Effects of Prenatal Ethanol Exposure on Juvenile Play-Fighting and Postpubertal Aggression in Rats

1990 ◽  
Vol 66 (2) ◽  
pp. 551-560 ◽  
Author(s):  
Joel Royalty
Keyword(s):  
Significant Positive Correlation ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Prenatal Treatment ◽  
Maternal Weight ◽  
Behavioral Measures ◽  
Treatment Groups ◽  
Play Fighting ◽  
Behavioral Variables ◽  
Eye Opening

The effects of prenatal ethanol exposure on juvenile play-fighting and postpubetal aggressive behavior in rats were longitudinally assessed in the context of more conventionally applied physical and behavioral measures. Pregnant animals were treated with either 2 gm/kg/day ethanol or isocaloric sucrose over gestation Days 6—19. Reproduction and somatic variables included maternal weight over gestation, offspring weight over Days 1—90, and age at eye opening and incisor eruption. Behavioral variables consisted of negative geotaxis, olfactory discrimination, activity, juvenile play-fighting, and postpubetal aggression. Ethanol offspring had lower birth weights, but there was no significant prenatal treatment effect on subsequent offspring weights or on any other reproductive or somatic variable. Both male and female ethanol-exposed offspring exhibited more play-fighting responses when paired with same-sex controls. Postpubertal aggression levels were assessed in males only. Ethanol-exposed offspring were more aggressive than controls and there was a significant positive correlation between play-fighting and postpubertal aggression ranks. No other behavioral measures discriminated between prenatal treatment groups and none were significantly correlated with either play-fighting or postpubertal aggression rank. The results are consistent with the position that juvenile play-fighting and postpubertal aggression are subserved by common substrates. They also are consistent with predictions derived from the hypothesis concerning a response-inhibition deficit as an effect of prenatal ethanol exposure on behavior.

scholarly journals Effects of prenatal ethanol exposure on the lungs of postnatal lambs

2011 ◽  
Vol 300 (1) ◽  
pp. L139-L147 ◽  
Author(s):  
Foula Sozo ◽  
Melissa Vela ◽  
Victoria Stokes ◽  
Kelly Kenna ◽  
Peter J. Meikle ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Phospholipid Composition ◽  
Lavage Fluid ◽  
Ethanol Exposure ◽  
Cytokine Gene Expression ◽  
Ethanol Administration ◽  
Mrna Levels ◽  
Prenatal Ethanol Exposure ◽  
Treatment Groups

Prenatal ethanol exposure increases collagen deposition and alters surfactant protein (SP) expression and immune status in lungs of near-term fetal sheep. Our objectives were to determine 1) whether these prenatal effects of repeated gestational ethanol exposure persist after birth and 2) whether surfactant phospholipid composition is altered following prenatal ethanol exposure. Pregnant ewes were chronically catheterized at 90 days of gestational age (DGA) and given a 1-h daily infusion of ethanol (0.75 g/kg, n = 9) or saline ( n = 7) from 95 to 135 DGA; ethanol administration ceased after 135 DGA. Lambs were born naturally at full term (146 ± 0.5 DGA). Lung tissue was examined at 9 wk postnatal age for alterations in structure, SP expression, and inflammation; bronchoalveolar lavage fluid was examined for alterations in surfactant phospholipid composition. At 134 DGA, surfactant phospholipid concentration in amniotic fluid was significantly reduced ( P < 0.05) by ethanol exposure, and the composition was altered. In postnatal lambs, there were no significant differences between treatment groups in birth weight, postnatal growth, blood gas parameters, and lung weight, volume, tissue fraction, mean linear intercept, collagen content, proinflammatory cytokine gene expression, and bronchoalveolar lavage fluid surfactant phospholipid composition. Although SP-A, SP-B, and SP-C mRNA levels were not significantly different between treatment groups, SP-D mRNA levels were significantly greater ( P < 0.05) in ethanol-treated animals; as SP-D has immunomodulatory roles, innate immunity may be altered. The adverse effects of daily ethanol exposure during late gestation on the fetal lung do not persist to 2 mo after birth, indicating that the developing lung is capable of repair.

Reversal of cardiomyopathy resulting from prenatal exposure to ethanol

1984 ◽  
Vol 42 ◽  
pp. 716-717
Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie
Keyword(s):  
Prenatal Exposure ◽  
Heart Development ◽  
Membrane Integrity ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Pathological Changes ◽  
Prenatally Exposed ◽  
Inner Mitochondrial Membrane ◽  
Fetal Alcohol ◽  
Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

Permanent abnormal response to a glucose load after prenatal ethanol exposure in rats

Alcohol ◽  
1989 ◽  
Vol 6 (6) ◽  
pp. 469-473 ◽  
Author(s):  
Dolores López-Tejero ◽  
Miquel Llobera ◽  
Emilio Herrera
Keyword(s):  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Glucose Load ◽  
Abnormal Response

Relief of pain and trismus in patients treated with naproxen or acetylsalicylic acid after tonsillectomy

1988 ◽  
Vol 102 (1) ◽  
pp. 39-42 ◽  
Author(s):  
S. Kristensen ◽  
K. Tveteraas ◽  
P. Hein ◽  
H. B. Poulsen ◽  
K. E. Outzen
Keyword(s):  
Clinical Trial ◽  
Acetylsalicylic Acid ◽  
Pain Intensity ◽  
Sleep Disturbances ◽  
Significant Positive Correlation ◽  
Controlled Trial ◽  
Double Blind ◽  
Treatment Groups ◽  
Significant Difference ◽  
Therapeutic Gain

AbstractThe pain-relieving efficacy of naproxen and acetylsalicylic acid (ASA) in tonsillectomized patients was compared in a double blind parallel clinical trial comprising 83 patients, among whom 42 were treated with naproxen and 41 with ASA. The patients were treated post-operatively for two days with either naproxen suppositories 500 mg. twice, or ASA effervescent tablets 1000 mg. three times, daily.The therapeutic gain was evaluated by recording the intensity of pain, reduced ability to open the mouth (trismus), consumption of supplementary analgesic (parcetamol), and pain-related sleep disturbances.The statistical analysis of the results revealed no differences in pain intensity, consumption of additional analgesics or pain-related sleep disturbances in the two treatment groups. A considerable degree of trismus was demonstrated in most of the tonsillectomized patients. This reduced ability to open the mouth was gradually overcome in the naproxen group while it remained unchanged in the ASA group, however, no statistical significant difference could be demonstrated. Additionally, no significant positive correlation between pain intensity and trismus was proven. The pain-relieving effect, however, was unsatisfactory in both the naproxen and the ASA group, and clinical controlled trial studies of alternative analgetics in tonsillectomized patients are still to be encouraged.

Prenatal ethanol exposure impairs the conduction delay at the atrioventricular junction in the looping heart

2021 ◽  
Author(s):  
Shan Ling ◽  
Michael W Jenkins ◽  
Michiko Watanabe ◽  
Stephanie M Ford ◽  
Andrew M Rollins
Keyword(s):  
Heart Development ◽  
Molecular Mechanisms ◽  
Early Stage ◽  
Heart Defects ◽  
Ethanol Exposure ◽  
Cardiac Conduction ◽  
Conduction Delay ◽  
Prenatal Ethanol Exposure ◽  
Endocardial Cushions ◽  
Atrioventricular Junction

The etiology of ethanol-related congenital heart defects has been the focus of much study, but most research has concentrated on cellular and molecular mechanisms. We have shown with optical coherence tomography (OCT) that ethanol exposure led to increased retrograde flow and smaller atrioventricular (AV) cushions compared to controls. Since AV cushions play a role in patterning the conduction delay at the atrioventricular junction (AVJ), this study aims to investigate whether ethanol exposure alters the AVJ conduction in early looping hearts and whether this alteration is related to the decreased cushion size. Quail embryos were exposed to a single dose of ethanol at gastrulation, and Hamburger-Hamilton stage 19 - 20 hearts were dissected for imaging. Cardiac conduction was measured using an optical mapping microscope and we imaged the endocardial cushions using OCT. Our results showed that, compared with controls, ethanol-exposed embryos exhibited abnormally fast AVJ conduction and reduced cushion size. However, this increased conduction velocity (CV) did not strictly correlate with decreased cushion volume and thickness. By matching the CV map to the cushion size map, we found that the slowest conduction location was consistently at the atrial side of the AVJ, which had the thinner cushions, not at the thickest cushion location at the ventricular side as expected. Our findings reveal regional differences in the AVJ myocardium even at this early stage in heart development. These findings reveal the early steps leading to the heterogeneity and complexity of conduction at the mature AVJ, a site where arrhythmias can be initiated.

Prenatal ethanol exposure potentiates isolation-induced ethanol consumption in young adult rats

Alcohol ◽  
2019 ◽  
Vol 75 ◽  
pp. 39-46 ◽  
Author(s):  
Macarena Soledad Fernández ◽  
Jorge Carrizo ◽  
Wladimir Plaza ◽  
Paola Haeger ◽  
Ricardo Marcos Pautassi
Keyword(s):  
Young Adult ◽  
Ethanol Consumption ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Adult Rats
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