Comparative development of the nervous, respiratory, and cardiovascular systems.

Monie, I. W.

doi:10.1289/ehp.761855

Cited by 18 publications

(13 citation statements)

References 8 publications

(6 reference statements)

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“…The neural tube closure occurs around 10.5 to 11.0 days of development in rats, between 9.0 to 9.5 days in mice, 9.5 to 10.5 days in rabbits, 8.25 to 8.5 days in hamsters and about 14.5 days of gestation in Oligoryzomys . According to Monie (1976) in the guinea pig the neural tube closure occurs at a more advanced gestational period when compared to these other species, around 15.25 to 16.5 days, similar to our study, where this closure was observed between 14 and 18 days post conception.…”

Section: Discussionsupporting

confidence: 90%

Development of the central nervous system in guinea pig (Cavia porcellus, Rodentia, Caviidae)

et al. 2016

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This study describes the development of the central nervous system in guinea pigs from 12th day post conception (dpc) until birth. Totally, 41 embryos and fetuses were analyzed macroscopically and by means of light and electron microscopy. The neural tube closure was observed at day 14 and the development of the spinal cord and differentiation of the primitive central nervous system vesicles was on 20th dpc. Histologically, undifferentiated brain tissue was observed as a mass of mesenchymal tissue between 18th and 20th dpc, and at 25th dpc the tissue within the medullary canal had higher density. On day 30 the brain tissue was differentiated on day 30 and the spinal cord filling throughout the spinal canal, period from which it was possible to observe cerebral and cerebellar stratums. At day 45 intumescences were visualized and cerebral hemispheres were divided, with a clear division between white and gray matter in brain and cerebellum. Median sulcus of the dorsal spinal cord and the cauda equina were only evident on day 50. There were no significant structural differences in fetuses of 50 and 60 dpc, and animals at term were all lissencephalic. In conclusion, morphological studies of the nervous system in guinea pig can provide important information for clinical studies in humans, due to its high degree of neurological maturity in relation to its short gestation period, what can provide a good tool for neurological studies.

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Section: Discussionsupporting

confidence: 90%

Development of the central nervous system in guinea pig (Cavia porcellus, Rodentia, Caviidae)

et al. 2016

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“…The postnatal rat is an established experimental model of human prematurity, as postnatal development of neuronal, cardiovascular, and respiratory function in this species compares with prenatal milestones in the human (17,18). Data in the present study show that postnatal treatment of rat pups with dexamethasone in human clinically relevant doses decreased regional brain volumes, cortical neuronal number and hippocampal soma volume, while increasing the density of GFAPpositive astrocytes in the white matter when measured at weaning.…”

Section: Discussionsupporting

confidence: 48%

Statins prevent adverse effects of postnatal glucocorticoid therapy on the developing brain in rats

et al. 2013

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Background: Postnatal glucocorticoid therapy in the treatment of chronic lung disease benefits lung function, however it adversely affects brain development. We hypothesized that combined postnatal glucocorticoid and statin therapy diminishes adverse effects of glucocorticoids on the developing brain. Methods: On postnatal days (P) 1-3, one male pup per litter received i.p. injections of saline (control (C), n = 13) or dexamethasone (0.5, 0.3, 0.1 µg/g; D, n = 13), ± pravastatin (10 mg/ kg i.p.; CP, n = 12; DP, n = 15). Statins or saline continued from P4-6. At P21, brains were perfusion fixed for histological and stereological analyses. results: Relative to controls, dexamethasone reduced total (837 ± 23 vs. 723 ± 37), cortical (378 ± 12 vs. 329 ± 15), and deep gray matter (329 ± 12 vs. 284 ± 15) volume (mm 3 ), cortical neuronal number (23 ± 1 vs. 19 ± 1 × 10 6 ), and hippocampal neuronal soma volume (CA1: 1,206 ± 32 vs. 999 ± 32; dentate gyrus: 679 ± 28 vs. 542 ± 24 µm 3 ; all P < 0.05). Dexamethasone increased the glial fibrillary acidic protein-positive astrocyte density in the white matter (96 ± 2 vs. 110 ± 4/0.1 mm 2 ); P < 0.05. These effects no longer occurred in brains from pups treated with combined dexamethasone and pravastatin. Pravastatin alone had no effect on these variables. conclusion: Concomitant dexamethasone with statins in premature infants may be safer for the developing brain than dexamethasone alone in the treatment of chronic lung disease. c hronic lung disease is a common outcome in extremely preterm neonates with severe respiratory distress syndrome and carries a high incidence of morbidity and mortality (1). Glucocorticoids, predominantly dexamethasone, are used to decrease inflammatory responses, accelerate surfactant production, and lung maturation, thereby improving respiratory function (2).Despite the well-established beneficial effects of postnatal glucocorticoid therapy, there has been serious growing concern regarding their clinical use because of unwanted side effects on somatic growth and weight gain in premature babies (3,4). Accumulating evidence from clinical trials has also demonstrated an association between postnatal steroid therapy and adverse neuromotor and cognitive outcomes (4,5). Furthermore, experimental studies in neonatal animals have demonstrated adverse effects of potent glucocorticoids, such as dexamethasone, on brain growth, cell division, differentiation, myelination, apoptosis, and neurogenesis (6-8).To date, the mechanism underlying the unwanted side effects of glucocorticoid therapy on the developing brain remains unknown, preventing the identification of plausible modified therapies to maintain the beneficial, but prevent the adverse, effects of steroid treatment. Glucocorticoids are known to decrease nitric oxide (NO) bioavailability and increases in NO via antioxidant treatment have been shown to prevent or partially restore glucocorticoid-induced cardiovascular dysfunction and hypertension (9,10), implying impaired NO physiology as the culprit mecha...

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“…, ). Interestingly, and perhaps surprisingly, the chronology of cardiac development in the chicken is much more comparable to the human than is the rodent, in which cardiac development continues into the postnatal period (Sissman, ; Monie, ; Marcela et al . ; see Fig.…”

Section: Introductionmentioning

confidence: 99%

The highs and lows of programmed cardiovascular disease by developmental hypoxia: studies in the chicken embryo

Itani

Salinas

Villena

et al. 2017

The Journal of Physiology

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It is now established that adverse conditions during pregnancy can trigger a fetal origin of cardiovascular dysfunction and/or increase the risk of heart disease in later life. Suboptimal environmental conditions during early life that may promote the development of cardiovascular dysfunction in the offspring include alterations in fetal oxygenation and nutrition as well as fetal exposure to stress hormones, such as glucocorticoids. There has been growing interest in identifying the partial contributions of each of these stressors to programming of cardiovascular dysfunction. However, in humans and in many animal models this is difficult, as the challenges cannot be disentangled. By using the chicken embryo as an animal model, science has been able to circumvent a number of problems. In contrast to mammals, in the chicken embryo the effects on the developing cardiovascular system of changes in oxygenation, nutrition or stress hormones can be isolated and determined directly, independent of changes in the maternal or placental physiology. In this review, we summarise studies that have exploited the chicken embryo model to determine the effects on prenatal growth, cardiovascular development and pituitary-adrenal function of isolated chronic developmental hypoxia.

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Comparative development of the nervous, respiratory, and cardiovascular systems.

Cited by 18 publications

References 8 publications

Development of the central nervous system in guinea pig (Cavia porcellus, Rodentia, Caviidae)

Development of the central nervous system in guinea pig (Cavia porcellus, Rodentia, Caviidae)

Statins prevent adverse effects of postnatal glucocorticoid therapy on the developing brain in rats

The highs and lows of programmed cardiovascular disease by developmental hypoxia: studies in the chicken embryo

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