Effects of pregnancy on mothers' sleep.

OBJECTIVES: To survey the effects of pregnancy on mothers' sleep. METHODS: Mothers were interviewed during and after pregnancy with a series of five questionnaires to assess alterations in their sleep. The first questionnaire covered the 3 months before becoming pregnant, the next three the trimesters of pregnancy and the last the 3 months after delivery. The study was carried out in a central hospital and the maternity care units in the nearby rural community. Altogether, 325 pregnant women completed all five questionnaires. RESULTS: The total amounts of reported sleep and of nocturnal sleep increased significantly during the first trimester of pregnancy, began to decrease thereafter and were shortest during the 3 months after pregnancy. During late pregnancy expectant mothers over 30 years of age reported less sleep than those under 30. During the whole pregnancy, but increasingly toward the end of pregnancy, sleep became more restless and fragmentary and its subjective quality worsened, due at least partly to increased restless legs and nightly awakenings increasing with advancing pregnancy. CONCLUSIONS: The subjective quality of sleep is disturbed as early as the first trimester of pregnancy, although total sleeping time increases. The amount of reported sleep begins to decrease in the second trimester. The frequency of reported sleep disturbances, such as restless legs syndrome and nocturnal awakenings, is maximum in the third trimester but is about normal within 3 months after delivery.

Thyrotropin-releasing hormone immunoreactivity in human blood, urine, spinal fluid, amniotic fluid, saliva, and gastric juice.

TRH immunoreactivity levels were measured in human blood, urine, saliva, spinal fluid, amniotic fluid and gastric juice. Urinary TRH excretion during a 48-h period was measured in 11 healthy persons. Blood and urinary TRH immunoreactivity were measured at 2 and 5 h, respectively, after administration of 40 mg of TRH. All the samples were prepurified by SP-Sephadex-C-25 cation-exchange chromatography and subjected to reverse-phase high-pressure liquid chromatography (HPLC). TRH immunoreactivity levels were then measured by our TRH radioimmunoassay. The TRH immunoreactivity (TRH-ir) levels found in urine were 14.6 +/- 2.5 pmol/l; in blood 7.5 +/- 2.0 pmol/l; in spinal fluid 2.8 +/- 1.4 pmol/l, and in gastric juice 23.2 +/- 7.1 pmol/l. In all of the amniotic fluid and saliva samples, in almost one half of the blood and spinal fluid samples, and in almost one third of the gastric juice samples, TRH-ir was below the detectable limit. In blood and urine samples taken after oral administration of TRH, TRH-ir was eluted at the same time as synthetic TRH. The recovery of synthetic TRH added to the samples ranged from 36 to 99%. In all of the biological fluid samples, endogenous TRH-ir was eluted at the same time in HPLC, at 15-18 min, as was synthetic TRH which had been added to the samples. Urine was found to contain two TRH immunoreactive peaks, the second of which was eluted at the same time as synthetic TRH. No diurnal variation in urinary TRH excretion or TRH-ir levels was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased urinary levels of thyrotropin-releasing hormone immunoreactivity in acute pancreatitis.

Thyrotropin-releasing hormone (TRH) has been shown to be present and have actions in the human gastrointestinal tract. We have studied urine TRH immunoreactivity (TRH-ir) levels in healthy subjects and patients with acute pancreatitis, gallstones, ulcerative colitis, or acute gastritis. The urine samples were prepurified by SP-Sephadex-C-25 cation exchange chromatography, subjected to reverse-phase high-pressure liquid chromatography, and assayed in our TRH radioimmunoassay. The mean urine TRH immunoreactivity values of healthy subjects were 4.42 +/- 1 ng/l (x +/- SEM); of patients with acute pancreatitis on the 1st day of hospitalization, 23 +/- 7 ng/l; on the 2nd day, 7 +/- 1 ng/l; and on the 3rd day 9 +/- 2 ng/l. Only the urine TRH levels of the pancreatitis patients on day 1 differed significantly (p less than 0.05) from the levels of the healthy subjects. Circulating TRH appears to be derived mostly from the pancreas, where the islets during acute pancreatitis are affected, and TRH is released into circulation and urine.