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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In chronically catheterized sheep fetuses, during normal pregnancy, the concentration of PGE in the fetal femoral arterial plasma is invariably greater than that of PGF, and increases during the 12 to 24 hr preceding delivery. The concentration of both PGE and PGF decreases repidly after birth. 2. These changes in fetal prostaglandin levels contrast with the marked increase in PGF, but negligible increase in PGE, in the maternal uteroovarian vein before parturition. 3. The changes in prostaglandin concentrations in fetal plasma at term are associated with only small changes in the concentrations of PGE and PGF in tracheal fluid. In amniotic fluid the concentrations of PGE and PGF increase during the last 4 days in utero. At birth the concentrations of PGE and PGF in fetal urine are similar to the concentrations in amniotic fluid. 4. The concentration of PGE in fetal plasma and in tracheal fluid is significantly elevated for up to 3 days after surgery. The concentration of PGF is significantly elevated in fetal plasma nad tracheal fluid for at least 24 hr after surgery. 5. Three fetuses which were chronically hypoxemic had elevated plasma PGE concentrations in utero. However, acute (1 hr) hypoxia or hypercapnia induced in the fetal lamb by making the ewe breathe appropriate gas mixtures did not produce consistent changes in fetal plasma prostaglandin concentrations. 6. During late pregnancy (day 128) exogenous PGE2 infused at about 1.6 microgram/min for 60 min into the fetal carotid artery achieved concentrations in the fetal femoral artery which were within the physiological range seen at term. At this infusion rate, there was no effect on fetal arterial Po2, Pco2, pH, or hematocrit, and no consistent effect on fetal blood pressure or heart rate. PGE2 infusion had no significant effect on the concentration of growth hormone or prolactin in fetal plasma. Within 30 min after beginning the infusion, however, there was a significant increase in the cortisol concentration in fetal plasma. This effect was seen even at times in pregnancy when the fetal adrenal gland responds only poorly to exogenous or endogenous ACTH.
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PMID:Prostaglandins in the sheep fetus: implications for fetal function. 64 1

The oxygenation and metabolism in appropriate (AGA) and small for gestational age (SGA) fetuses has been investigated by cordocentesis. The umbilical venous and arterial pO2 and pH decrease with gestational age while pCO2 increases and blood lactate concentration does not change. The mean umbilical venous blood glucose concentration is higher than in the umbilical artery indicating that there is fetal glucose uptake from the placenta. Similarly, the maternal glucose concentration is higher than the fetal and the levels in the two compartments are significantly correlated. The plasma insulin concentration increases exponentially with gestation reflecting the progressive maturation of the fetal pancreas. The fetal plasma cortisol does not change but the fetal plasma ACTH increases with gestation. Fetal plasma triglyceride concentration decreases exponentially with gestation and this is likely to be the result of increased utilization by the fetus for deposition into adipose tissue. There is a high correlation between fetal and maternal levels for individual amino acids and the concentration in the fetus is higher than in the mother, supporting the active transport of amino acids by the placenta. Some SGA fetuses are compromised by hypoxemia, hypercapnia, hyperlacticemia and acidosis, are starved of glucose and amino acids, and are hypertriglyceridemic. Furthermore, some of these fetuses are hypoinsulinemic and the degree of hypoinsulinemia is disproportional to the degree of hypoglycemia suggesting pancreatic dysfunction. In SGA fetuses the plasma cortisol is increased and the plasma ACTH decreased. Knowledge of human fetal oxygenation and metabolism may help in deciding the optional timing of delivery but may also constitute a basis for future fetal therapy in the form of oxygen and nutrient supplementation.
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PMID:Metabolic and endocrine findings in appropriate and small for gestational age fetuses. 165 88

We studied the effect of chronic carotid body denervation on renin (plasma renin activity, PRA), adrenocorticotropin (ACTH), blood pressure, and hematocrit responses to acute normocapnic (arterial CO2 partial pressure, PaCO2, 35 Torr) and hypercapnic (PaCO2, 65 Torr) hypoxia (arterial O2 partial pressure, PaO2, 31 Torr) in five anesthetized, artificially ventilated dogs. Animals were studied at least 3 days before and again at least 10 days after carotid body denervation (bilateral carotid sinus nerve resection). Increases in PRA during hypercapnic normoxia [21.8 +/- 6.4 ng angiotensin I (ANG I) X ml-1 X 3 h-1] and normocapnic hypoxia (13.3 +/- 4.2 ng ANG I X ml-1 X 3 h-1) were not attenuated by carotid body denervation. Increases in ACTH during normocapnic hypoxia (117 +/- 34 pg/ml) were attenuated but not eliminated by carotid body denervation; the increase in ACTH during hypercapnic hypoxia (295 +/- 93 pg/ml) was not attenuated by carotid body denervation. Both the blood pressure and hematocrit responses to normocapnic and hypercapnic hypoxia were attenuated by carotid body denervation. We concluded that 1) the renin response to hypercapnia and hypoxia is not a carotid chemoreflex, 2) the ACTH response to hypoxia is partially a carotid chemoreflex, and 3) blood pressure and hematocrit responses to hypoxia are primarily carotid chemoreflexes.
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PMID:Renin and ACTH responses to hypercapnia and hypoxia after chronic carotid chemodenervation. 608 93

The dispersed neuroendocrine (NE) system is represented in the bronchopulmonary tract by the solitary neuroendocrine cells and the neuroepithelial bodies (NEBs). Immunohistochemically, neuron-specific enolase, serotonin, bombesin, and calcitonin are demonstrable in both components, whereas leu-enkephalin is demonstrable only in solitary NE cells. The precise function of and interplay between these two components under physiologic and pathologic conditions are not entirely clear. Current indications are that NEBs act as intrapulmonary chemoreceptors sensitive to hypoxia and hypercapnia, whereas solitary NE cells may have a paracrine, regulatory function. Even less clear is the possible role of solitary NE cells and NEBs in the processes associated with intrauterine and neonatal pulmonary growth and maturation. Various experimental manipulations have resulted in proliferation of solitary NE cells and NEBs. Of particular interest is the apparently selective proliferative effect on NEBs shown by several nitroso compounds. Diethylnitrosamine administration to hamsters for several weeks results in an increase in the number of NEBs and an increase in the number of cells per NEB. These hyperplastic NEBs express the same immunoreactive hormones as their normal counterparts. However, when NEB cells from diethylnitrosamine-treated hamsters are cultured in vitro a notable proportion of the resulting endocrine cells express ACTH immunoreactivity. Interestingly, the neoplasms that eventually develop in these hamsters are not comprised of NE cells. Studies on human bronchi from specimens resected for various types of neoplasms and for bronchiectasis with and without associated chronic obstructive pulmonary disease have revealed frequent hyperplasias of solitary NE cells and NEBs. In about 10% of the specimens, dysplastic aggregates of solitary NE cells and NEBs are found. Unexpected "microcarcinoids" and tumorlets are also seen. The mildly and moderately hyperplastic solitary NE cells and NEBs tend to express the hormones indigenous to the bronchi, whereas in the severely hyperplastic and dysplastic cells, "ectopic" hormones may also be expressed; the latter include predominantly ACTH and vasoactive intestinal polypeptide. A distinct hyperplasia of NEBs has been found in the lungs from individuals living at altitudes ranging from 3400 to 4300 meters; these changes may represent an adaptive response to chronic hypoxia parallel to the hyperplastic carotid paraganglia that may be found in the same type of population. Bronchopulmonary NE neoplasms comprise a spectrum that includes typical carcinoids, well-differentiated NE carcinomas, and NE carcinomas of intermediate and small cell types. Typical carcinoids are predominantly central, display little if any pleomorphism, are richly granulated by electron microscopy, and by immunohistochemistry express predominantly, although not exclusively, hormones indigenous to their site of origin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuroendocrine components of the bronchopulmonary tract: hyperplasias, dysplasias, and neoplasms. 613 58

We examined the interaction of graded hypoxia and hypercapnia on stimulation of vasopressin (AVP), ACTH, and corticosteroids in nonsurgically stressed, pentobarbital-anesthetized, gallamine-paralyzed ventilated dogs. Partial pressure of O2 in arterial blood (PaO2) levels of approximately 26-29, 38-41, 54-57, and 83-88 Torr were achieved by altering the fractional concentration of O2 in dry inspired gas with a normocapnic (PaCO2, 35 Torr) and hypercapnic (PaCO2, 59 Torr) background. Normocapnic hypoxia produced a PaO2-dependent increase in AVP, ACTH, and corticosteroids. The threshold PaO2 for AVP was lower (approximately 35 Torr) than for ACTH (approximately 45 Torr). AVP, ACTH, and corticosteroids at all PaO2 levels were higher during hypercapnia. In addition, an ACTH and corticosteroid dose-response correlation estimated the threshhold ACTH to be 20-30 pg/ml. The PaO2-dependent hormone increases and the augmentation of these relationships by hypercapnia are consistent with a peripheral chemoreceptor-mediated reflex. In addition, hypoxia and hypercapnia did not seem to alter the high sensitivity of the adrenal cortex for ACTH.
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PMID:Vasopressin, ACTH, and corticosteroids during hypercapnia and graded hypoxia in dogs. 630 30

In recent years, the expanding literature in fetal cardiovascular physiology and endocrinology has improved our understanding of the afferent mechanisms involved in the reflex hormonal and neural responses to cardiovascular distresses, such as hypotension, hypoxia, hypercapnia, and asphyxia. For some endocrine systems, the relative roles of peripheral and central baroreceptors and chemoreceptors are well understood. The best example of such a system is AVP, summarized in Fig. 6. Published experiments have demonstrated that AVP secretion is influenced by arterial baroreceptors, but not by arterial chemoreceptors. On the other hand, there is most likely a chemosensitive area within the central nervous system controlling AVP secretion which responds to hypoxia as well as hypercapnia. Cardiac receptors are less important in the control of AVP secretion in fetal life than in postnatal life. Our understanding of the control of other hormonal systems, including renin and ACTH, is less complete. The challenge for the future in this field will be to fill in the gaps in our knowledge of these fetal reflexes, and to provide a functional understanding of the mechanisms underlying the quantitative differences between fetus and adult. For example, does the rearrangement of the circulation at birth 'activate' the cardiac receptors by changing intracardiac pressures, or are the neuronal pathways poorly developed in the fetus compared with the postnatal animal? Also, what is the mechanism of the chemoreflex control of AVP which is independent of peripheral chemoreceptor integrity in the fetus? The answers to these questions and others will significantly improve our understanding of fetal cardiovascular and endocrine physiology. These answers will also provide information which will prove to be of practical importance in a modern age of obstetrics, paediatrics, and surgery, where the fetus will increasingly be treated as a young patient.
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PMID:Baroreflex and chemoreflex control of fetal hormone secretion. 860 59