Changes in the content of vasopressin-immunoreactive material in neurons and their projections were examined in pregnant and nonpregnant guinea pigs as well as in mother and newborn animals. Before sacrifice all animals used in the present study were submitted to a pyrogen test, during which the pregnant animals displayed a reduced fever response to exogenous pyrogen. The unlabeled enzyme-immunoperoxidase method was used in the present study. Light microscopic examination showed that, in comparison to all other groups examined, the pregnant animals exhibited a reduced content of the vasopressin-immunoreactive substance in the supraoptic nucleus (SON), in the neuronal pathways extending between the paraventricular nucleus (PVN) and the SON, as well as in the axons projecting to the neural lobe of the pituitary. An increased amount of vasopressin-immunoreactive material was observed during pregnancy especially in the medial portion of the PVN, in axonal distensions in the external zone of the median eminence and in the extrahypothalamic projection sites of the PVN in the lateral septum and in the amygdala. In the pregnant animals neurovascular contacts of vasopressinergic perikarya and fibers were abundant in the PVN; in the lateral septum and in the amygdala vasopressinergic terminals appeared to contact neurons of other types. It is suggested from the present immunocytochemical results that activation of neurons in the medial portion of the PVN and the increased number of vasopressinergic terminals and preterminals in the lateral septum and in the amygdala might be functionally involved in fever suppression at the term of pregnancy.
The synthetic polyribonucleotide pyrogen Poly I:Poly C (800 micrograms.kg-1) was injected intramuscularly on alternate days into pregnant and non-pregnant female guinea pigs. Pregnant animals, close to term, had smaller fevers in response to the pyrogen than did non-pregnant animals. Repeated injections of the pyrogen caused sequentially smaller fevers for the first 3-4 injections, particularly in non-pregnant animals, and this appeared to be like the tolerance usually developed to repeated injections of endotoxin. Continued pyrogen injections then caused, in non-pregnant animals, fevers of increasing magnitude until the original fever levels were reached, whereas in pregnant guinea pigs the fever responses remained reduced until parturition. The development of tolerance was associated with an increase in immunoreactivity for arginine vasopressin (AVP) in some neurons in the medial part of the paraventricular nucleus, and in terminals in the lateral septum and amygdala similar to changes found in these areas at term of pregnancy. These observations raise the possibility that AVP in these regions may have a role in the development of tolerance to pyrogens, and further quantitative studies of the AVP content of, and release from, nerve terminals projecting to the limbic system seem warranted.
In acute hypoxemic respiratory failure of term and near-term neonates, extra- and intrapulmonary right-to-left shunting contribute to refractory hypoxemia. Inhaled nitric oxide (NO) decreases pulmonary arterial pressure and improves ventilation-perfusion mismatch in a variety of animal models and selected human patients. We report on 10 consecutive term and near-term newborns with severe acute hypoxemic respiratory failure due to diaphragmatic hernia, meconium aspiration syndrome, group B streptococcus sepsis, pneumonia or acute respiratory distress syndrome, who received increasing doses of inhaled NO (up to 80 ppm) to improve the arterial partial pressure of oxygen (PaO2). The response to NO and the optimum NO concentration which improved PaO2 varied considerably between patients. Improvement of PaO2 was absent or poor (less than 10 mm Hg) in the 4 newborns with meconium aspiration syndrome and in 1 patient with congenital diaphragmatic hernia, while in the other 5 patients inhaled NO increased the mean (+/- SE) PaO2 from 41 +/- 6 to 57 +/- 9 mm Hg (P < 0.05). Optimum NO concentrations determined by dose-response measurements performed during the first 8 hr of NO inhalation were 8-16 ppm except for 2 newborns with congenital diaphragmatic hernia who required 32 ppm to effectively increase PaO2. Four of the 5 patients in whom the PaO2 rose by more than 10 mm Hg received inhaled NO for extended periods of time (5 to 23 days) with no signs of tachyphylaxis. The optimum NO concentration dropped to less than 3 ppm after prolonged mechanical ventilation or when intravenous prostacyclin was given concomitantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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