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Biomedical subjects

F Fyhrquist

Publications and source records attributed to F Fyhrquist.

At least 181 records · Page 10Linked to original sources
PubMed1984

Inhibitor binding assay for angiotensin-converting enzyme.

We describe a new principle for the determination of enzymes, here applied to angiotensin-converting enzyme (ACE, EC 3.4.15.1) in human serum. The enzyme inhibitor binding assay is based on specific binding of labeled inhibitor to the active center of the enzyme. Serum (10-15 microL) is incubated with 125I-labeled ACE inhibitor (" 351A ," a p- hydroxybenzamidine derivative of N-(1-carboxy-3-phenylpropyl)-L-lysyl-L-proline) at pH 7.0 at 37 degrees C for 2 h in a non-equilibrated system. Inhibitor bound to ACE is separated by adsorption to coated charcoal, the radioactivity remaining in the supernate is counted, and the ACE value is calculated from a standard curve. Sensitivity for ACE in serum is 200 U/L, corresponding to 5.0 ng of ACE purified from human lung. The coefficient of variation was 3.9% within assay, and 6.4% between assays for normal ACE activities. Correlation with a comparison spectrophotometric method (Am J Med 59: 363-372, 1975) for ACE assay was excellent (r = 0.98) in 59 samples from healthy subjects and from patients with various diseases including active sarcoidosis. The novel assay principle presented here is simple and specific, and can be extended to use with various biological fluids and tissues, and to other enzymes as well.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

The effect of fentanyl on arginine vasopressin and cortisol secretion during anesthesia.

The effects of nitrous oxide-oxygen plus small doses of fentanyl with (N = 7) and without (N = 15) naloxone and the effects of nitrous oxide-oxygen plus halothane (N = 13) on plasma concentration of arginine vasopressin (AVP) and cortisol were studied in normal patients before and during gynecologic laparotomies. Patients given fentanyl alone received incremental doses of 0.002 mg/kg before, during, and after induction of anesthesia. Naloxone, when given, was injected in doses of 0.005 mg/kg before administration of fentanyl. In the fentanyl group, the induction of anesthesia resulted in a significant increase in the plasma AVP levels and a significant decrease in cortisol levels. In contrast, while the halothane group also showed a decrease in plasma cortisol level, there was no change in the AVP levels. There were comparable increases in AVP and cortisol levels in both groups during surgery. Administration of naloxone before fentanyl prevented the increase of plasma AVP levels during anesthesia and surgery and blunted the elevation of plasma cortisol during surgery. Our results suggest that the increase in plasma AVP levels after induction of fentanyl anesthesia may not be induced by the stress of intubation and that small doses of fentanyl may cause AVP release during anesthesia.

Adult↗
PubMed1983

Immunological features of patients with chronic sclerosing osteomyelitis of the mandible.

Immunological status was studied in 15 patients, aged 11 to 71 years, with chronic sclerosing mandibular osteomyelitis. Duration of disease ranged from 1 to 16 years. Routine serological and immunological tests revealed some abnormality in all patients. All except one had an accelerated ESR. The Waaler-Rose titre was raised in 3 patients; in 1 it was 2000 (normal less than 32). Nuclear antibodies were detected in 2 patients, organ-specific antibodies in 3, and antibodies to double-stranded DNA in 1. In only 4 patients were the serum concentrations of immunoglobulins IgG, IgA, IgM and IgE within normal limits; all had normal concentrations of C3 and C4. None had raised antibody titres against viruses or precipitating antibodies to either milk protein or gluten. In none could evidence of food allergy be detected. PHA stimulation of lymphocytes was normal in all patients. HLA-typing in 12 patients showed that 4 had the antigen B13, 3 had B27, and of these 3 patients had the combination B13, B27. The function of neutrophils was studied in 5 patients. In all these patients the chemokinesis was significantly increased, whereas other phagocytic activities were normal. Most of our patients had a hyperactive humoral immune response. The clinical relevance of this finding awaits further, mainly immunogenetic, study.

Adolescent↗
PubMed1983

Immunogenetic markers and immune response in patients with recurrent oral ulceration.

20 patients, aged 20 to 72 years (mean 36.5 years), 14 with recurrent (RAS) and 6 with recurrent cicatrizing (RCAS) aphthous stomatitis were studied. 3 patients (15%) had the HLA locus A11 antigen, whose frequency in the Finnish population is 8%. 5 patients (25%) had B12, which occurs in 15% of the normal population. Results of routine serological tests were normal. All had normal serum levels of IgG, IgM, IgA and complements C3 and C4. 4 patients, 2 with RAS and 2 with RCAS, had raised serum IgE. Precipitating antibodies against milk protein were detected in 2 patients and against gluten in 1. In 4 patients, tests for immediate allergy were positive. 5 patients had antibodies to double-stranded DNA. Delayed hypersensitivity reactions were normal, and the PHA stimulation of lymphocytes elicited normal T-cell responses in all patients except one with RCAS. In this patient, there was a striking parallelism between an increase in PHA-reactive lymphocytes and clinical improvement. The serum of this patient contained a binder for 125I-labelled PHA, a binder not consistently detected in the other patients with ROU. Lymphocyte dysfunction may play a rôle in ROU. Of the 16 biopsy specimens of aphthous tissue studied by direct immunofluorescence for IgG, IgM, IgA, fibrinogen and C3, 15 specimens contained deposits of C3 in and along mucosal vessels, whereas among the 15 controls only 1 specimen of erosive lichen planus showed deposits of C3 along capillary walls. Immune complexes precipitating in capillary walls appear to be a common feature of ROU.

Adult↗
PubMed1983

Marathon run: effects on plasma renin activity, renin substrate, angiotensin converting enzyme, and cortisol.

Altogether 33 Finnish amateur runners were studied before and after a non-competitive Marathon run over the classical itinerary in Athens in 1976 (n = 8), 1977 (n = 14) and 1978 (n = 11). Plasma renin activity (PRA) rose 3-fold in all runs, whereas plasma renin substrate (RS) concentration did not change significantly. Serum angiotensin converting enzyme (ACE) activity was not changed. Serum cortisol concentration was increased 2-3 fold. The unchanged plasma RS concentration, in spite of increasing PRA, indicates that plasma RS is kept within normal limits during prolonged strenuous physical exercise. One contributing mechanism may be stimulation of RS biosynthesis by cortisol. Low PRA levels in two old runners, 65 and 83 years old, may indicate a decreased ability to respond with renin release to the stimuli of physical exercise.

Adult↗
PubMed1983

Sustained antihypertensive effect of captopril combined with diuretics and beta-adrenergic blocking drugs in patients with resistant hypertension.

Ten patients with severe hypertension and unsatisfactory blood pressure control during combined therapy with beta-adrenergic blocking drugs, diuretics, and vasodilators were treated with gradually increasing doses of captopril. Vasodilators were discontinued 24 hours prior to captopril administration. Six patients had essential, two renal, and two renovascular hypertension. Mild renal impairment was observed in four patients. Captopril effectively decreased blood pressure for 3 hours in all patients after the first dose. The antihypertensive effect appeared to be triphasic and was sustained in all but one patient during 12 months of observation. Captopril doses of 25-75 mg t.i.d. were sufficient to achieve acceptable blood pressure control (RR less than or equal to 160/100 mmHg) when given in the above mentioned combination. Side-effects were few and tolerable and discontinuation of captopril was not required.

Adrenergic beta-Antagonists↗
PubMed1983

Long-term 1,25-dihydroxycholecalciferol treatment in renal failure.

1,25-Dihydroxycholecalciferol (1,25-DHCC) was administered to four patients on maintenance hemodialysis and to four patients with renal failure not requiring hemodialysis. Secondary hyperparathyroidism was found in both groups of patients. Before initiation of 1,25-DHCC treatment both groups had serum 1,25-DHCC levels below the normal range (33.1 +/- 15.3 pg/ml). During the treatment period, serum 1,25-DHCC concentrations were normalized. Parathormone concentration in serum decreased in both groups during the observation period. Serum calcium concentration was normalized in patients with renal failure and within the upper normal range in patients on maintenance hemodialysis. Bone biopsy and densitometry, of the radius showed a trend towards normalization of bone during the treatment period, while X-ray studies showed no clear effect of 1,25-DHCC treatment. This study shows that changes in bone mineralization can be reversed by normalization of 1,25-DHCC.

Adolescent↗
PubMed1983

Decrease of serum angiotensin converting enzyme activity after discontinuation of captopril treatment.

Serum ACE activity increased as expected about three-fold following six weeks of captopril (30 mg/kg/day) treatment in Wistar rats (n = 9). The effect on serum and lung ACE activity and concentration, respectively, was studied after captopril discontinuation. Serum ACE activity was measured at start and 3, 6, and 12 days after captopril withdrawal. The approximal half-life of serum ACE activity was 72 hours as judged from the decrease rate after stimulated ACE biosynthesis induced by captopril. No differences in lung plasma membranes and lung homogenate ACE concentrations between treated and untreated rats were observed 12 days after discontinuation of captopril treatment. Serum ACE activity remained unchanged in the control rats (n = 9). We conclude that induction of ACE biosynthesis in the rat is reversible after withdrawal of captopril.

Animals↗
PubMed1983

Vasopressin, ACTH and neonatal haemodynamics.

In 21 normal deliveries, high concentrations of AVP and ACTH in cord blood were associated with higher blood pressure and lower skin temperature, indicating peripheral vasoconstriction. Following Caesarean section after the onset of labour (n = 8), cord AVP concentrations and blood pressures were lower than after normal delivery but higher than after elective Caesarean section (n = 9). Maternal AVP concentrations at delivery were normal, as were plasma AVP concentrations in all infants 3 days after delivery. The relationship between vasopressin, a potential ACTH releasing factor, and ACTH was interesting. We conclude that the massive release of vasopressin is associated with normal delivery, elevated ACTH values and with peripheral vasoconstriction. These findings reflect favourable adaptation to hypoxia and stress of delivery, intended to redistribute cardiac output to vital organs and may provide for physiological adjustments necessary for extrauterine life.

Adrenocorticotropic Hormone↗
PubMed1983

The induction of angiotensin converting enzyme by its inhibitors.

The inhibitors of angiotensin converting enzyme (ACE), captopril and enalapril, were found to increase ACE concentration in cultured human endothelial cells from cord artery as measured with a novel ACE assay employing MK 351A, an inhibitor of ACE, and with immunofluorescense labeling using anti-human lung ACE antibody. Dexamethasone (10 nM) also increased ACE and potentiated the increase of cellular ACE caused by captopril. Similar effects of ACE inhibitors were seen in cultured human macrophages, particularly after prestimulation with E. coli lipopolysaccharide. In Wistar Kyoto rats, captopril caused a 3-fold increase of serum ACE, while dexamethasone (40 ug/day, 14 days) did not increase serum ACE. Combined treatment with captopril and dexamethasone caused a 5-fold increase of ACE in purified lung plasma membranes. ACE inhibitors induce increased ACE biosynthesis in endothelial cells, and in macrophages. The rise of cellular ACE with ACE inhibitors is potentiated by glucocorticoid.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

Regulation of angiotensin converting enzyme.

Angiotensin converting enzyme (ACE;EC 3.4.15.1), or kininase II, was studied in serum, cultured endothelial cells from cord artery, in macrophages of humans, and in serum and purified plasma membranes of rats following treatment with inducers of ACE biosynthesis. ACE activity was measured in biological fluids with an enzyme kinetic method employing synthetic 1-hipp-1-his-l-leu tripeptide as a substrate, and with a new method using 125I-labelled specific inhibitor of ACE as a sensitive probe for ACE binding sites. The latter technique also proved suitable for the quantification of ACE in cells. Anti-human ACE antibody was employed for immunofluorescence studies in human cells. Dexamethasone treatment caused an increase in ACE in cultured human endothelial cells, macrophages and in rat pulmonary plasma membranes, but failed to increase serum ACE activity in rats. Captopril and enalapril treatment of hypertensive patients increased total serum ACE, the increase being evident after removal of the active drug from the serum by prolonged storage or chloramine T treatment (captopril) or by dialysis (enalapril). Captopril increased the ACE content of endothelial cells and macrophages. Macrophages appeared sensitive to captopril induction of ACE biosynthesis after pre-stimulation with Escherichia coli lipopolysaccharide. Dexamethasone treatment potentiated the known induction of ACE in rat pulmonary tissue. Thus ACE biosynthesis may be enhanced by three categories of treatment: (1) glucocorticoid; (2) macrophage activation; (3) ACE inhibitors. The precise mechanism of ACE induction and its possible biological relevance await further clarification.

Adult↗
PubMed1983

Plasma renin substrate and oestrogens in normal pregnancy.

Relationship between concentrations of serum oestrogens, plasma renin substrate and plasma renin activity were studied in six women throughout pregnancy. There was a significant positive correlation between serum oestradiol-17 beta and plasma renin substrate concentrations (r=0.60). Serum oestriol concentrations also correlated significantly with plasma renin substrate concentrations (r = 0.68). Correlation coefficients calculated separately for each subject throughout pregnancy were higher than those for the whole group. Also, there was much individual variation in dose-response of serum oestrogens to plasma renin substrate concentrations. There was no significant correlation between serum oestrogens and plasma renin activity. Our results support the view that oestrogens cause the increase in plasma renin substrate concentration during pregnancy, and emphasize the individual variation in response of renin substrate concentration to serum level of oestrogens.

Estradiol↗