Biomedical subjects

Hugo Lagercrantz

Publications and source records attributed to Hugo Lagercrantz.

20 records · Page 2Linked to original sources

PubMed2002

Long-term prenatal hypoxia alters maturation of adrenal medulla in rat.

Catecholamine release from the adrenal medulla glands plays a vital role in postnatal adaptation. A number of pathologic situations are characterized by oxygen deficiency. The objective of the present study was to determine the influence of long-term prenatal hypoxia on maturation of the adrenal medulla. Pregnant rats were subjected to hypoxia (10% O2) from the fifth to the 20th d of gestation. The offspring were examined on the 19th d of gestation (E19), the day of birth (P0), and at postnatal (P) day of life P3, P7, P14, P21, and P68. The catecholamine content and activity of tyrosine hydroxylase (TH) in vivo were assayed by HPLC with electrochemical detection. Cellular expression of TH and phenylethanolamine N-methyl transferase was evaluated by protein immunohistochemistry and in situ hybridization of the corresponding mRNA species. Exposure to prenatal hypoxia reduced the epinephrine content of the adrenal medulla on E19, P0, P3, and P7 while increasing the norepinephrine content on E19, P0, and P14. Furthermore, the peak epinephrine to norepinephrine ratio appearing between P7 and P10 in the normoxic offspring was absent in the hypoxic offspring. The in vivo TH activity was increased on P3 and P14 and decreased on P68. The percentage of chromaffin cells in the medulla expressing TH and phenylethanolamine N-methyl transferase was lowered on E19, P0, and P7. TH and phenylethanolamine N-methyl transferase mRNA levels were reduced on P7. Clearly prenatal hypoxia results in major changes in adrenal catecholamine stores and synthesis during the perinatal period, which persist into adulthood. The capacity to cope with postnatal stress might be disturbed as a consequence of prenatal hypoxia.

Adrenal Medulla↗

PubMed2002

Perinatal nicotine attenuates the hypoxia-induced up-regulation of tyrosine hydroxylase and galanin mRNA in locus ceruleus of the newborn mouse.

The effect of perinatal nicotine exposure on the hypoxic response in the newborn mouse was examined, with special reference to the catecholaminergic system. We studied transcripts for the catecholamine synthesizing enzyme tyrosine hydroxylase (TH) and the neuropeptide galanin (GAL) in locus ceruleus (LC) and adrenal medulla at different times after birth and postnatal hypoxia. We thereafter investigated how perinatal nicotine affected these mRNA levels, as well as the ability of the newborn to survive severe hypoxia. TH mRNA levels increased postnatally in both LC and adrenals, reaching peak values at 24 h postnatally and thereafter stabilizing at lower levels. GAL mRNA also increased in the LC but did not decrease after 24 h. Acute hypoxia (5% O(2) for 60 min) elicited increases in TH and GAL mRNA levels in the LC after 24 h. However, TH mRNA levels in the adrenals did not change. Perinatal nicotine exposure increased mortality after hypoxia (from 0% to 16.9%). Moreover, hypoxia-induced increases in TH and GAL mRNA levels in the LC were not observed in nicotine-treated pups. Nicotine also decreased basal TH mRNA levels in the adrenals. The present results suggest (1) that the postnatal increases in adrenal TH mRNA levels are not directly due to hypoxia at birth, and (2) that the increased mortality seen after hypoxia in nicotine pups concurs with a perturbed LC function in these animals. A deficient catecholamine synthesis in the adrenals may also contribute to the detrimental effect of prenatal exposure to nicotine on the response to hypoxia.

Acute Disease↗