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Biomedical subjects

H Rauch

Publications and source records attributed to H Rauch.

At least 37 records · Page 2Linked to original sources
PubMed1994

Evoked potential monitoring during repeatedly induced ventricular fibrillation for internal defibrillator implantation.

Repeated induction of ventricular fibrillation (VF) with circulatory compromise during implantable cardioverter defibrillator (ICD) testing may cause cerebral injury. To test this hypothesis, somatosensory evoked potentials (SEP), a more sensitive marker of injury, were recorded in patients (N = 10) undergoing ICD implantation. SEP were recorded before induction of anesthesia, after induction of anesthesia, before and at several times following induction of VF. Possible modifying factors of the SEP measurements such as anesthetic application, blood pressure, body temperature, and hematocrit remained constant throughout the operations. Central conduction time was unaffected by ICD defibrillation testing. Amplitude of SEP primary complexes was transiently reduced at 34.9% (P < 0.01) by defibrillation testing, but returned to control within 10 minutes after testing. It is concluded that while ICD defibrillation testing may produce transient changes in SEP, there is no evidence of residual cerebral injury.

Adult↗
PubMed1992

Hepatic metallothionein gene expression in toxic milk mice.

The toxic milk mutation (tx) in mice is an autosomal recessive condition that causes a marked hepatic accumulation of copper in adults and severe copper deficiency in the pups of tx/tx dams. We determined the concentration of metallothionein-I (MT-I) mRNA in mutant and normal animals at various stages of development and following administration of copper and zinc. In two tx/tx males the average MT-I mRNA was 329 molecules/pg RNA compared with 38 molecules/pg in normal animals. In fetal and neonatal animals the concentration of MT-I mRNA was generally the same in normal and mutant mice and was independent of copper status. Copper or zinc administration to 7-d-old pups caused a marked induction of MT-I mRNA. There was an increased response to copper administration in one mutant group, but no clear pattern of hyper-induction of the MT gene in tx/tx animals was demonstrated. The elevation of MT-I mRNA in adult toxic milk mice is likely to be a secondary consequence of copper accumulation and not a primary effect of the mutation, because high MT-I mRNA levels would have been observed in the mutant neonates and fetuses. However, the possibility that the tx mutation causes overexpression of MT in post-weaning animals cannot be excluded by these data. The results also show that copper deficiency has no effect on the fetal or neonatal expression of the MT genes.

Animals↗
PubMed1991

Hepatic ceruloplasmin gene expression is unaltered in the toxic milk mouse.

The toxic milk mutation in mice is an autosomal recessive condition that causes a marked hepatic accumulation of copper in the adults, but is also characterized by severe copper deficiency in the pups of toxic dams. To establish whether the mutation affects ceruloplasmin (CP) gene expression, we analyzed the steady state levels of CP mRNA in mutant and normal animals at various stages of development and following administration of copper and zinc. In fetal and neonatal animals, the expression of the CP gene is unaltered by the mutation or the copper deficiency in the pups of mutant dams. Copper and zinc administration to 7-d-old pups caused a significant increase (35%) in CP mRNA in all genotypes. In the adults that had accumulated 600-700 micrograms/g dry wt of copper in the liver, the CP mRNA level was normal, but pregnancy produced two-to fourfold elevation of the mRNA in both normal and mutant females. These results suggest that the toxic milk mutation does not affect the regulation of the CP gene and that the gene is not responsive to copper deficiency, copper administration or copper excess in the liver.

Animals↗
PubMed1989

Serum aluminium levels of intensive care patients treated with two different antacids for prevention of stress ulceration.

We studied the serum aluminum levels of 30 intensive care patients receiving six daily doses of magaldrate (Riopan) or aluminium hydroxide (Trigastril). In both groups we found a significant rise of the serum aluminium concentration (p less than 0.01) following administration of the antacid solutions. Examination on day 9 and 15 the magaldrate group showed significantly (p less than 0.05) lower aluminium levels than the aluminium hydroxide group. An increase up to the critical serum aluminium level of 100 ng/ml occurred in none of the patients that all had normal or slightly impaired renal function. Therefore routine measurements of serum aluminium levels in patients without renal impairment are not considered necessary following antacid therapy. However, we recommend the use of antacids with an aluminium absorption rate as low as possible.

Adult↗
PubMed1988

Morphologic and chemical studies on a murine mutation (toxic milk mice) resulting in hepatic copper toxicosis.

The accumulation of excessive amounts of copper in the livers of toxic milk mice results in gross morphologic, histologic, and ultrastructural changes that are progressive with age even though the concentrations of copper tend to decrease in mice older than 6 months. Striking differences in morphologic integrity between regenerative nodules and the intervening parenchyma were observed. Profound changes in mitochondria, endoplasmic reticulum, and nuclei as well as accumulation of microvesicular lipid droplets were observed in injured hepatocytes. By contrast, the hepatocytes of regenerative nodules appeared well preserved. Comparisons with other inherited mammalian disorders associated with hepatic copper toxicosis indicate that copper causes species specific organelle injury.

Animals↗
PubMed1985

Pathological findings in coronary arteries associated with sudden death in Austria.

50 witnessed sudden cardiac deaths in the age group between 20-50 years have been studied at autopsy. The most remarkable findings were a high percentage of stenosis and arteriosclerosis of the descending branch of the left coronary artery and a large amount of three vessel disease. It is clear that severe stenosis and sclerosis of the coronary arteries are not essentially related to sudden cardiac death, but a high number of vessels with moderate stenoses and sclerosis has been found. The severity of vessel disease has been evaluated by a coronary score, which takes the haemodynamic effects of the injured coronary arteries on the myocardium into account. We also noted that patients below 35 years of age who died of sudden cardiac death showed a very low coronary score.

Adult↗