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Biomedical subjects

W H Reinhart

Publications and source records attributed to W H Reinhart.

At least 19 recordsLinked to original sources
PubMed1999

[Angioedema induced by ACE inhibitors and angiotensin II-receptor antagonists: analysis of 98 cases].

Angiooedema has been reported as a rare but in most cases serious adverse effect of ACE inhibitors. Recent reports have indicated that angiotensin II-receptor antagonists may also induce angiooedema. As part of the spontaneous reporting scheme in Switzerland the Swiss Drug Monitoring Centre (SANZ) has received reports on 94 cases of ACE inhibitor-induced and 4 cases of angiotension II-receptor antagonist-induced angiooedema. These 98 spontaneously reported cases were analysed in detail. 28 cases were classified as serious and in three patients intubation was even required. In 35% of cases angiooedema was induced within the first week of therapy and in 64% within the first year. In one case the angio-oedema displayed latency of 8 years. Latency of this duration shows that this adverse drug reaction (ADR) may be hard to detect. In 45 of the 98 cases the oedema persisted for more than one day (maximum 2 months), although in some instances the patients continued ACE-inhibitor therapy. In 25 cases the oedema recurred, in one instance as many as 20 times. In rare cases angiooedema may also be induced by angiotensin II-receptor antagonists, although in such instances the course of the oedema was usually milder. In two of the four reported cases angiooedema recurred after switching from an ACE inhibitor to an angiotensin II-receptor antagonists. The four reported cases from Switzerland showed a similar profile when compared with 25 internationally documented cases. Our data indicate that angiooedema is a specific ACE inhibitor ADR. A protracted latency period may be observed and recurrence of oedema is frequent. Angiotensin II-receptor antagonist-induced angiooedema may also occur in rare instances.

Adult↗
PubMed1999

Ifosfamide-induced stomatocytosis and mesna-induced echinocytosis: influence on biorheological properties of blood.

Ifosfamide is an alkylating agent which has poorly understood toxic side effects such as encephalopathy. We hypothesized that ifosfamide and concomitantly applied mesna could have an influence on the flow properties of blood, and thus carried out an in vitro study. Whole blood was incubated in vitro with increasing concentrations of ifosfamide (0-50 mg/ml), mesna (0-20 mg/ml) and combinations thereof. Chloroacetaldehyde, a major metabolite of ifosfamide, was also studied (0-5 mmol/l). Ifosfamide led to a dose-dependent stomatocytic shape transformation and mesna to an echinocytic shape transformation of erythrocytes. These shape changes were reversible upon removal of the causing agent. Both shape changes increased whole blood viscosity. Erythrocyte aggregation was decreased by both drugs at high concentration. Erythrocyte deformability, as measured with the transit time through 5-microm pores, was decreased by mesna and remained unaffected by ifosfamide. These effects were seen at concentrations which may be reached in vivo at the infusion site of the drugs into a vein and in the urinary tract. We conclude that ifosfamide and mesna interact with the lipid bilayer of the cell membrane, which may contribute to the toxicity of the compounds.

Adult↗
PubMed1998

Influence of exercise training on blood viscosity in patients with coronary artery disease and impaired left ventricular function.

Exercise training has recently become an accepted therapeutic modality in chronic heart failure after myocardial infarction. Because the therapeutic mechanism behind it is controversial and not well understood, we analyzed the influence of exercise training on blood viscosity. Twenty-five patients with chronic heart failure (ejection fraction < 40%) after myocardial infarction were randomly assigned to either an 8-week intensive exercise program at a residential rehabilitation center or 8 weeks of sedentary life at home. Exercise consisted of two 1-hour walking sessions per day and four intensive bicycle ergometer training sessions of 40 minutes at 70% to 80% peak exercise capacity per week. Whole blood viscosity, viscosity at standardized hematocrit of 45% (P45) at high and low shear rates, and plasma viscosity were measured in a Couette-type viscometer before, during, and at the end of the study period. Exercise training, which significantly increased maximal cardiac output and oxygen uptake, did not change plasma viscosity, whole blood viscosity, and P45 significantly. Sedentary controls, however, had a higher whole blood viscosity and P45 after 8 weeks. No statistical difference was found, however, between the two groups. We conclude that blood rheology remains unaffected by exercise training in patients with chronic heart failure. The improvement of blood viscosity remains an interesting therapeutic option for the symptoms of these patients, which must be achieved by methods other than exercise training.

Blood Viscosity↗
PubMed1998

Lethal pulmonary hypertension in a young woman caused by unrecognized haemangiosis carcinomatosa.

A 38-year-old female is described, who was admitted with increasing respiratory distress, cough and visible blood stasis in the jugular veins. The most likely diagnosis in this young women taking oral contraceptives was pulmonary embolism, however, a ventilation-perfusion lung scan was normal. Echocardiography showed a dilated right ventricle and increased systolic pulmonary pressure. Despite administration of oxygen and intravenous heparin the patient died in circulatory collapse before further investigations could be initiated. Post-mortem examination revealed diffuse adenocarcinoma of the stomach (linitis plastica) with metastasis to local lymphnodes, lymphangiosis carcinomatosa of the liver, pancreas and spleen and tumour cell masses within the lumen of small pulmonary arteries leading to variable occlusions of the vessels. Fibrocellular intimal proliferation was found, leading to further obstruction and increased resistance to flow through the pulmonary vascular bed and to subacute cor pulmonale.

Adenocarcinoma↗
PubMed1998

Echinocytosis induced by haemodialysis.

BACKGROUND: Haemodialysis, widely used to treat patients with renal failure, is not always well tolerated. Different mechanisms have been postulated for this. We analyzed the influence of haemodialysis on erythrocyte morphology and blood rheology. METHODS: Twenty-two haemodialysed patients were studied immediately before haemodialysis, after 30 min, and at the end of haemodialysis with biocompatible membranes. Haematological routine was measured, the erythrocyte morphology was assessed on glutaraldehyde-fixed cells and blood viscosity was determined. RESULTS: Erythrocytes underwent various degrees of echinocytic shape transformation after 30 min of haemodialysis, which was completely reversible at the end. In a repetition of the investigations during a subsequent haemodialysis other patients were affected. A plasmatic factor caused echinocytosis since the incubation of control erythrocytes in patients plasma induced a similar, even more marked shape transformation and, vice versa, patient echinocytes regained a discocytic shape when incubated in buffer. The degree of echinocytosis was related to an increased blood viscosity at high shear rates (r=0.800, P<0.01). Echinocytosis was not accompanied by obvious clinical reactions. CONCLUSIONS: Reversible echinocytosis and an increase in blood viscosity is often seen during haemodialysis, which may affect the circulation in patients at risk.

Adult↗
PubMed1998

High prevalence of bronchial hyperresponsiveness and asthma in ice hockey players.

The prevalence of asthma was studied in a ice hockey team compared with both a floor ball team and the Swiss population. Lung function, bronchial hyperresponsiveness to methacholine, asthma symptoms and exercise-induced asthma were measured in a cross-sectional prospective study. A positive response to the methacholine bronchial provocation test was found in 34.6% of the ice hockey players and 20.8% of the floor ball players (Swiss population 16.4%). The provocative dose causing a 20% fall in the forced expiratory volume in one second (PD20) was significantly lower in ice hockey players than in floor ball players, but there was no significant difference in the dose-response slopes between the two groups. Asthma was diagnosed in 19.2% of the ice hockey players and in 4.2% of the floor ball players (Swiss population 6.8%), whereas exercise-induced asthma was found in 11.5% of the ice hockey players and in 4.2% of the floor ball players. In conclusion, asthma and bronchial hyperresponsiveness seemed to be more common in ice hockey players than in floor ball players and in the Swiss population. Strenuous exercise at lower temperatures may be a risk factor for the higher prevalence of asthma and bronchial hyperresponsiveness, as well as the increased severity of bronchial hyperresponsiveness, particularly in ice hockey players.

Adolescent↗
PubMed1998

The non-ionic surfactant Poloxamer 188 (RheothRx) increases plasma and whole blood viscosity.

RheothRx injection is an intravenous formulation of Poloxamer 188, a non-ionic block copolymer surfactant which is actually used in clinical studies, e.g., during thrombolysis in acute myocardial infarction. We have analysed the influence of RheothRx on plasma and whole blood viscosity of healthy individuals in vitro. For that purpose plasma was incubated with 0, 0.75, 3.75 and 18.75 mg/ml RheothRx and whole blood with a constant hematocrit of 41.4% with 0, 0.4, 2 and 10 mg/ml RheothRx at 37 degrees C. Viscosity was measured with a Couette viscometer at shear rates of 94, 11, 0.9 and 0.1 s-1 as well as with a newly developed oscillating viscometer. In contrast to other studies, we found no favourable effect of RheothRx on plasma and whole blood viscosity. At the highest RheothRx concentration an increase in high and low shear viscosity was observed. Erythrocyte morphology remained unchanged. These data, although on normal blood in vitro, suggest that the positive effects of RheothRx in vivo may not be caused by improved flow properties of blood, but could rely on other mechanisms.

Adult↗
PubMed1998

No influence of furosemide on human erythrocyte shape and volume and blood viscosity in vitro.

Furosemide is a diuretic agent which is often given in high concentration intravenously. Since erythrocytes have a furosemide-sensitive transport system and oral application of furosemide was found to induce an echinocytic shape transformation in horses, we have analysed the influence of furosemide on erythrocyte shape, volume and blood viscosity in vitro. Increasing plasma furosemide concentrations of 0, 1, 10, 100 and 1000 micrograms/ml did not affect the erythrocyte volume or shape and left blood viscosity unaffected. We conclude that furosemide has no influence on blood rheology in humans.

Administration, Oral↗
PubMed1998

Rheological properties of blood as assessed with a newly designed oscillating viscometer.

A newly designed type of oscillating viscometer was tested for blood viscosity measurements. The viscometer consists of a probe (either a tube or a rod) oscillating at a resonance frequency with amplitudes in the micro- and nanometer range. The torsional oscillations are dampened by fluids flowing through the tube or surrounding the rod. The degree of damping depends on the viscosity of the fluid, which allows to measure viscosity. Data obtained with these instruments were compared with those obtained with a conventional Couette viscometer. An increase of erythrocyte aggregation by the addition of dextran 70 in vitro led to the expected increase of viscosity in the Couette viscometer; in the oscillating tube viscometer, however, it remained unchanged, which may be explained by a decreased erythrocyte concentration near the tube wall due to increased aggregation and flow of erythrocytes in the tube center. In ex vivo experiments on blood flowing without anticoagulant directly through the tube viscometer an inverse correlation between viscosity and fibrinogen concentration was found. This is in contrast to actual knowledge and may indicate that high fibrinogen levels have a beneficial rheological effect at the tube or vessel wall. Our data suggest that the new oscillating tube viscometer is an interesting tool, which may contribute to a more comprehensive understanding of blood flow.

Adult↗
PubMed1998

[Leg edema].

The legs are preferentially affected by systemic edematous states. Pathogenetic factors are: increased hydrostatic pressure, increased capillary permeability (leak), reduced colloid-oncotic pressure, reduced lymph drainage and miscellaneous rare conditions. The most frequent cause of increased hydrostatic pressure is right heart failure, which can be treated with diuretic drugs. Increased capillary leak is seen in septic-toxic events, where the underlying disease must be treated. Reduced oncotic pressure is caused by hypoalbuminemia, either due to reduced production, e.g., in liver cirrhosis, or to increased albumin loss, e.g., through the kidney in nephrotic syndrome or the gut in protein-loosing enteropathy. Lymphedema is classified either as primary or secondary and is treated by lymph drainage. Idiopathic edemas, primarily seen in females, often lead to chronic abuse of diuretics, which in turn can cause diuretic-induced edemas.

Diagnosis, Differential↗
PubMed1997

[Fever: friend or enemy?].

Normal body temperature values are distributed in a Gaussian manner and are subject to circadian variation. Therefore, the usually accepted upper limit of 37 degrees C for normal body temperature should be replaced by a value of 37.1 degrees C in the morning and 37.4 degrees C in the afternoon. Fever develops when cytokines increase the thermostatic set point in the hypothalamus, which in turn results in increased body temperature via increased heat production and decreased heat dissipation. Hyperthermia is a distinct entity in which the thermostatic set point is normal but the heat control mechanism fails. Increased body temperature has positive effects (e.g. decreased bacterial growth, stimulation of host defence mechanisms) as well as negative effects (e.g. increased heart rate, oxygen consumption and metabolism). Whether fever is a friend or foe depends on the actual clinical circumstances. Antipyretic treatment should, therefore, not be applied routinely. In the case of pure hyperthermia (e.g. heat stroke), physical cooling is appropriate, while in the case of fever the thermostatic set point must first be normalized with drugs before cooling can be applied.

Body Temperature Regulation↗
PubMed1997

[Fatal central pulmonary embolism under heparin therapy: white-clot syndrome].

A 75-year old female underwent coronary angiography for chest pain. Significant proximal stenosis of the left coronary artery was found. During the waiting time for bypass surgery, intravenous heparin treatment was established for several days because of recurrent unstable angina pectoris. 10 days after coronary angiography an acute event with chest pain, hypotension, tachycardia and a new right bundle branch block suspect for myocardial infarction occurred, which was treated with rt-PA. Fever, persistent hypotension, acute progressive renal failure and thrombocytopenia suggested septic shock, and the patient was transferred to our hospital. A pulmonary artery catheter could not be advanced beyond the main stem of the pulmonary artery. The patient died suddenly 24 hours later from acute right ventricular failure. Autopsy demonstrated multiple white clots in both pulmonary arteries. The histological finding of clots rich in leukocytes and fibrin was compatible with the diagnosis of heparin-induced thrombosis-thrombocytopenia or white clot syndrome. Heparin-induced thrombocytopenia may occur after about 5 days of treatment. Two distinct types have been described. The first type occurs in up to 25% of patients receiving heparin and is a result of temporary platelet aggregation, margination and peripheral sequestration. The less common second type of thrombocytopenia is thought to be mediated by a heparin-dependent IgG antibody inducing platelet aggregation and may be associated with thromboembolic events leading to the white clot syndrome, which is rarely reported in the literature. In these cases heparin should be stopped immediately and replaced by oral anticoagulation. Other therapies such as low molecular weight heparin, synthetic heparinoids, hirudin, fibrinolytic agents, plasmapheresis and intravenous immunoglobulins are discussed. Monitoring of the platelet count every 5 days in patients receiving heparin for any extended period should become standard medical practice to avoid potential fatal complications.

Aged↗
PubMed1997

The anti-neoplastic drug 5-fluorouracil produces echinocytosis and affects blood rheology.

The anti-neoplastic agent 5-fluorouracil (5-FU) in high therapeutic doses can induce angina pectoris and myocardial infarction. The pathophysiological mechanism of this side-effect has not yet been elucidated. We analysed the influence of 5-FU on blood rheology in vitro. Whole blood, blood cell suspensions and plasma were incubated with increasing concentrations of 5-FU (final concentrations 0, 0.08, 0.4, 2, 10 and 25 mg/ml 5-FU) at 37 degrees C. Erythrocyte morphology was analysed after fixation with glutaraldehyde. Viscosity was measured at high and low shear rates (94 and 0.1 s[-1]). Erythrocyte aggregation and the cell transit times of erythrocytes through 5 microm pores and polymorphonuclear leucocytes through 8 microm pores were determined. 5-FU induced a dose-dependent formation of echinocytes within minutes and was reversible upon removal of 5-FU, which reflected a preferential intercalation of the drug in the outer hemileaflet of the cell membrane. High shear blood viscosity was increased at the highest 5-FU concentration (148 +/- 12%), and at low shear rate a dose-dependent decrease was found (0 mg/ml: 100%, 0.08 mg/ml: 87 +/- 10%, 0.4 mg/ml: 80 +/- 19%, 2 mg/ml: 70 +/- 15%, 10 mg/ml: 40 +/- 19%, 25 mg/ml: 33 +/- 5%). Erythrocyte aggregation was decreased by the 5-FU-induced echinocytosis. The transit time of erythrocytes through narrow pores was increased in a dose-dependent manner by 5-FU, whereas the transit time of polymorphonuclear leucocytes was initially decreased at 10 mg/ml and returned to control after 60 min incubation. We conclude that 5-FU interacts with the cell membrane, induces echinocytosis and vesiculation and affects blood rheology in several ways which may contribute to cardiovascular complications.

Antimetabolites, Antineoplastic↗
PubMed1997

Cisapride increases peak plasma and saliva ethanol levels under fasting conditions.

OBJECTIVES: Alcohol absorption is influenced by gastric first-pass metabolism through an alcohol dehydrogenase and the gastric emptying time. Whilst an influence of antisecretory drugs and aspirin on gastric alcohol metabolism has been described, the role of prokinetic drugs has not been determined. DESIGN: A randomized, placebo-controlled double-blind cross-over study was performed. SETTING: Out-patient facilities of a referral hospital. SUBJECTS: Eight male volunteers (age range 25-46 years). INTERVENTION: Treatment with two doses of either placebo or cisapride 150 micrograms/kg 7 h and 20 min before drinking 0.5 g/kg alcohol either in a fasting state or during a standardized meal (12 kcal/kg). MAIN OUTCOME MEASURES: Plasma and saliva ethanol concentrations were measured during 4 h. RESULTS: Cisapride increased peak plasma ethanol levels in fasting subjects from 15.6 (SD 1.4, 95%-KI 14.7;16.6) to 17.8 (SD 2.7, 95%-KI 15.9;19.7) mmol/L and saliva ethanol 30 min after alcohol ingestion from 11.4 (SD 2.2. 95%-KI 9.9;12.9) to 15.9 (SD 4.3, 95%-KI 12.9;18.8) mmol/L. A significant interaction between fasting state and drug intake was found for the 30 min saliva ethanol values (P < 0.05, ANOVA for repeated measurements). CONCLUSIONS: Cisapride may increase ethanol levels under fasting conditions. Patients treated with prokinetic drugs should be informed about this possibility.

Adult↗