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Biomedical subjects

C Merkel

Publications and source records attributed to C Merkel.

At least 109 records · Page 6Linked to original sources
PubMed1982

Renal haemodynamic in essential hypertension assessed by 133-Xenon washout and selective renal angiography.

The renal and intrarenal haemodynamic pattern in 17 patients with essential hypertension of different severity and duration was studied by means of the 133-Xenon washout technique and the selective renal angiography. The mean and the cortical renal blood flows were on average significantly decreased as compared to the controls. A good agreement was found between the reduction in renal perfusion and the degree of vascular abnormalities as shown by angiography; on the contrary no correlation was found between the impairment in renal blood flow and the degree and/or duration of hypertension.

Adult↗
PubMed1981

Evaluation of renal tubular damage in liver cirrhosis by urinary enzymes and beta-2-microglobulin excretions.

To assess the renal tubular damage in liver cirrhosis the fractional clearances of beta-2-microglobulin (B2m-fr.cl) and malate-dehydrogenase (MDH-fr.cl) were measured respectively in sixty-four and in forty-six out of seventy-nine patients with liver cirrhosis of different aetiology; furthermore the fractional excretions of gammaglutamyl-transpeptidase (fr-GGT) and of alpha-glucosidase (fr-AGL) were determined in fifty-three and in forty of them respectively. In all patients glomerular filtration rate (GFR) and renal plasma flow (RPF) were also measured. Twenty-five subjects were studied as a control group for the enzyme excretions, sixteen for B2m-fr.cl. B2m-fr.cl and MDH-fr.cl--indexes of tubular functions--on the average were normal and only slightly increased respectively in cirrhotics compared to controls. Nevertheless fr-GGT and fr-AGL--indexes of cytolysis of tubular cells--on the average were massively increased in cirrhosis compared to controls, particularly in those with reduced RPF and/or GFR. No clear relationship between the indexes of tubular damage studied and the indexes of liver function was found. Our results show that (1) A renal tubular anatomical damage was found by means of an increase in the release of enzyme from tubular cells in patients with liver cirrhosis, particularly in those with a significant reduction of RPF and/or GFR; even so renal reabsorption of low molecular weight proteins is generally maintained. (2) The tubular damage does not seem to be related to the degree of liver impairment.

Adult↗
PubMed1981

Hypotensive and renal effects of captopril.

The effects of Captopril on blood pressure and renal function were evaluated in ten patients with different degrees of hypertension. In seven, blood pressure was reduced after 7 weeks of therapy; in three it remained practically unchanged. No correlation was found between the standing plasma renin activity before treatment and the hypotensive response. Plasma renin activity increased significantly from the median value of 5.4 (range 1-16.7) to 9.5 (range 2.6-19.8) ng ml-1 h-1 (P less than 0.05) and urine aldosterone significantly fell from 13 (range 2.3-52.5) to 7.4 (range 1.6-14) microgram 24 h-1 (P less than 0.01) during therapy. Renal plasma flow decreased from 534 (range 300-616) to 471 (range 333-606) ml min-1, but the difference was not significant, and glomerular filtration rate fell significantly form 122 (range 64-143) to 88 (range 71-116) ml min-1 (P less than 0.05). No urinary excretion of alpha 2-macroglobulin was observed during Captopril. 24 h proteinuria, albumin and transferrin clearance, alanine-amino transferase, gammaglutamyl transferase and alpha glucosidase excretion rate and malate-dehydrogenase clearance remained unaltered throughout the treatment. This indicates that neither glomerular permeability nor renal tubular function were affected by the drug.

Adult↗
PubMed1981

Intrarenal blood flow, circulation time, and cortical vascular volume in patients with cirrhosis.

The pathogenesis of renal functional impairment in patients with cirrhosis is still poorly understood, although it is probably linked to intrarenal haemodynamic alterations, such as renal cortical vasoconstriction and opening of intrarenal shunts. To elucidate the intrarenal haemodynamic pattern in patients with cirrhosis, in eight patients with this disease mean renal blood flow (MRBF) and cortical blood flow (CBF) were determined by means of the xenon-133 washout technique; in the same subjects mean intrarenal circulation time for plasma (t) and fastest circulation time for plasma(t0) were determined by means of injection of human serum albumin tagged with technetium-99m into the renal artery. Moreover, cortical vascular volume (CVV) was obtained in all subjects by means of the following formula: CVV = CBF x t. Fourteen normal subjects constituted a control group for MRBF, 9 subjects for CBF, and 4 subjects for t, t0, and CVV. In patients with cirrhosis MRBF and CBF were significantly less than in controls; t did not show any significant alterations, whereas t0 was significantly shorter than in controls. CVV was also significantly impaired. It is concluded that renal cortical vasoconstriction is a characteristic of the renal haemodynamic pattern in patients with cirrhosis. It is suggested that the decrease in t0 is due to the opening of intrarenal shunts and that is likely to be the consequence of renal vasoconstriction.

Adult↗
PubMed1981

Distal renal tubular acidosis in hepatic cirrhosis: clinical and pathogenetic study.

The mechanism of the renal tubular acidosis (RTA) occurring in patients with hepatic cirrhosis remains uncertain although it has been suggested that renal and intrarenal hemodynamic alterations could play a role in its pathogenesis. To verify this hypothesis, renal acidification was studied with an intravenous acid load of arginine hydrochloride in 51 patients with cirrhosis due to various causes. In 22 patients renal and intrarenal blood flow was also measured using the 133-Xe washout technique. RTA was found in 17 of 51 patients (33%) with the greatest incidence in alcoholic cirrhosis. The tubular defect did not appear related either to the degree of liver functional impairment or to the renal and intrarenal hemodynamic alterations.

Acidosis, Renal Tubular↗
PubMed1980

The tRNA genes punctuate the reading of genetic information in human mitochondrial DNA.

A detailed transcription map of HeLa cell mitochondrial DNA (mtDNA) has been constructed by using the S1 protection technique to localize precisely the sequences coding for the ribosomal RNA (rRNA) and poly(A)-containing species on the physical map of the DNA. This transcription map has been correlated with the positions of the tRNA genes derived from the mtDNA sequence. It has been shown that, with the exception of the D loop and another small segment near the origin of replication, the mtDNA sequences are completely saturated by the rRNAs, poly(A)-containing RNAs and tRNA coded for by the two strands. No evidence for intervening sequences has been found. The sequences coding for the individual poly(A)-containing RNA and rRNA species appear to be immediately contiguous on one side, and most frequently on both sides, to tRNA coding sequences. Furthermore, the H strand sequences coding for the two rRNAs, the poly(A)-containing RNAs and the tRNAs appear to be adjacent to each other, extending from coordinate 2/100 to coordinate 95/100 of the genome relative to the origin taken as 0/100. The results are consistent with a model of transcription of the H strand in the form of a single molecule which is processed into mature RNA species by precise endonucleolytic cleavages, occurring in almost all cases immediately before and after a tRNA sequence. The tRNA sequences may play an important role as recognition signals in the processing of the primary transcripts.

Chromosome Mapping↗
PubMed1980

Renal and intrarenal blood flow in patients with cirrhosis before and after portal-systemic shunt.

Portal hypertension has been considered a pathogenetic factor in the onset of renal haemodynamic alterations in patients with cirrhosis. This hypothesis is based on experimental evidence, whereas the clinical data are few and contradictory. Mean and cortical renal blood flows were studied in 16 patients with liver cirrhosis before and 20-40 days after a portal-systemic shunt performed by different techniques: nine patients had a non-selective shunt and seven a selective shunt (distal splenorenal according to Warren). Despite a decrease in portal pressure, mean and cortical renal blood flows did not change significantly after surgery, and there was no significant correlation between decrease in portal pressure and modification of renal blood flow. It is concluded that portal hypertension is not a pathogenetic factor in renal hypoperfusion in cirrhosis.

Adult↗
PubMed1979

Cardiac involvement in progressive systemic sclerosis.

The case of a patient with progressive systemic sclerosis (PSS) who developed electro- and vectorcardiographic patterns of myocardial necrosis without clinical picture of myocardial infarction is reported. The coronarography showed no obstruction of coronary arteries and cineventriculography a hypodynamic enlarged left ventricle. The analysis of electrocardiograms from 43 other patients affected with PSS revealed myocardial necrosis in 5 of them. The clinical syndrome of myocardial infarction was absent in all these cases. Moreover, the hemodynamic investigation in 13 cases allowed to record a dip-plateau figure on the right ventricle pressure curve in 3 of them. In PSS, the electrocardiographic aspects of "necrosis" as well as hemodynamic restrictive findings or ventricular enlargement at ventriculography could indicate myocardial disease.

Adult↗
PubMedDate not supplied

Randomised trial of nadolol alone or with isosorbide mononitrate for primary prophylaxis of variceal bleeding in cirrhosis. Gruppo-Triveneto per L'ipertensione portale (GTIP)

BACKGROUND: The risk of having a first cirrhosis-associated variceal bleed is lowered by about 50% by beta-blockers. Use of beta-blockers is currently recommended for patients with cirrhosis and oesophageal varices that are at risk of bleeding. We aimed to test the effectiveness of isosorbide mononitrate as an adjunct to the beta-blocker nadolol in the prophylaxis of first variceal bleeding in these patients. METHODS: We did a randomised multicentre study to compare the non-selective beta-blocker, nadolol, with nadolol plus isosorbide mononitrate in 146 relatively well (Child-Pugh score < or = 11) patients who had oesophageal varices at risk of bleeding. Patients on nadolol alone received a single oral 40 mg daily dose. Every second day the dose was titrated to achieve 20-25% decrease in resting heart rate (maximum dose 160 mg daily). Patients receiving both drugs received nadolol as above then isosorbide mononitrate was added starting with 10 mg orally twice daily, which was increased to 20 mg unless hypotension or severe headache occurred. The main endpoint was the occurrence of variceal bleeding of any severity. Patients were followed up for up to 40 months. FINDINGS: During the study period 11 of 74 patients from the nadolol alone group and four of 72 from the nadolol plus isosorbide mononitrate group had variceal bleeding (log-rank test p = 0.03). Cumulative risk of variceal bleeding was 18% in the nadolol group and 7.5% in the combined treatment group (95% CI for difference 1-25%). Two patients in each group had a non-variceal bleed related to portal hypertension. 14 patients from the nadolol only group and eight from the combined treatment group died during the study period (log-rank test p = 0.09). Four and eight patients, respectively, had to discontinue one of the drugs because of side-effects. INTERPRETATION: Nadolol plus isosorbide mononitrate is significantly more effective than nadolol alone in the primary prophylaxis of variceal bleeding in relatively well patients with cirrhosis, and has few side-effects.

Administration, Oral↗