Prenatal High-Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring.

SCOPE: Maternal nutrition during pregnancy is related to intrauterine fetal development. The authors' previous work reports that prenatal high sucrose (HS) diet impaired micro-vascular functions in postnatal offspring. It is unclear whether/how prenatal HS causes vascular injury during fetal life. METHODS AND RESULTS: Pregnant rats are fed with normal drinking water or 20% high-sucrose solution during the whole gestational period. Pregnant HS increases maternal weight before delivery. Fetal thoracic aorta is separated for experiments. Angiotensin II (AII)-stimulated vascular contraction of fetal thoracic arteries in HS group is greater, which mainly results from the enhanced AT1 receptor (AT1R) function and the downstream signaling. Nifedipine significantly increases vascular tension in HS group, indicating that the L-type calcium channels (LTCCs) function is strengthened. 2-Aminoethyl diphenylborinate (2-APB), inositol 1,4,5-trisphosphate receptors (IP3Rs) inhibitor, increases vascular tension induced by AII in HS group and ryanodine receptors-sensitive vascular tone shows no difference in the two groups, which suggested that the activity of IP3Rs-operated calcium channels is increased. CONCLUSION: These findings suggest that prenatal HS induces vascular dysfunction of thoracic arteries in fetal offspring by enhancing AT1R, LTCCs function and IP3Rs-associated calcium channels, providing new information regarding the impact of prenatal HS on the functional development of fetal vascular systems.

The Blood Supply of the Breast Revisited.

BACKGROUND: Many surgeons are under the impression that the blood supply is clearly defined in textbooks. Unfortunately, the majority of textbooks supply inadequate information and illustrations can be misleading in many instances. None of the textbooks describe a segmental pattern of blood supply when in actual fact a basic segmental pattern does exist. The reason for inadequate information is the perpetuation of facts since the work of the pioneers Cooper and Manchot from one textbook to another. A paucity of research studies thereafter and the fact that the results of some of these studies did not find their way into textbooks is another contributing factor. METHODS: The findings of research studies since the descriptions by Cooper and Manchot are analyzed and compared in an effort to find common ground and its clinical implication. RESULTS: Researchers concurred on the main sources of blood supply; these are internal thoracic, lateral thoracic, anterior intercostal, and acromiothoracic (thoracoacromial) arteries. However, the different research studies showed considerable variation in the branches from the main sources to supply the nipple-areola complex. CONCLUSIONS: Even though the locations of the main sources of blood supply are constant, partial or complete absence of branches from the main sources does occur and therefore the blood supply to the nipple-areola complex is unpredictable. Cognizance of the basic segmental pattern and the variations resulting from embryologic development will be helpful for the surgeon to use or adapt a technique to minimize the risk of nipple necrosis.

Frizzled 2 is transiently expressed in neural crest-containing areas during development of the heart and great arteries in the mouse.

Frizzled 2 acts as a 7-transmembrane receptor in the Wnt-Dishevelled signal transduction cascade. Among others, this cascade has been associated with neural crest cell proliferation and early migration during development in mammals. The genes for some components of this cascade are located in chromosomal regions that are deleted in human syndromes associated with neural crest cell defects, like DiGeorge and Velo-Cardio-Facial Syndrome. These syndromes are often accompanied by abnormalities in cardiac morphology. Furthermore, we have reported in previous studies the upregulation of the tissue polarity gene frizzled 2 in myofibroblasts during their migration into the necrotic area after myocardial infarction in the adult heart. It is known that genes that are upregulated during cardiac remodeling due to pathology often play a role during development. To investigate whether frizzled 2 can be associated with the process of cardiac morphogenesis we studied its expression in the thoracic arterial system and heart of mouse embryo's of 10, 12, 14, 16 and 18 days after conception by means of in situ hybridization. At day 10 after conception signal could be found in the pharyngeal arches and arch arteries. The outflow tract, the ascending aorta and the pulmonary trunk were positive for frizzled 2 from day 12 on. This expression decreased with time and at day 18 only some signal could be detected in the aorta and pulmonary trunk. In contrast, in coronary and pulmonary arteries no expression was observed at any time point. Minor myocardial expression was observed in the ventricular septum at days 12 and 14. Atrial expression, although considerably lower than ventricular expression, could be detected somewhat later at days 14 and 16. Our results indicate that there is transient expression of frizzled 2 in areas that are invested by neural crest cells. This expression is downregulated upon neural crest cell differentiation. The frizzled 2 expression supports a role for the Wnt-frizzled pathway in neural crest-related disorders.

Patterns of paired-related homeobox genes PRX1 and PRX2 suggest involvement in matrix modulation in the developing chick vascular system.

PRX1 (MHox) and PRX2 (S8) were previously shown to be expressed throughout embryogenesis in complex, mostly mesenchyme-specific patterns. In the developing cardiovascular system both genes were highly expressed in prospective connective tissues, that is, endocardial cushions and valves, the epicardium, and the wall of the great arteries and veins. We further scrutinised expression of PRX1 and PRX2 in the developing vascular system of the chicken embryo and compared patterns with those of established vascular differentiation markers (muscle-actin, procollagen I, and fibrillin-2). PRX1 and PRX2 expression were associated with the primary vessel wall from early stages onward and became increasingly restricted to the adventitial and outer medial cell layers. PRX1 eventually colocalised strikingly with procollagen I and fibrillin-2 expression and generally excluded high smooth muscle actin expression. Furthermore, PRX1 expression preceded the segregation of very distinct nonmuscular cells and smooth muscle cells in the media of the great arteries. PRX2 patterns deviated at later stages from those of PRX1 and showed specific and high transcript levels in the ductus arteriosus from embryonic day 6 onward. Results suggest that PRX genes are not essential in smooth muscle contractile differentiation, but may be involved in matrix modulation in the vascular system and possibly in defining the noncontractile cellular phenotype and in media-adventitia definition.

Abnormal origin of internal thoracic and vertebral arteries.

The aim of this study was to evaluate the variability of the origin of the internal thoracic and vertebral arteries after a cadaver demonstrated abnormal origins for both vessels. The arteries were studied in 60 adult cadavers and measurements taken to adjacent structures. In one cadaver the right internal thoracic artery originated from the third part of the subclavian artery (one of 120 arteries; 0.83%). The same cadaver presented with the left vertebral artery originating directly from the aortic arch between the left common carotid and left subclavian arteries. Two other cadavers also presented with abnormal vertebral arteries, making it three of 60 left vertebral arteries (5%). These results are comparable to the established range in the literature. The internal thoracic artery is used for revascularization in coronary artery diseases and as this area is also used for subclavian vein catheterization, it is important to be aware of this rare variation concerning the internal thoracic artery. This study reports an important variation in the origins of the internal thoracic and vertebral artery in a singular cadaver.

Changes observed in Doppler studies of the fetal circulation in pregnancies complicated by pre-eclampsia or the delivery of a small-for-gestational-age baby. I. Cross-sectional analysis.

The aim of this study was to compare changes in Doppler ultrasound studies of the fetal circulation in normal pregnancies with a group of pregnancies complicated by proteinuric pregnancy-induced hypertension (PPIH), delivery of a small-for-gestational-age (SGA) baby, or both. A total of 167 uncomplicated pregnancies with a term delivery of an appropriately grown baby (AGA) were used to define the normal range. Altogether, 123 high-risk pregnancies with a known outcome constituted the study group. A color duplex ultrasound machine was used to perform biometry and fetal Doppler studies. Measurements obtained from the fetal circulation included the umbilical artery (UA) pulsatility index (PI), the middle cerebral artery (MCA) PI and time-averaged velocity (TAV), the thoracic aorta (AO) PI and TAV. In addition, the ratio between the MCA PI and UA PI, the MCA PI and the AO PI, and the product of the MCA PI and AO TAV were used in the analysis. A total of 105 pregnancies had a complicated outcome. They were divided into three categories: PPIH only (pregnancies complicated by PPIH with the delivery of an AGA fetus, n = 17), SGA only (delivery of an SGA baby, with no evidence of PPIH, n = 55), and PPIH + SGA (pregnancies complicated by pre-eclampsia and delivery of an SGA baby, n = 37). The PPIH + SGA group represented true clinical intrauterine growth retardation. Cross-sectional reference ranges were created using the observations from the normal group. z-scores (standard deviation from the mean of the normal range) of the last observations made before delivery were calculated for each of the vessel velocimetry measurements and ratios. The statistical significance of z-score values was calculated using analysis of variance. The MCA and UA PI values showed the greatest deviation for any single-vessel parameter. The ratios of fetal Doppler indices (MCA/UA PI ratio, MCA/AO PI ratio and the MCA PI/AO TAV index) demonstrated greater deviation from normal than any individual vessel. The UA PI z-score for PPIH+SGA delivering < 34 weeks gestation (2.92) was significantly greater than the z-score for PPIH+SGA delivering > or = 34 weeks (1.20, p < 0.05). Fetal Doppler indices, in particular ratios that include measurements obtained from the cerebral circulation, help in the recognition of the small fetus that is growth-retarded. At term, evidence of fetal hemodynamic redistribution may exist in the presence of a normal umbilical artery PI. Fetal Doppler indices provide information that is not readily obtained from more conventional tests of fetal well-being.(ABSTRACT TRUNCATED AT 400 WORDS)