 by an as yet unknown mechanism.
Adult↗
The effect of aortic coarctation on expression of endothelin-1 and endothelin receptors in heart and lungs.
Expression of prepro-endothelin-1 (ppET-1), and endothelin (ET) receptor subtype (ETA, ETB) mRNAs was studied in atria, ventricles, and lungs of aortic coarctated rats. During 8 weeks following aortic banding, rats developed ventricular hypertrophy. The levels of expression of ppET-1, ETA- and ETB-receptors were significantly lower in the ventricles of coarctated rats than in sham-operated animals. In atria, the level of expression of ppET-1, ETA and ETB-receptors was not significantly changed. These results indicate that production of ET-1 is decreased and ETA and ETB-receptors are down-regulated in hypertrophied ventricles 8 weeks after aortic coarctation. This may be a compensatory response to pressure overload.
Animals↗
Role of angiotensin II in blood pressure regulation and in the pathophysiology of cardiovascular disorders.
Angiotensin II (Ang II) raises blood pressure (BP) by a number of actions, the most important ones being vasoconstriction, sympathetic nervous stimulation, increased aldosterone biosynthesis and renal actions. Other Ang II actions include induction of growth, cell migration, and mitosis of vascular smooth muscle cells, increased synthesis of collagen type I and III in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. These actions are mediated by type 1 Ang II receptors (AT1), and may be blocked by losartan, a specific blocker of AT1 receptors. In particular, studies employing losartan have shown that Ang II is an important contributor to BP regulation and plays a significant role in hypertension and in the pathophysiology of vascular damage during the course of hypertension. Ang II is also involved in the process of atherosclerosis and in remodelling and repair processes of the myocardium following myocardial infarction. Finally, increased Ang II is an important part of neurohumoral activation in heart failure. Exciting new discoveries concerned with polymorphisms of genes coding for angiotensin converting enzyme (ACE) and angiotensinogen suggest that Ang II may be genetically associated with increased risk for myocardial infarction, hypertension and left ventricular hypertrophy.
Angiotensin II↗
Insulin increases the release of endothelin in endothelial cell cultures in vitro but not in vivo.
Endothelin-1 (ET-1), a potent vasoconstrictor and mitogenic peptide for vascular smooth muscle cells, may be a marker for development of vascular disorders in diabetic patients. The aim of this study was to elucidate the possible role of insulin in the regulation of ET-1 production. The effect of hyperinsulinemia (with and without concomitant hyperglycemia) on the release of ET-1 was studied in 23 healthy men in vivo, as well as in human umbilical cord vein endothelial cell (HUVEC) cultures in vitro. Plasma glucose and insulin were maintained at four desired levels (from 5 to 22 mmol/L and 0.065 to 12.9 nmol/L, respectively) during the in vivo studies. The mean (SEM) plasma ET-1 during normoglycemia and a fasting insulin concentration in healthy men was 3.8 (0.4) pg/mL, and ET-1 levels did not change in response to changes in the concentration of glucose (from 5.0 to 22 mmol/L) or insulin (from 0.065 to 12.9 nmol/L). The ET-1 concentration in HUVEC culture medium increased linearly during 24 hours, and insulin further enhanced the release of ET-1 dose-dependently. ET-1 release was stimulated by angiotensin II, thrombin, and transforming growth factor-beta (TGF-beta), whereas treatment with glucose and insulin-like growth factor-1 (IGF-1) was not associated with changed ET-1 levels in culture medium. Our results show that although high insulin concentrations stimulate ET-1 release in vitro, hyperinsulinemia is not associated with increased plasma ET-1 levels in healthy men in vivo. The role of insulin in the regulation of ET-1 production in vivo, if any, remains unsettled.
Adult↗
Endothelin antiserum decreases volume-stimulated and basal plasma concentration of atrial natriuretic peptide.
BACKGROUND: Endothelin-1 (ET-1) is the most powerful factor known to release atrial natriuretic peptide (ANP) in vivo and in cultured cardiac myocytes or preparations of atrium. We tested the role of endogenous ET-1 in the regulation of ANP release by passive immunization in anesthetized rats. METHODS AND RESULTS: Intravenous injection of antiserum against ET-1 was shown to decrease basal and volume-stimulated plasma concentrations of ANP, whereas control serum was without effect. Antiserum generated in rabbits cross-reacted 100% with endothelin-2 and -3. In pentobarbital-anesthetized Wistar rats treated with ET-1 antiserum, plasma ANP concentration measured by radioimmunoassay was reduced by 37% from starting level after 10 minutes and by 30% after 60 minutes. Control rat serum had no effect on plasma ANP. Rapid intravenous infusion of 8 mL of 0.9% NaCl caused a sixfold increase of plasma ANP concentration in control rats but only twofold in rats pretreated with ET-1 antiserum (P < .01). This effect of ET-1 antiserum was dose dependent. ET-1 antiserum changed neither blood pressure nor heart rate significantly in anesthetized rats. Pretreatment with ET-1 antiserum did not affect the initial hypotensive response to intravenous ET-1 0.5 nmol/kg but significantly attenuated the subsequent hypertensive response to endothelin. CONCLUSIONS: Endothelin may be a physiological modulator of both basal and stimulated ANP release.
Animals↗
Biocompatibility of polyethylene and host response to loosening of cementless total hip replacement.
A human lymphocyte culture protocol was used to identify the biocompatibility pattern of fine particulate ultra-high molecular weight polyethylene. Polyethylene did not cause an increase in lymphocyte DNA synthesis as assessed by the 3H-thymidine incorporation method on culture Days 1, 3, nor 5. As analyzed with monoclonal activation markers, the polyethylene dependent expression of major histocompatibility complex (MHC) class II antigen as well as interleukin-2 receptor (CD25) was virtually nonexistent. An apparent increase in the amount of CD11b positive monocytes/macrophages from 7% +/- 2% to 22% +/- 6% was recorded. Samples of pseudocapsules of the totally replaced hips (THR) obtained at revision operations for aseptic loosening of cementless prostheses with polyethylene lining of the acetabular component, were obtained from ten patients for immunopathologic studies. In seven cases the prostheses consisted of chromium-cobalt-molybdenum steel alloy and in three cases of titanium. Revisions were performed on average 4.6 years (range, 2.5-7) after insertion of the prostheses. The predominant cell in the lining cell layer of the periprosthetic cavity was in each case the CD11b, CD68, and nonspecific esterase positive but endogenous peroxidase-negative macrophage. Proline 4-hydroxylase positive fibroblasts dominated the stroma that was also inhabited by usually perivascular mononuclear cell infiltrations of mainly CD11b/CD68 phenotype with occasional CD4-positive cells. Only few mononuclear cells were activated CD25 positive T cells or CD19-positive B-lymphocytes. In titanium-based THRs, the cytoplasm of the macrophages contained a large number of small metallic particles, although this phenomenon was not seen in chromium-cobalt-molybdenum steel-based THRs. Fine particulate ultra-high molecular weight polyethylene is immunologically relatively insert. Nevertheless, it causes a clear foreign body type of phenomenon in vitro. The loosening of cementless acetabular components was associated with CD11b- and CD68-positive macrophage reaction in the pseudocapsular tissue. In any case, there is no clinical or experimental evidence to suggest that the use of cementless THR prostheses with polyethylene sockets would prevent an adverse biologic host response.
Adult↗
[The endothelial cell as an endocrine organ--endothelin].
Endothelin is a newly discovered potent vasoconstrictive polypeptide released by endothelial cells in response to various stimuli, including vasoactive peptides such as angiotensin II, adrenaline and vasopressin, and thrombocyte products like transforming beta growth factor and thrombin. Endothelin is believed to exert its main effects locally, in a paracrine or autocrine way. In vascular tissue, endothelin induces longlasting contraction of smooth muscle cells, leading to decreased blood flow, especially in the coronary and renal circulation, together with an increase in systemic blood pressure. It acts also mitogenically in vascular smooth muscle cells. Endothelin stimulates release of aldosterone and catecholamines in non-vascular tissue, and inhibits release of renin. A physiological function of endothelin may be to modulate vascular tone, and increased levels of circulating endothelin are seen after the "cold pressor test". Moreover, plasma endothelin concentration is elevated during acute myocardial infarction, in acute renal failure, in patients with hypertension, and during cardiogenic chock. What role endothelin plays in the development of these conditions, and in other disorders such as vascular spasm and atherosclerosis is uncertain.
Endothelins↗
Cytokine and acute-phase reactant levels in serum of children with cancer admitted for fever and neutropenia.
Serum concentrations of tumor necrosis factor-alpha (TNF alpha), interleukin (IL)-1 beta, IL-6, and the acute-phase reactants C-reactive protein (CRP) and serum amyloid A (SAA) were measured on admission in 46 neutropenic children with cancer in 81 episodes of fever. The aim was to find out whether any of these variables would differentiate true bacteremia from fever due to other causes. In most episodes serum concentrations of TNF alpha and IL-1 beta were elevated. IL-6 was detectable in 68%, but the serum concentration was elevated in only 15%. SAA proved to be more sensitive than CRP for the early detection of bacteremia. However, not even SAA was sufficiently accurate at the individual level. We conclude that the cytokine and acute-phase protein levels found were related to the febrile response but did not correlate with documented bacterial etiology.
Acute-Phase Proteins↗
Outcome of patients with secondary amyloidosis in dialysis treatment.
Between the years 1974 and 1987, 37 patients with secondary amyloidosis entered dialysis treatment at our department. All had amyloidosis secondary to chronic arthritic disease (35) or to other chronic inflammatory causes (2). Only two patients were maintained on CAPD throughout follow-up; 12 patients (32%) received a kidney transplant. Survival in dialysis at 1 year was 82%, at 2 years 46%, and at 3 years 37%. Survival of amyloidosis patients transplanted at the Finnish transplant centre within the same period was worse at 1 year, but better at 2 and 3 years, 70%, 62%, and 62% respectively, but the difference was not significant. Populations are not compatible, since patients were selected for transplantation. Infection was a common cause of death, 7/18 (39%) deaths; cardiac deaths were less common, only two myocardial infarctions and one cardiac arrhythmia (17%). Symptoms of cardiac amyloid infiltration indicated a poor prognosis, although it did not necessarily predict death of a cardiac cause. Cardiac infiltration of amyloid was more common in autopsy than previously reported (10 of 13 patients), probably indicating longer duration of amyloidosis in patients treated with renal replacement therapy. Patients who died within follow-up had a shorter interval between the start of primary disease and the development of amyloidosis than those who survived, 11.8 versus 17.7 years (P = 0.041), and also a slightly shorter period between diagnosis of amyloidosis and start of dialysis, 3.0 versus 4.4 years (P = 0.129). This indicates that the rate of progression of amyloidosis determines the development of disease-associated complications, and fast progression may predict serious outcome.
Adult↗
Immunoreactive interleukin-6 in serum of patients with B-lymphoproliferative diseases.
Serum immunoreactive interleukin-6 (ir-IL-6) concentration was measured by radioimmunoassay in nine patients with chronic lymphocytic leukaemia (CLL), 16 patients with multiple myeloma (MM), 12 patients with monoclonal gammapathy of undetermined significance (MGUS), 22 patients with primary Sjögren's syndrome (SS), and in 32 control subjects. Measurable quantities of ir-IL-6 were detected in every sample studied. Patients with MGUS and SS had significantly higher serum ir-IL-6 (mean +/- SD) concentrations (337 +/- 92 ng l-1 and 299 +/- 100 ng l-1, respectively) than controls (92 +/- 77 ng l-1) and patients with CLL and MM (120 +/- 32 ng l-1 and 113 +/- 58 ng l-1, respectively). Longitudinal studies of ir-IL-6 concentration in a few patients with MM showed a decrease before remission and an increase prior to relapse, but no consistent pattern was detected. In conclusion, we found that serum ir-IL-6 levels are higher in patients with benign hypergammaglobulinaemic states than in patients with malignant neoplastic B-cell disorders.
Adult↗
Radioimmunoassay of interleukin-6 in plasma.
We present a double-antibody radioimmunoassay for determining human interleukin-6 (IL-6) in biological fluids. The detection limit of the assay is 20 ng/L (B0 - 2 SD). Bound radioactivity in the range of 30% to 90% of the B0 counts corresponds to IL-6 concentrations of 100 to 14,000 ng/L. Analytical recovery of IL-6 added to EDTA-treated plasma averaged 25% more than that added to serum. The plasma concentration of IL-6 was therefore approximately 85 ng/L more than the concentration in simultaneously drawn serum. The mean serum concentration of IL-6 in 45 healthy subjects was 83 ng/L (range 20-290 ng/L), in 20 patients with multiple myeloma 303 ng/L, in 20 patients with rheumatoid arthritis 234 ng/L, and in 13 patients with systemic lupus erythematosus 183 ng/L. Markedly increased (greater than 3000 ng/L) concentrations of IL-6 were found in sera of patients with meningococcus meningitis and infectious peritonitis.
Adult↗
Increased plasma interleukin 6 and renin substrate levels during bacterial peritonitis in CAPD patients.
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Angiotensinogen↗
Raised plasma endothelin-I concentration following cold pressor test.
Plasma concentration of immunoreactive endothelin-1 was measured by radioimmunoassay in 6 healthy subjects before and following cold pressor test by immersion of one fore-arm into ice-water. Mean (SEM) plasma endothelin-1 concentration rose from 1.2 (0.7) to peak value 8.4 (2.3) pg/ml in venous plasma from the immersed hand, and, reaching peak 2 minutes later, from 1.4 (0.5) to 4.6 (2.3) pg/ml in venous plasma from the contralateral hand. In 66 healthy control subjects, venous plasma concentration of endothelin-1 was 2.9 +/- 1.2 pg/ml (mean +/- SD). Exposure to cold is associated with raised blood levels of endothelin-1, which points to a relation between endothelin-1 and vasoconstriction associated with low temperature.
Cold Temperature↗
Tissue distribution and half-life of 125I-endothelin in the rat: importance of pulmonary clearance.
Plasma half-life and organ uptake of endothelin 1 (ET-1) was studied in anaesthetized Wistar rats administering a bolus of 125I-labeled ET-1 into jugular vein, with and without a preceding dose of 1-80 ng of unlabeled ET-1, via the same route. Plasma half-life of intact 125I-ET-1 was 40 sec and that of total radioactivity 68 sec. Immunoreactivity of circulating 125I-ET was rapidly reduced, by 23% at 30 sec and by 43% at 360 sec, respectively. High power liquid chromatography of plasma extracts revealed a corresponding decrease of intact 125I-ET-1 peak with time. There was a predominant uptake of 125I-ET-1 in the lungs, 82%, and lesser by kidneys, 10%, heart 3.6%, liver, 2.7%, and spleen, 1.5%, respectively. Pretreatment with unlabeled ET-1 caused a dose-dependent shift of uptake from lungs to kidneys. We conclude that circulating ET-1 is rapidly cleared, primarily by the lungs, which may play an important role in protecting the systemic circulation from the vasoconstricting actions of ET-1.
Animals↗