[Acute respiratory insufficiency after inhaling concrete dust--a case report]. / Akute respiratorische Insuffizienz nach Inhalation von Betonstaub--eine Kasuistik.

UNLABELLED: Inhalation of inorganic, inert dusts, like concrete dust, has generally not been considered dangerous. Very rarely alterations following chronic exposures can be observed, such as airflow obstruction and increased mucous secretion. Acute reactions in terms of acute respiratory failure have not been described so far. CASE REPORT: The present case report introduces a 54-year old male patient who developed acute respiratory failure after sawing a concrete block for several hours without wearing a face mask. Save for a chronic obstructive pulmonary disease he was unremarkable for his past medical history. When the emergency physician arrived, oxyhaemoglobin saturation was only 54%. Severely obstructed breathing sounds and coarse bubbling rales over both lungs were audible. After endotracheal intubation, a great deal of white viscous mucus could be aspirated via the tubus. The chest radiograph after admission demonstrated cloudy, shadowed areas with emphasis on both lower lung fields. As pulmonary function did not improve inspite of drug therapy with prednisolone, theophylline, fenoterol, n-acetylcysteine and respiration therapy with 100% oxygen concentration, the patient was treated daily with bronchoscopic aspiration of the mucus. Only on the fourth day, after an additional ten hours in prone position, the lung function improved. The patient could be extubated on the fifth day. The final chest radiograph indicated no residuum apart from a very small shadowed area on the right angle between heart and diaphragm. CONCLUSION: The inhalation of dusts, which have long been considered inert, can cause acute pulmonary reactions. We suggest that the massive, mechanical covering on the alveolar layer with still alkaline concrete dust in conjunction with a history of chronic bronchitis was responsible for the acute inflammation and oedematous swelling of the bronchial mucosa, bronchospasm, secretion of a highly viscid mucus, atelectasis, and thus for the ARDS.

[Modification of blood coagulation by antihypertensive therapy? Effect of enalapril and hydrochlorothiazide on blood coagulation parameters in patients with essential hypertension]. / Beeinflussung der Blutgerinnung durch antihypertensive Therapie? Wirkung von Enalapril und Hydrochlorothiazid auf Blutgerinnungsparameter bei Patienten mit essentieller Hypertonie.

An increased tendency of the blood to clot in patients with arterial hypertension is not desirable, since cardiovascular and cerebrovascular sequelae may be aggravated. Recently, activation of coagulation under ACE inhibition with captopril has been described. In an open, randomized study, we compared the influence of enalapril on various coagulation parameters with that of hydrochlorothiazide. In contrast to the latter, we detected no unfavorable influence of enalapril on the coagulation factors investigated. A transient increase in fibrin monomeres was observed in one patient each on enalapril and hydrochlorothiazide.

Baseline and stimulated ANF plasma levels: is an impaired stimulus-response coupling diagnostically meaningful?

Plasma levels of ANF were determined and chromatographically analysed in normotensive controls, cirrhotic patients with and without ascites, hypertensive patients, patients with congestive heart failure and heart transplant recipients. A comparison of baseline plasma levels allowed for the conclusion that cirrhotic patients do not differ in this regard from control subjects (9.0 +/- 1.3, n = 41 vs. 9.6 +/- 1,0 fmol/ml, n = 51). Cirrhotic patients with ascites do not have lower plasma levels than cirrhotic patients without ascites (8.8 +/- 1.4, n = 8 vs 8.6 +/- 1.5 fmol/ml, n = 10). Stimulation of the ANF-system by head-out water immersion, however, revealed an impaired increase in ANF release in cirrhotic patients with ascites (146 +/- 18% vs 204 +/- 16%). Patients with cardiovascular disease display tonically-elevated ANF plasma levels. Heart failure patients displayed the highest plasma concentration (81.5 +/- 32.7 fmol/ml, n = 17), whereas plasma levels in hypertensive patients ranged from normal to greatly elevated (61.7 +/- 13.2 fmol/ml, n = 36). Heart transplant recipients also had significantly elevated plasma levels as compared to control subjects (31.2 +/- 7.9 fmol/ml, n = 14) but levels were lower than in hypertensive patients in spite of a comparable arterial pressure. Short term ventricular pacing (f = 150/min for 5 min) revealed an impaired phasic activity of the ANF system in heart failure patients and heart transplant recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic factor in plasma of patients with arterial hypertension, heart failure or cirrhosis of the liver.

Since the discovery of the atrial natriuretic factor (ANF) an endocrine function has been attributed to the mammalian heart. This function may include definition of optimal conditions for efficient performance of the heart, e.g. by reduction of afterload in hypertension or of preload and afterload in heart failure. Plasma ANF levels were measured in various cardiovascular disease states and compared with those of controls and of patients with liver cirrhosis. Plasma ANF levels in hypertensive patients were sevenfold higher than in controls, and in patients with heart failure 40-fold higher than normal values. Small differences were detected between controls and patients with cirrhosis of the liver, in spite of the impaired renal sodium handling seen in cirrhotics. Plasma ANF levels were significantly correlated with haemodynamic parameters and were inversely related to the cardiac index. Treatment with an angiotensin converting enzyme inhibitor led to a significant decrease in plasma ANF levels in parallel with the haemodynamic improvement. Preliminary chromatographic analysis suggested differences in the structure of plasma ANF between normotensive and hypertensive subjects.

Basis and clinical significance of regression of hypertensive hypertrophy.

The basis of every therapy in hypertensive heart disease is blood pressure normalization. However, blood pressure should be lowered through antihypertensive drugs, which can regress LV hypertrophy, increase myocardial perfusion and improve LV function depending on the stage of hypertensive heart disease. Such a step-care of hypertensive heart disease must not be understood as a therapeutic scheme, but should be considered as an attempt to cover the clinical therapy of common hypertensive cardiac complications.

Regression of heart muscle hypertrophy after nifedipine therapy: changes in cardiac gene expression.

Changes in cardiac gene expression were studied during development and regression of cardiac hypertrophy in spontaneously hypertensive rats (SHR) in an attempt to determine some of the biochemical factors responsible for alterations in cardiac mass. Chronic nifedipine treatment of SHR (30 mg/kg per day for 20 weeks) led to a marked reduction in arterial blood pressure and to a subsequent regression of cardiac hypertrophy. Cardiac mRNA concentration decreased, whereas cardiac protein concentration remained unchanged. Changes in cardiac gene expression, as reflected by the decrease in cardiac mRNA concentration, were thus identified as a major factor responsible for the regression of cardiac hypertrophy after nifedipine therapy of SHR.

Demonstration and characterization of alpha-human atrial natriuretic factor in human plasma.

This paper describes a highly specific and sensitive radioimmunoassay for alpha-human atrial natriuretic factor (alpha-hANF), the C-terminal 28-amino-acid residue portion of human prepro-ANF in human plasma. A novel extraction and prepurification procedure allowed for detection of levels of immunoreactive-alpha-hANF as low as 0.5 fmol/ml. In normotensive subjects, levels in the range 1-23 fmol/ml (mean = 8.9 fmol/ml) were found. Combined gel permeation and HPLC analysis demonstrated that this ir-alpha-hANF was comprised virtually exclusively of authentic 28-residue alpha-hANF. No evidence for occurrence of larger precursor forms in human plasma was acquired. A heterogenous group of hypertensive patients displayed considerably higher levels (mean = 62.2 fmol/ml), of interest in view of the hypotensive properties of ANF.

Virus myocarditis: molecular hybridization allows the detection of virus-RNA in heart muscle after virus infection.

In most patients with virus myocarditis, the diagnosis is still based on clinical data alone. Endomyocardial biopsies subjected to electron microscopy, immunofluorescence techniques and virus isolation procedures provide additional, but only occasionally conclusive information. In this communication we describe a new method which could possibly be used to improve the diagnostic possibilities in patients with suspected virus myocarditis. The method is based on the hybridization of radioactive complementary nucleotide sequences to virus-RNA. It is shown that in an experimental model (reovirus infected baby mice) this method can be used to demonstrate the virus infection of cardiac muscle. It is suggested that the method could be adapted to other viruses (e.g. coxsackie virus) and to endomyocardial biopsies derived from patients with suspected virus myocarditis.

Influence of starvation and total protein deprivation on cardiac mRNA levels.

The effect of starvation and of protein-deprivation on the extractable amount of cardiac mRNA was investigated in male rats. Cardiac mRNA was determined by either (a) isolation of cardiac mRNA by SDS-Phenol/oligo-dT-cellulose, or by (b) hybridization of cardiac mRNA to 3H-Poly(U). During starvation (1-6 days) the extractable amount of cardiac microsomal RNA decreased from 870 micrograms/g heart (controls) to 606 micrograms/g (3 days) and to 547 micrograms/g (6 days), the extractable amount of mRNA fell from 28.6 micrograms/g heart (controls) to 18.7 micrograms/g (3 days) and to 14.5 micrograms/g (6 days). When a normocaloric but protein-deficient diet was fed, the decreases in cardiac microsomal RNA and mRNA were qualitatively similar, but slightly less severe. An analysis of the intracellular distribution of cardiac microsomal RNA and mRNA in the hearts of normal animals and of animals starved or fed a protein-deficient diet indicates that during starvation cardiac mRNA does not accumulate in the cell sap, but gets rapidly degraded. In the refeeding period, mRNA is transported from the nucleus to the cytoplasm and engages in polyribosome formation. The specific mRNA species coding for the major myofibrillar cardiac proteins are affected to a similar extent by these changes during starvation/protein-deprivation and refeeding.

[Regression of biochemical changes in heart muscle hypertrophy]. / Biochemische Veränderungen bei Herzmuskelhypertrophieregression.

Reduction in arterial blood pressure caused by ACE inhibitors, calcium antagonists and beta-blockers leads to regression of heart muscle hypertrophy. However, this regression may also occur in the absence of a significant reduction in blood pressure (alpha-Methyldopa), whereas no decrease in heart muscle mass may be observed in the presence of pronounced decreases in blood pressure (hydralazine, minoxidil, diuretics). In the present review, biochemical factors are analyzed that might be important in the regression of heart muscle hypertrophy. It will be seen that angiotensin II and cardiac catecholamines play important roles in modifying the influence of various drugs on regression of heart muscle hypertrophy. Reductions in angiotensin II and cardiac catecholamines lead to decreases in cardiac mRNA contents and thus to a decrease in the myocardial protein synthesis. Changes in myocardial protein degradation do not contribute to the regression of heart muscle hypertrophy.

Quantitation of cardiac messenger RNA in heart-muscle biopsies.

A method has been developed that allows the direct quantitation of cardiac messenger RNA in heart-muscle biopsies. This provides a new tool to directly assess changes in cardiac gene expression in cardiac biopsies. Using this method, we have analyzed changes in cardiac gene expression during induction and regression of triiodothyronine-induced heart hypertrophy, during development of heart atrophy secondary to starvation and protein depletion, in adriamycin cardiomyopathy, and in patients with mitral-valve diseases.

Gene expression in cardiac hypertrophy in rat and human heart muscle.

Changes in the cardiac contents of microsomal RNA and poly(A)-containing mRNA have been examined during induction and regression of heart muscle hypertrophy in rat hearts, as well as possible changes in the subcellular distribution and protein-synthetic activity of cardiac mRNA. In addition, cardiac biopsies from patients with mitral valve diseases were evaluated for their mRNA contents. Induction of heart muscle hypertrophy was accompanied by substantial increases in cardiac microsomal RNA (30-60%) and cardiac mRNA (20-80%). During regression of hypertrophy increased levels of cardiac microsomal RNA and mRNA returned to normal values within 10-16 days. In general, cardiac mRNA levels were lower in human heart muscle than in rat heart muscle. Since the subcellular distribution of the microsomal RNA and of the mRNA as well as the protein-synthetic activity of the mRNA were not changed in the hypertrophied animals as compared with normal animals, and since the cardiac contents of most specific cardiac mRNA species (mRNAs for MHC, MLC1 and MLC2, actin, tropomyosin, troponin-T, myoglobin) increased proportionately, it is concluded that during induction of hypertrophy activation of gene expression occurs and affects the genes coding for the major cardiac proteins to a similar extent. This does, however, not exclude the possibility of more specific shifts in isoprotein patterns and in the levels of their corresponding mRNAs. It is proposed that changes in cardiac mRNA levels are the major regulatory factor in causing changes in cardiac protein synthesis rates leading to the induction and regression of cardiac hypertrophy.

Plasma exchange and concomitant therapy in TTP.

Since plasma exchange was introduced in the management of thrombotic thrombocytopenic purpura (TTP) in 1977, patient survival rate has increased from 10 to 80%. However, approximately 50 subsequent case reports in the literature provide no consensus as to the optimal therapy. We review here 4 episodes of TTP in 3 patients. In all cases, treatment was started with intensive FFP plasma exchange combined with administration of antiplatelet agents and corticosteroids. Remission was achieved in 3 out of 4 episodes although all required individualization of the medication regimen. In the remaining patient, cytotoxic therapy (vincristine) and ultimately splenectomy were required to achieve stable remission. The variable clinical response to these therapeutic protocols indicates that TTP may not represent a single homogeneous disease entity but rather may involve various underlying pathologies. We conclude that the most effective present therapy for the management of TTP is daily plasma exchange with fresh frozen plasma infusions combined with antiplatelet agents and steroids. Vincristine and splenectomy should only be employed if this protocol proves ineffective.