Total-, free-, and acylcarnitine concentrations were determined in whole blood, plasma, and red blood cells of 88 women during pregnancy. Already in the 12th week of gestation the mean whole blood carnitine level was significantly (p < 0.01) lower than those of the controls. From the 12th gestational week up to parturition there was a further significant (p < 0.01) decrease. This reduction of total carnitine in whole bloods was mainly caused by a significant (p < 0.01) decrease of free carnitine levels, since no marked changes of short chain acylcarnitine values were found throughout pregnancy. The contribution of red blood cell L-carnitine to whole blood carnitine increased significantly (p < 0.05) to 61% at delivery versus 39% (controls). In umbilical cord blood free and total carnitine levels were significantly (p < 0.05) higher than the corresponding maternal levels. The contribution of red blood cell L-carnitine to whole blood carnitine was higher in cord blood than in maternal blood. The results of the present study demonstrate that during pregnancy whole blood and plasma carnitine levels decrease to those levels found in patients with carnitine deficiency. Also the percentage of acylcarnitine on total carnitine, found in the present study, is characteristic for a secondary carnitine deficiency. Thus L-carnitine substitution in pregnant women, especially in risk pregnancies, may be advantageous.

Lungs of fetal rats between the 18th and 20th gestational day (total gestation lasting 22 days) were examined. There was a significant increase (p < 0.01) of the dipalmitoyl phosphatidylcholine content from day 19 to day 20 of gestation. In the second trial, pregnant rats were treated with different doses of betamethasone, L-carnitine, betamethasone-L-carnitine combinations, and saline (controls) for three days before Cesarean section on the 19th gestational day. Maternal injections of 0.10 mg/kg body weight betamethasone and 100 mg/kg body weight L-carnitine significantly (p < 0.05, p < 0.01 respectively) increased the dipalmitoyl phosphatidylcholine content of fetal lungs. Combinations of either 0.05 or 0.10 mg/kg body weight betamethasone with 100 mg L-carnitine also significantly increased the dipalmitoyl phosphatidylcholine content of the fetal lungs above control values (p < 0.001) and values achieved with betamethasone alone (p < 0.05). Maternal treatment with a betamethasone-L-carnitine combination on day 19 of gestation resulted in dipalmitoyl phosphatidylcholine levels comparable to those found on the 20th gestational day during normal lung maturation. Fetal rats delivered on the 20th gestational day survived, while fetuses delivered on the 19th gestational day did not survive.

No abstract

No abstract

Patients on chronic hemodialysis with hyperlipidemia were found to respond either with decreased levels (responders) or with a further increase of the plasma triglyceride levels (nonresponders) to a carnitine substitution therapy. The aim of the present study was to find possible predictors to distinguish between responders and nonresponders prior to the initiation of therapy. Since it is suggested that erythrocytes are involved in carnitine transport to tissues, it was of interest to determine plasma and erythrocyte carnitine concentrations in the hemodialyzed patients before and during carnitine substitution therapy and to compare the results with those of healthy controls. Before therapy, comparatively lower plasma levels of both free and total carnitine, but higher portions of short-chain acylcarnitine on total carnitine were found in all patients. In erythrocytes, the nonresponders showed significantly higher total carnitine levels, compared to responders and controls. After the start of carnitine substitution, the increase of total plasma carnitine during the substitution period corresponded with the carnitine dose administered in responders, in nonresponders the highest carnitine values were found in the second week when the lower carnitine dose was administered. The changes of the plasma short-chain acylcarnitine levels with time were very similar to those of plasma triglycerides. All patients showed a time-delayed accumulation of carnitine in erythrocytes and, interestingly, markedly higher concentrations in the second week when the lower carnitine dose was administered. The results of the present study demonstrate that the erythrocyte carnitine content is a reliable predictor to distinguish between responders and nonresponders prior to the start of a carnitine substitution therapy.

No abstract

No abstract

No abstract