Biomedical subjects
Publications and source records attributed to P Wunderlich.
From 1972 through 1983 there were 10 near-drowned children (7 boys and 3 girls) aged 1 to 4 years, treated as inpatients at the Children's Hospital of the Medical Academy Dresden. Three of them showed a severe aspiration pneumonia which in one case was complicated by bilateral pneumothoraces. In a further five children there were radiological signs of pulmonary oedema. Only in two children were the X-ray pictures of the chest normal.
Twenty two patients with cystic fibrosis, 7 to 17 years of age, underwent each two bronchoscopic investigations, the second six months later than the first, in general anaesthesia with muscle relaxation using a ventilation bronchoscope and taking small biopsies of the mucous membrane. The degree of reddening, swelling of the mucous membranes and hypersecretion was in some agreement with the intensity of the cellular infiltration and the production of pus (microscopic investigation). Secondary ultrastructural changes were detected in nearly all children: e.g. cellular oedema, protrusion of cells and fusion of cilia, microtubular abnormalities of the cilia, lesions of the apical cell membranes and increased number of goblet cells. These changes of ultrastructure were not correlated to the mentioned signs of inflammation.
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More than 4000 children with chronic and recurrent bronchopulmonary diseases have been cared for in the Dresden district, GDR (just under 2 million inhabitants) in 28 out-patient clinics over the past 7 years. The prevalence of this disease group is thus around 1.2%. There was a marked increase in children with bronchial asthma from initially 1000 to 1600, corresponding to 26 and 40%, respectively, within the disease group. By contrast, there was a continuous decrease in children requiring bronchological investigations (24 to 13%). Bronchiectasis was also encountered with diminished frequency. One third and one quarter of the patients dropped out of care over two three-year periods, respectively. Of these 70 to 75% were discharged symptom-free. The remaining patients were referred to adult out-patient clinics for continued care. Whereas nearly 80% of the discharged children with chronic or recurrent bronchitis became symptom-free, only 30% of the asthmatics showed this satisfactory result. The analysis of this large group of patients confirms the clear-cut success of out-patient clinic treatment of children with chronic and recurrent bronchopulmonary disease.
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Acute renal functional impairment not infrequently accompanies liver dysfunction and, particularly with bile duct obstruction, may be extremely severe. Recent studies suggest that tubuloglomerular feedback (TGF) activated by circulating non-electrolyte factors which occur during liver dysfunction may contribute to the intense renal vasoconstriction thought to be central to the functional renal impairment. In this study, serum from two patients with obstructive jaundice (OJ) and renal impairment, and from rats with OJ due to bile duct ligation were either dialysed or treated with furosemide, known to block electrolyte-mediated TGF. These sera, when perfused into loops of Henle in rat nephrons, induced a significant fall of 28% in stop-flow pressure, an indirect measure of glomerular capillary pressure thus implying arteriolar vasoconstriction. These findings are consistent with the hypothesis that circulating, non-electrolyte factors, which stimulate TGF, occur in cases of obstructive jaundice and that these may contribute to the renal impairment.
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A factor activating tubuloglomerular feedback in the rat by an unknown mechanism was extracted from the plasma of patients with hepatic damage and acute renal failure except for patient 9, but not from healthy volunteers or patients with chronic renal failure. GFR in such patients appears to be correlated inversely to the level of this activity.
Within 20 years 22 children with congenital lobar emphysema were observed. 13 children were infants, 9 were already older than a year, thus, clearly deviating from the age structure reported in literature. 15 children underwent an operation, in 2 children the alterations disappeared completely respectively partially. One child prematurely born died before operation. The upper lobe was concerned most frequently (11 times), followed by the right upper lobe (6 times) and the right middle lobe (4 times). Bronchoscopy was showing in surprising frequency a stenosis of the trachea (2 times) respectively of the main bronchus (7 times). In 13 of 15 cases bronchographically investigated the displacement and compression of the adjacent lobar bronchi were predominant. The regression of the emphysema observed in a x-ray picture series initially with an "opaque lung" and later on with spontaneous disappearance of the lobar emphysema is more fully described. In the opinion of the authors the analysis of their cases is justifying a change in the conception concerning age structure and urgency of surgery. Bronchological examination is considered of importance for differential diagnostics especially to delimit cystic pulmonary alteration.
The effect of intravenous endotoxin (Sal. abortus equi) in a semilethal dose in rats was very individual. Animals showing a drop in creatinine clearance were termed sensitive (E II), and animals without effect on the creatinine clearance non sensitive (E I). In the sensitive animals a reduction of intravascular space by albumin loss into the extravascular space, a decrease of renal blood flow and an average fall in creatinine clearance of 40% were found. The non sensitive animals (E I), on the other hand, showed no significant change in albumin space but, in contrast to E II, their hematocrit fell, a fact interpreted as vasodilatation and inflow of fluid. In these animals (E I) no change in creatinine clearance was measured. Orthograde tubular perfusion of endotoxin through the loop of Henle elicited no tubular glomerular feedback response. In these sensitive animals (E II), the absence of tubular glomerular feedback vasoconstriction, hypovolemia and a fall in blood pressure suggest a prerenal cause for this type of acute renal failure. Additional factors responsible for acute renal failure are discussed.
Acute renal failure was induced in rats by subcutaneous injection of 200 mg/kg body weight gentamicin on 3 consecutive days. Following the last gentamicin injection, the animals began to produce increased amounts of dilute urine and usually remained polyuric throughout the experimental period which lasted up to 2 weeks. Plasma concentrations of creatinine rose to values between 2 and 10 mg%, of urea to values between 100 and 1,000 mg% 5-7 days after the last gentamicin injection and returned to levels slightly above control after 14 days. Average proximal tubular pressure was slightly elevated to 13.7 +/- 0.5 mm Hg on the 2nd day after the last gentamicin dose, decreased to 6.1 +/- 0.4 mm Hg after 1 week, and returned to 11.8 +/- 0.2 mm Hg after 2 weeks (control proximal tubular pressure 11.6 +/- 0.2 mm Hg). These average values hide the fact that early in this model of gentamicin-induced acute renal failure many tubules had proximal tubular pressures increased to values between 18 and 25 mm Hg, suggesting tubular obstruction. Decreased proximal tubular pressures and the histological finding of wide-spread necrosis of proximal convolutions is suggestive of tubular leakage. Dehydration, similarly to other models of acute renal failure, markedly potentiated gentamicin-induced acute renal failure. Salt diuresis induced either by DOCA-saline or by furosemide failed to afford functional protection and increased the degree of morphological damage. No relation was found between the concentration of gentamicin in renal tissue and the degree of functional or morphological impairment.
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