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Biomedical subjects

C Hasslacher

Publications and source records attributed to C Hasslacher.

At least 19 recordsLinked to original sources
PubMed1992

Effects of combined renovascular hypertension and diabetes mellitus on myocardial cells, non-vascular interstitium and capillaries: a stereological study on rat hearts.

The effects of combined renovascular hypertension and diabetes mellitus on the rat heart were investigated in order to detect possible synergistic effects of the two conditions. Hypertensive diabetic and hypertensive non-diabetic animals were compared to diabetic and non-diabetic controls. Hypertension was established for 12 weeks by a surgical stenosis of the left renal artery; diabetes mellitus was maintained for 8 weeks by a single intraperitoneal injection of 60 mg/kg streptozotocin. Light microscopic stereology did not reveal significant divergences between diabetic hypertensives and non-diabetic hypertensives. Hypertension induced a focal perivascular and interstitial fibrosis with increased volume densities of non-vascular interstitium and fibrosis (P less than 0.001). Capillary density (QA) was decreased in transverse sections (P less than 0.01) and increased in longitudinal sections (P less than 0.01). This indicates a three-dimensional remodelling of the capillary bed with an increased number of obliquely running capillaries. At least the length density (LV) of capillaries (mm/mm3) tends to be normalized in long-term renovascular hypertension. At the ultrastructural level, a synergism of hypertension and diabetes mellitus was observed: the volume ratio of mitochondria to myofibrils was significantly decreased in hypertensive diabetics, but not in non-diabetic hypertensives or in diabetics. This may enhance the risk of cardiac deterioration. We conclude that the primary target of the synergistic damage in hypertensive diabetic heart muscle disease is the myocardial cell and not the cardiac interstitium.

Animals↗
PubMed1992

The response of GFR to amino acids differs between autosomal dominant polycystic kidney disease (ADPKD) and glomerular disease.

We compared the glomerular filtration rate (GFR) response to amino acids in patients with glomerular disease and polycystic kidney disease. The GFR response to infusion of amino acids (75 g/12 h), of dopamine (2 micrograms/kg per min), or their combination was evaluated in nine healthy probands and in patients with two types of renal diseases at various degrees of renal function: 15 patients with ADPKD and 11 patients with glomerular disease (IgA glomerulonephritis or diabetic nephropathy). Steady-state inulin infusion technique was used. In healthy subjects amino acids increased median C(in) in response to amino acids was not found in glomerular disease. In contrast in most ADPKD patients median C(in) increased after amino acids (+6.0 ml/min; range -4 to +68), (P less than 0.05). The response to amino acids was not modified by dopamine. The results demonstrate that amino acid-induced acute changes of glomerular filtration differ in polycystic kidney disease compared with glomerular disease. These observations may have implications with respect to mechanisms of progression.

Adult↗
PubMed1992

[ACE inhibitor effects on structure and function of the glomerular basement membrane].

Metabolism of proteins which compose capillary basement membrane is altered in diabetic patients. In the kidney, this leads to an impaired permselectivity of glomerular basement membrane and consequently to onset of proteinuria. Proteinuria which is often increased by hemodynamic factors, initiates and promotes the development of diabetic glomerusclerosis. Aside from near-normal metabolic control, special antihypertensive treatment can reduce proteinuria and retard loss of kidney function in proteinuric diabetic patients. The beneficial effect of ACE-inhibitors on course of diabetic nephropathy is generally thought to be a consequence of decreased systemic and intraglomerular pressure. However, recent longterm studies in Type I and Type II diabetic patients with nephropathy showed that ACE-inhibition can reduce proteinuria independent from their hemodynamic effects and, thus, improves the filtration properties of glomerular basement membrane. This may be due to an influence of ACE-inhibition on metabolism of basement membrane proteins.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

[Excretion of beta-N-acetylglucosaminidase in urine in type I and type II diabetic patients with and without nephropathy].

The clinical aspects of the excretion of beta-N-acetylglucosaminidase (beta-NAG, EC 3.2.1.30) in urine of type I and type II diabetics with and without nephropathy are evaluated. Correlation between concentration of albumin and of beta-NAG activity in urine is determined and the circadian rhythm of beta-NAG excretion in urine is examined, the indication of glomerular and tubulointerstitial damage is discussed. Longitudinal studies should demonstrate, whether an increased beta-NAG activity in urine of diabetics with normoalbuminuria is an indicator of nephropathy or a predictor of nephropathy if raised albuminuria is observed.

Acetylglucosaminidase↗
PubMed1991

[Albuminuria in diabetes mellitus].

A critical overview on different procedures and methods for an early diagnosis of diabetic nephropathy is given. Genetic markers, morphology and function of glomerula, blood pressure and the metabolic state of diabetics are especially discussed. From the risk markers available today microalbuminuria (20 to 200 micrograms/min resp. 20 to 200 mg/l) is shown to be most suitable for recognizing patients developing nephropathy.

Albuminuria↗
PubMed1990

[Diagnosis and therapy of diabetic nephropathy].

Diabetic nephropathy continues to be a common complication and has an unfavorable prognosis. Metabolic and hemodynamic factors determine the natural history of the condition. Of importance for the prognosis is the detection of nephropathy at an early stage. Such early diagnosis is not possible through the detection of microalbuminuria (incipient nephropathy stage). At this stage, further progress can be reversed by optimizing the metabolic situation and initiating early treatment of increasing blood pressure. For this reason, all diabetics should be submitted to early screening for microalbuminuria. When proteinuria persists (clinically manifest nephropathy stage), renal function usually declines progressively. Vigorous treatment of hypertension, optimal metabolic management, and normalization of protein intake can slow down the rate of continued loss of renal function.

Albuminuria↗
PubMed1990

[Improved prognosis of Type I and Type II diabetics with nephropathy].

Between 1966 and 1985, 72 type I and 75 type II diabetics developed persistent proteinuria. These patients were divided into two groups according to time of onset of proteinuria (1966 to 1975 and 1976 to 1985, respectively). In these groups, we investigated both the quality of antihypertensive treatment and metabolic control as well as the course of nephropathy and life prognosis. Control of hypertension was markedly improved in type I and type II diabetics with later onset of proteinuria (1976 to 1985), compared with patients who developed proteinuria between 1966 and 1975. However, metabolic control was improved only in type I diabetics. Compared with the previous decade, prevalence of renal insufficiency was lowered by one-third in type I and type II diabetics with later onset of proteinuria (1976 to 1985). During the six-year observation period, 32% of type I and 72% of type II diabetics who developed proteinuria between 1966 and 1975 died, whereas all type I and 54% of type II diabetics with later onset of proteinuria (1976 to 1985) survived. The study shows that conservative treatment methods, especially lowering of blood pressure, may improve prognosis for proteinuric type I and type II diabetic patients.

Adolescent↗
PubMed1990

Diabetic nephropathy--are there differences between type I and type II?

It has commonly been assumed that the renal risk in type II diabetes is markedly lower than in type I diabetes since only approximately 5% of the former but 40% of the latter experience renal failure. Based on our observations in the diabetes outpatient department of the University of Heidelberg, we conclude that the cumulative risk of developing proteinuria for the nonproteinuric type II diabetic and the cumulative risk of developing renal failure for the proteinuric type II diabetic are comparable with the respective risks of the type I diabetic. This observation is noteworthy since there is no uncontroversial evidence of hyperfiltration in early type II diabetes. Type II diabetes may be an interesting model for testing the hyperfiltration theory.

Diabetes Mellitus, Type 1↗
PubMed1979

[Pathogenesis of diabetic microangiopathy. Protein and basement membrane synthesis in isolated kidney glomeruli of diabetic and non-diabetic rats].

In incubation experiments with isolated glomeruli, an increased synthesis of protein and basement membranes was detected in streptozotocin-diabetic rats compared to metabolically healthy controls. Chemical analysis of isolated basement membranes and incorporation studies did not give any indication of enhanced hydroxylation of lysine in the diabetic membrane. Different glucose concentration in the incubation medium and insulin in vitro did not influence protein and basement membrane synthesis of non-diabetic glomeruli. On the other hand, in diabetic glomeruli the synthetic activity depends on glucose concentration. Insulin had a stimulatory effect on protein and basement membrane synthesis diminished at lower glucose concentration and did not inhibit the increased synthetic activity demonstrated at higher glucose concentration. Therefore, these results may be attributable to an energy deficit of incubated glomeruli and not to a lower glucose stimulation of synthesis. By treatment of diabetic rats with insulin in vivo the synthetic activity was not affected by brief normalization of blood sugar. Insulin treatment from the beginning of diabetes only lead to a normalization of protein synthesis in moderate metabolic control. On the other hand, a rise of basement membrane synthesis could only be prevented by strict metabolic control of the rats. These results show that basement membrane synthesis reacts more sensitively to the diabetic situation than overall protein synthesis. Insulin deficiency does not appear to be one of the factors directly influencing basement membrane synthesis.

Animals↗
PubMed1978

[Lipid-lowering effect of bezafibrate in patients with diabetes mellitus and hyperlipidaemia (author's transl)].

600 mg of bezafibrate daily were administered to 13 well controlled diabetics with hyperlipidaemia for 12 weeks. Placebo was given before and after the treatment period. Compared with pretreatment placebo, bezafibrate reduced triglycerides (between 37 and 47%) and cholesterol (between 12 and 19%) significantly. Blood glucose levels during treatment were significantly lower at 8 and 12 weeks compared with post-treatment placebo values. Urinary glucose excretion did not change. Hypoglycaemia was not observed. No change in antidiabetic medication was necessary. Bezafibrate was well tolerated. It lowered blood lipids effectively in diabetics with hyperlipidaemia. No additional precautions have to be taken to control carbohydrate metabolism during bezafibrate treatment.

Blood Glucose↗
PubMed1978

[Hypoglycemia].

Explore the source record for details and available documents.

Female↗
PubMed1977

[Influence of the beta-receptor blocker nifenalol on insulin secretion in normal subjects and diabetic patients (author's transl)].

In 10 insulin-independent diabetic patients and 5 healthy volunteers the basal and glucose-stimulated insulin secretion was tested before and during oral treatment with the beta-blocker 1-(4-nitrophenyl)-2-isopropylaminoethanol (nifenalol, Inpea). In diabetic patients the insulin secretion was not changed by Inpea. The fasting blood sugar levels were slightly elevated in 8 of these patients. This result, which could not be ascertained statistically, may be due to a slight intrinsic activity of this beta-blocker. The normal subjects showed different responses. In one person the glucose tolerance deteriorated by Inpea.

Adult↗
PubMed1977

Antibodies against the hepatitis B surface antigen in diabetics.

The frequency of antibodies to the hepatitis B surface antigen was determined in 406 diabetics in two study series separated in time (1971-1972 and 1974-1975). In the 1971-1972 series, the antibody frequency in insulin and orally treated patients was significantly higher, and the incidence of hepatitis was also greater. The decline in the antibody frequency in the 1974-1975 series is primarily attributed to improved hygienic measures. Anti-HBs was more frequently demonstrable in insulin-dependent diabetics than in orally treated patients. Since the duration of diabetes was about three times as long in this treatment group and the frequency of metabolic checks twice as great, the raised antibody frequency in insulin-injecting diabetics was attributed to greater exposure to the virus.

Administration, Oral↗
PubMed1976

[Risk factors of arteriosclerosis in patients with severe bradycardia arrhythmias].

The frequency and distribution of risk factors of arteriosclerosis were determined in 405 patients with implanted cardiac pacemakers and compared with the corresponding results of patients with cardiac infarction. The most frequent risk factors were smoking (43,5%), hypertension (35,2%), and diabetes (34,3%) in males, hypertension (52,3%) and diabetes (49,7%) in females. The frequency of cardiac infarction was in average 19,5%. In the infarction group diabetes was lower in both sexes (23,5% and 35,8%), respectively), hyperlipoproteinemia and smoking were more frequent. From the different distribution of risk factors it is suggested, that coronary arteriosclerosis is not the most important etiologic factor in the development of bradycardic dysrhythmias. The higher percentage of diabetes in the pacemaker group could point to metabolic disturbances or specific diabetic vascular disease as harmful factors to the conduction system.

Aged↗