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Biomedical subjects

M Stäubli

Publications and source records attributed to M Stäubli.

At least 55 records · Page 3Linked to original sources
PubMed1986

Plasma volume and proteins in voluntary hyperventilation.

In a controlled study the changes of the plasma volume and plasma proteins induced by voluntary hyperventilation (HV) were investigated in nine splenectomized volunteers. The plasma volume changes were calculated from the changes of the hemoglobin and hematocrit. After 20 min of HV in supine position, which lead to a decrease of the venous CO2 partial pressure by 19 Torr and to an increase of plasma epinephrine and norepinephrine levels, the plasma volume was reduced by 12.9%. The intravascular masses of total protein, albumin, and several other proteins decreased during HV but a similar decrease of these proteins was also observed during the control study (C), i.e., rest in supine position without HV. The differences between changes during HV and C were not significant, indicating that the loss of protein was not due to HV. It is concluded that acute HV leads to a rapidly reversible loss of a virtually protein-free solution from the vascular space. The red cell compartment participated in fluid shifts in that the mean red cell volume decreased by 2.2% (P less than 0.02 compared with C). Comparison with earlier work shows that addition of erythrocytes from the normal spleen does not play a part in the HV-induced increase of hemoglobin and hematocrit.

Adolescent↗
PubMed1985

Amiodarone-treated patients with suppressed TSH test are at risk of thyrotoxicosis.

Therapeutic use of the potent antiarrhythmic drug amiodarone requires early detection of impending hyperthyroidism, a potentially life-threatening adverse reaction in cardiac patients. Since amiodarone inhibits peripheral conversion of thyroxine (T4) to triiodothyronine (T3), serum T4 and T3 levels become unreliable parameters of thyroid function. In 44 patients treated with amiodarone for a median period of 7.3 months, up to seven TRH-TSH tests were performed. The TSH response to TRH was normal in 23 patients, partially suppressed in eight, totally suppressed in eight and overshooting in five patients. Two of the eight patients with suppressed TRH-TSH tests were clinically hyperthyroid, in four others thyrotoxicosis developed within 1 to 2 1/2 months after the first observation of a suppressed TSH response, while two patients remained euthyroid. In all patients with negative TRH-TSH tests. TSH response to TRH returned to normal between 2 and 29 months after withdrawal of amiodarone. We conclude that the TRH-TSH test, repeated at intervals, is a reliable tool for assessing thyroid function in patients on long-term treatment with amiodarone. Patients with a suppressed response under amiodarone therapy are at risk of developing thyrotoxicosis. Normalization of the TSH response indicates that this risk is over.

Adolescent↗
PubMed1985

Creatine kinase and creatine kinase MB in endurance runners and in patients with myocardial infarction.

Following a 100 km race creatine kinase (CK) creatine kinase MB (CKMB) activities were serially measured in well trained athletes and compared with enzyme activities in patients with acute myocardial infarction (AMI). The half-time of disappearance of CK (CKt1/2) was 1.75 +/- 0.70 days in runners who trained within the 1st week after the race, and was 0.81 +/- 0.18 days in patients with AMI, P less than 0.005. CKt1/2 in runners was shorter (1.17 +/- 0.28 days) when no training was performed in the first postrace week. CKt1/2 was linearly correlated with age (P less than 0.01) in the runners but not in the patients. CKMBt1/2 was 1.30 and 1.11 days in two runners and 0.56 +/- 0.10 days in patients with AMI (P less than 0.05). In line with histologic and enzymatic findings in skeletal muscle of long distance runners as reported by other workers, our kinetic data provide further evidence that CK and CKMB are released from muscular compartments in runners other than those in patients with AMI.

Adult↗
PubMed1985

Pharmacokinetics of amiodarone, desethylamiodarone and other iodine-containing amiodarone metabolites.

In 23 patients treated with the iodine-containing antiarrhythmic drug amiodarone, the plasma concentrations of amiodarone, desethylamiodarone and iodine have been studied. Besides amiodarone and desethylamiodarone, a pool of iodine-containing substances, NANDAI (non-amiodarone-, non-desethylamiodarone-iodine), was present. At steady state the iodine content of NANDAI amounted to 64% and the iodine content of amiodarone plus desethylamiodarone to 36% of total serum iodine. At steady state 26% of the NANDAI fraction was made up of inorganic iodide, the average plasma concentration of which was at least 40 times above the upper limit of the normal range. The serum elimination half-life of NANDAI of 57-160 days exceeded that of amiodarone (35-68 days) and of desethylamiodarone (31-110 days). At steady state the serum concentration of desethylamiodarone appears to be related to the concentration of amiodarone by a Michaelis-Menten type function, yielding a Km of amiodarone of 2.45 mumol/l and a maximal desethylamiodarone concentration of 3.61 mumol/l.

Adolescent↗
PubMed1985

Amiodarone-induced vasculitis and polyserositis.

A dose-dependent cutaneous leukocytoclastic vasculitis developed in a 34 year old man who was given amiodarone for supraventricular tachycardias resistant to other drugs. This adverse reaction disappeared within 2 weeks after discontinuation of amiodarone despite its very long half-life of 52 days in this patient. During previous treatment periods with amiodarone, the patient had experienced photosensitivity and dose-dependent polyserositis. Since high doses of amiodarone have been recently proposed for the treatment of resistant cardiac arrhythmias, dose-dependent adverse effects as described here may be encountered with increasing frequency.

Adult↗
PubMed1985

Hyperventilation-induced changes of the blood picture.

In a controlled study of 11 male volunteers the following changes (means +/- SD) were observed in venous blood during (D) and 75 min after (A) a period of 20 min of voluntary hyperventilation in comparison with before (B) hyperventilation (P values referring to the difference between D and B) erythrocyte count 5.18 +/- 0.17 X 10(6) (B), 5.70 +/- 0.21 X 10(6) (D) (P less than 0.001), and 5.18 +/- 0.16 X 10(6)/microliter (A); hemoglobin 15.7 +/- 0.6 (B), 17.2 +/- 0.7 (D) (P less than 0.001), and 15.8 +/- 0.6 g/dl (A); centrifuged hematocrit 46.6 +/- 1.0 (B), 50.4 +/- 1.7 (D) (P less than 0.001), and 47.0 +/- 1.8% (A). The platelets increased from 159 +/- 30 X 10(3) (B) to 205 +/- 40 X 10(3) (D) (P less than 0.001) and returned to 157 +/- 26 X 10(3)/microliter (A). The leukocytes (WBC) were 4,210 +/- 630 (B), 6,220 +/- 1,660 (D) (P less than 0.001), and 6,190 +/- 1,870/microliter (A) (P less than 0.002, as compared with B). The rise of WBC during hyperventilation was mainly due to a 83% increase of lymphocytes, whereas a 93% increase of neutrophil leukocytes accounted for the increased WBC 75 min posthyperventilation. The increase of the ratio of band forms to segmented neutrophils from 9 (B) to 19% (A) (P less than 0.01) indicates that band forms were released from the bone marrow. The results show that WBC and platelets can be mobilized by hyperventilation by as yet unidentified mechanisms.

Adult↗
PubMed1985

Erythrocyte adenosine triphosphate depletion during voluntary hyperventilation.

Chronic hypophosphatemia in humans is associated with a slow depletion of adenosine triphosphate (ATP) and 2,3-diphosphoglycerate (2,3-DPG) in erythrocytes, combined with shape alteration, impaired deformability, and viability of the cells. Likewise, incubation of erythrocytes in alkaline solution is associated with ATP depletion. Since in hyperventilation both hypophosphatemia and alkalosis are present, we have investigated red cell organic phosphates, shape, deformability, and osmotic fragility before, during, and after 20 min of voluntary hyperventilation. On the average, red cell ATP decreased by 42%, the blood pH increased by 0.2 units, and plasma inorganic phosphorus decreased by 46% compared with the initial values. Red cell 2,3-DPG, shape, deformability, and osmotic fragility remained unchanged. After the end of hyperventilation ATP increased rapidly to control values in parallel with the normalization of the blood pH, whereas inorganic plasma phosphorus remained at the low level observed during hyperventilation. It is concluded that the combined effects of hypophosphatemia and alkalosis in acute hyperventilation lead to an isolated fall of red cell ATP, which occurs as rapid as after total inhibition of red cell glycolysis in vitro.

2,3-Diphosphoglycerate↗
PubMed1985

The influence of L-sorbose on red cell flow properties, shape and packing ability.

Since the sweet ketohexose L-sorbose causes overt hemolysis in dogs but not in man, we examined the possibility that L-sorbose induces a "prehemolytic state" of human red cells, manifesting itself as impairment of rheological red cell properties. After 2 hours incubation at 37 degrees C relative viscosity of red cell suspensions measured by radial spreading in filter paper and packing ability of red cells were normal. Incubation for 24 and 48 hours of red cells in media containing L-sorbose, glucose or no sugar showed that relative viscosity was best maintained in glucose. Relative viscosity and packing ability of red cells in L-sorbose containing suspensions decreased less than in suspensions without sugar. This difference was independent of the glucose metabolism, red cell ATP, osmolality and pH of the suspending media, but appeared to be related to different degrees of spheroechinocytic red cell shape transformation observed in different suspending media. It is possible that L-sorbose has some antiechinocytic properties and/or that it induces an alteration of red cell membrane flexibility. There is no indication of an L-sorbose induced "prehemolytic state" in human red cells.

Adenosine Triphosphate↗
PubMed1984

Does amiodarone affect heart rate by inhibiting the intracellular generation of triiodothyronine from thyroxine?

The hypothesis that the antiarrhythmic drug amiodarone slows down the heart rate by its inhibitory action on the intracellular conversion of thyroxine (T4) to 3,5,3' triiodothyronine (T3) was investigated. For this purpose we compared the effect of amiodarone with that of another potent inhibitor of the T4----T3 conversion, i.e. the radiographic contrast medium iopanoic acid, on the heart rate of unanaesthetized guinea-pigs. Both amiodarone and, to an even greater extent, iopanoic acid induced an increase in serum 3.5',3' triiodothyronine (reverse T3), indicating effective inhibition of T4----T3 conversion. Both amiodarone and iopanoic acid were accumulated in the liver and in the heart (measured as iodine). While amiodarone induced bradycardia, iopanoic acid did not change the heart rate. Supraphysiological amounts of exogenous T3 reverted the amiodarone induced bradycardia to near normal values. A comparable effect was observed with isoprenaline. The intracellular inhibition of the T4----T3 conversion is not the ultimate mode of the action of the amiodarone effect on heart rate. It is thought that amiodarone interacts with T3 at its receptor or somewhere later along the pathway from the T3-receptor interaction to the final effect of T3 on heart rate.

Amiodarone↗
PubMed1983

Serum concentrations of amiodarone during long term therapy. Relation to dose, efficacy and toxicity.

In 17 patients on long term therapy with amiodarone, serum drug levels measured by HPLC were related to pharmacological effects. At steady state, serum levels were directly proportional to the dose, 5 mg/kg per day leading to an average serum level of approximately 2.5 mumol/l. The non-amiodarone level of iodine averaged 4-times higher than the level of amiodarone iodine. The elimination half-life of amiodarone ranged from 21 to 78 days, and of non-amiodarone iodine from 24 to 160 days. Control of arrhythmias was satisfactory in all 12 evaluable patients, when the serum amiodarone level exceeded 1.5 mumol/l. Deterioration of vision and polyserositis occurred only at amiodarone levels above 4 mumol/l. Tentatively, a therapeutic range of 1.5 to 4 mumol/l is proposed. In contrast, thyroid dysfunction was observed at any amiodarone level. In view of the narrow therapeutic window, therapy with amiodarone may be optimized by monitoring its serum level and in addition, thyroid function should be regularly checked.

Adult↗
PubMed1983

Abnormalities of gut vessels in Turner's syndrome.

We describe a 57-year-old patient with Turner's syndrome, iron deficiency anaemia and intestinal vascular abnormalities. Colonoscopy revealed 2 widely dilated, tortuous veins in the terminal ileum and several smaller ectatic veins and haemangioma-like malformations throughout the colon. Laparotomy for herniotomy showed only minimal vascular abnormalities of the serosal surface. Patients with Turner's syndrome and anaemia should be checked for these lesions by endoscopy, and conversely, in patients with such lesions, Turner's syndrome should be considered.

Colon↗
PubMed1982

Creatine kinase and MB-fraction after a long distance race.

In 18 well-trained athletes creatine kinase (CK) and the CK-MB isoenzyme were measured immediately after a 100 km race and 10 days later for control purposes. The CK was 1970 +/- 1505 U/l (mean +/- SD, range 481--5558 U/l) after the race and 50 +/- 23 U/l on the control day (p less than 0.001). The CK-MB fraction was 72 +/- 70 U/l (range 14--228 U/l) and 8.6 +/- 2.3 U/l (p less than 0.01). The ratio CK-MB/CK was 3.4 +/- 1.1% and never exceeded 6%. The study indicates that elevated CK and CK-MB are a common finding after a long distance race. CK-MB/CK ratios up to 6% may be observed.

Creatine Kinase↗
PubMed1982

Erythrocyte deformability in dialysed and non-dialysed uraemic patients.

In thirty-one uraemic patients, fourteen on conservative treatment and seventeen on long-term haemodialysis, erythrocyte deformability, measured as filtration half-time in a paper filtration experiment, was studied. The two groups were comparable concerning age, sex and kidney disease. Although the mean filtration half-time for erythrocyte suspensions was normal in non-dialysed patients there was a positive linear correlation (P less than 0.01) between serum creatinine and filtration half-time in this group. Filtration half-time was increased in dialysed patients, indicating impaired deformability in the latter (P less than 0.001). Filtration half-time showed a good inverse correlation with the packed red cell volume in the non-dialysed (P less than 0.001) and in the dialysed group (P less than 0.01). As pre- and post-dialysis filtration half-times were the same, it appeared that the more severe uraemic state of dialysed patients was responsible for the impairment of erythrocyte deformability and not the dialysis procedure itself.

Adult↗
PubMed1982

Changes in the rheologic properties of blood as induced by sodium/meglumine ioxaglate compared with sodium/meglumine diatrizoate and metrizamide.

The influence of the new angiographic contrast medium sodium/meglumine ioxaglate on the rheologic properties of blood in vitro was assessed by measurements of blood viscosity and by observation of red cell shape and aggregation. Compared with iodine-similar concentrations of sodium/meglumine diatrizoate and metrizamide, exposition of blood to the new compound was associated with a lower impairment of blood viscosity, rouleaux formation of red cells and with only minor alterations of red cell shape. These favourable results are due to the low hyperosmolality and to absence of direct influence on the red cell membrane of sodium/meglumine ioxaglate.

Adult↗
PubMed1981

[Amiodarone and the thyroid gland].

In an estimated 5% of patients, antiarrhythmic therapy with amiodarone (Cordarone) may have side effects involving thyroid function. These unwanted effects on the thyroid gland can be classified into three entirely different categories. In addition, amiodarone invariably interferes in a characteristic way with the peripheral metabolism of thyroid hormones at the cellular level. These effects are reviewed. 1. Amiodarone contains 39% of iodine. Since its metabolism involves deiodination to inorganic iodide, classical iodine-induced thyrotoxicosis may occur in patients with nodular goiters containing autonomous follicles. 2. An entirely different form of thyrotoxicosis, resembling Graves' disease, may be induced by amiodarone in individuals with previously normal thyroid. The pathogenesis of this phenomenon is unknown. 3. In rare patients of the thyroid gland is unable to cope with pharmacological quantities of iodide, possibly due to genetic anomaly of thyroid metabolism. In these individuals amiodarone may induce hypothyroidism. 4. In contrast to the possible side effects of amiodarone involving the thyroid gland, the drug has an obligate impact on the metabolism of thyroid hormones at the level of the peripheral cells. It inhibits the peripheral conversion of thyroxin to triiodothyronine (T3) and favours the generation of reverse T3, which has no T3 activity. This and other arguments favour the assumption that the effects on the heart observed after prolonged amiodarone treatment are in fact due to selective local hypothyroidism.

Adult↗