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Biomedical subjects

L Longerich

Publications and source records attributed to L Longerich.

41 records · Page 3Linked to original sources
PubMed1982

Digoxigenin biotransformation.

Two healthy subjects took 3H-digoxigenin-12 alpha and unlabeled digoxigenin. Metabolites were assayed by high-pressure liquid chromatography (HPLC) in serum and urine. Of the tritium activity in the serum at 30 min, less than 26% chromatographed with digoxigenin; the rest chromatographed as metabolites, most of which were polar. The main polar metabolites identified were glucuronides of 3-epidigoxigenin. An important route of biotransformation to polar metabolites appears to be from 3 beta-digoxigenin through 3-keto-digoxigenin to 3-epidigoxigenin. Several HPLC peaks remain unidentified. There was extensive cross reactivity between metabolites and antisera to digoxin. The digoxigenin route of digoxin biotransformation to polar metabolites may be important in some patients receiving digoxin and such metabolites could contribute an important fraction to the serum digoxin concentration measured by radioimmunoassay.

Biotransformation↗
PubMed1981

Influence of gastric pH on digoxin biotransformation. II. Extractable urinary metabolites.

High-performance liquid chromatography (HPLC) analysis was performed on methylene chloride extracts of urine from six subjects after administration of 3H-digoxin-12 alpha and unlabeled digoxin by nasogastric tube under four conditions: pentagastrin and control saline infusions, each in the supine and ambulatory states. There were no differences with change in position. With pentagastrin stimulation of acid secretion, there was extensive intragastric hydrolysis, mainly to digoxigenin; there was further extensive biotransformation leading to an increase in both extractable and unextractable metabolites in urine, particularly the latter. In the first 5 hr mean digoxin was only 17% and unextractable metabolites were 54% of total urine radioactivity. Extractable radioactivity was found under HPLC peaks with retention times of digoxin, digoxigenin, and its mono- and bis-digitoxosides. There were also three other peaks that were not identified; two correlated with gastric H+ activity and with the peak for digoxigenin, which is probably their precursor since similar peaks were found after ingestion of digoxigenin. The third unidentified peak eluted immediately after the digoxin, with which it correlated; it may have a close structural relationship to digoxin. Gastric acid stimulation induced a major increase in the production of urinary metabolites and may prove a useful model for the study of digoxin biotransformation, which is not yet well defined.

Biotransformation↗
PubMedDate not supplied

Ischemic heart disease, serum cholesterol, and apolipoproteins in CAPD.

Thirty-one patients, mean age 54 years, had been on chronic ambulatory peritoneal dialysis (CAPD) for an average of 38 months. Mean values (mg/dl) for triglycerides (567), total-C (267), LDL-C (133), and Apo-B (154) were elevated, and HDL-C (30) were low. The low values for total-C/Apo-B and LDL-C/Apo-B suggest an increase in the number of low density lipoprotein (LDL) particles, rather than in the amount of cholesterol per LDL particle. Without knowledge of lipids, ischemic heart disease for the 31 patients was categorized into five grades in the following manner. All patients were graded based on history (angina, myocardial infarction, and bypass surgery), electrocardiogram (EKG), and echocardiography. In addition, five patients underwent coronary angiography, the results of which were considered in their grading. The five grades were assigned as follows: Grade I, no evidence (n = 15); Grade II, angina with EKG ischemia (n = 4); Grade III, myocardial infarction (MI) (n = 1); Grade IV, MI with dyskinesia-akinesia on echo (n = 4); Grade V, severe three vessel disease on angiography, or multiple infarcts, or Grade IV with heart failure (n = 7). Only Apo-B (r = 0.56) and total-C/HDL-C (r = 0.57) correlated with severity of grade, with p less than 0.001. When patients with and without detectable ischemic heart disease were compared by stepwise logistic regression, Apo-B was the only variable that independently predicted heart disease (p = 0.001). However, contribution of the lipid changes induced by CAPD has not been established.

Apolipoprotein A-I↗
PubMedDate not supplied

Higher plasma Na+,K+-ATPase inhibitory activity in essential hypertensive patients.

The ability of plasma to inhibit 86 rubidium uptake in rat aorta and to displace [3H]-ouabain from hog brain Na+,K+-ATPase was used as a measure of plasma Na+,K+-ATPase inhibitory activity in seven normotensive and eight hypertensive subjects. Rat aortae rings were incubated in oxygenated plasma containing 86 rubidium (2 microCi/mL) for 30 mins at 37 degrees C and uptake measured and expressed as mumol/kg wet weight/min. Plasma was extracted with a mixture of chloroform and methanol (2:1) and the extract separated by silicic acid column followed by thin layer chromatography and fractions assayed for ouabain displacement using digoxin as a standard. Total ouabain displacement was calculated as the sum of all fractions. There was a strong correlation between the two methods for total plasma Na+,K+-ATPase inhibitory activity (r = 0.761, P less than 0.01). There was a significant positive correlation between plasma Na+,K+-ATPase inhibitory activity and blood pressure in all subjects. Na+,K+-ATPase inhibitory activity was significantly higher in plasma of hypertensives by both methods (P less than 0.001). The increased Na+,K+-ATPase inhibitory activity in plasma from hypertensives was due to the nonesterified fatty acid, long chain acylcarnitine and diphosphatidylglycerol fractions.

Adult↗