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Journal of the Anatomical Society of India

Gastric and Cystohepatic teratogenicity - related to altered blood flow during development phase-Extrapolation using observations from adult Specimens

Author(s): Kumar Keshaw

Vol. 51, No. 2 (2002-07 - 2002-12)

Department of Anatomy, Institute of Medial Sciences, B.H.U., Varanasi INDIA.

Abstract

Abdomen of 216 cadavers was dissected in order to study the teratogenic effect of greater and lesser blood supply on development of stomach and liver with gall bladder respectively. Only in one cadaver stomach and left gastric as well as right gastroepiploic arteries were larger in size while liver with gall bladder and cystic as well as hepatic arteries were smaller in size. Gastric hyperplasia and cystohepatic hypoplasia were teratogenic effects of greater arterial blood supply to stomach and lesser arterial blood supply to liver with gall bladder respectively because during ontogeny arteries develop prior to organs.

Key words: Teratogenecity, Hyperplasia, Hypoplasia, Blood Supply, Stomach.

Introduction:

Brent and Franklin (1960), Franklin and Brent (1964), Leist and Grauwiler (1972, 1974) reported the effects of uterine vessel clamping on the development of rat embryos. Danielsson et al (1989, 1990) described digital defects induced by vasodilating agents and its relationship to decreased uteroplacental blood flow. Caplan and Koutrouspas (1973) described the role of differential vascularization in control of muscle and cartilage development in chick limb. Grabowski (1970) showed embryogenic oxygen deficiency as a physiological approach to analysis of teratological mechanism. However the teratogenic effects of increased blood supply on the development of stomach and decreased blood supply on the development of liver with gall bladder have not been observed till now by any author.

The present study is conducted to observe the teratogenic effects of greater arterial blood supply on gastric development and lesser arterial blood supply on cystohepatic development.

Material and Method:

Abdomen of 216 cadavers were dissected to find out anomalies in the arteries supplying stomach, liver and gall bladder and also to observe the teratogenic effects of greater arterial blood supply on gastric development with lesser blood supply on cystohepatic development if any.

Observations:

While dissecting abdomen in cadavers only in one out of 216 cadavers it was found that stomach was enlarged twice to its normal size having quadrangular shape and lying in left as well as right hypochondriac regions of abdomen. The position and shape of liver was normal but it was reduced to half of its normal size and its left lobe was represented by a fibrous band. Size of quadrate lobe, caudate lobe and gall bladder was also reduced according to reduction in size of right lobe of liver. Histologial study of these viscera did not reveal any abnormality.

Superior mesentric artery gave common hepatic artery which divided into a large gastroduodenal and a small hepatic branch to supply right lobe of liver which was reduced to half of its normal size. From hepatic artery a smaller cystic artery arose to supply gall bladder which was also reduced to half of its normal size. Right gastroepiploic branch arising from gastroduodenal artery was larger sized and superior pancreaticoduodenal artery was normal sized. After giving normal sized splenic artery coeliac trunk continued as a larger left gastric artery which gave a slender branch to fibrosed rudimentary left lobe of liver before reaching the lesser curvature of stomach.

Discussion:

Findings of Grabowski (1970) in chick embryo that hypoxia caused disturbance of fluid and electrolyte balance and an increase in the body fluid was associated with oedema and haemorrhage produces maldevelopment, support the observations made in the present study where under nutrition due to lesser blood supply to the gall bladder and right lobe of liver and least blood supply to left lobe of liver resulted into cystohepatic hypoxia causing hypoplasia of gall bladder as well as right lobe of liver and fibrosis of left lobe of liver proving the oedema syndrome described by Danielsson (1990) and "Hypoxia hypothesis" put forth by Leist and Grauwiler (1974) who maintained that foetal hypoxia leads to a dramatic increase of the diameter and rupture of thin walled vessels of the limb plate, localized oedema, haemorrhage (producing further hypoxia) and finally necrosis of the most distal digital phalanges. Clamping experiments performed by Leist and Grauwiler (1972) in the rat have shown that effects on foetus depend not only on degree of blood flow decrease but also on the duration of the block in blood flow which further support the findings in the present study where persistently and permanently lesser blood supply to gall bladder as well as right lobe of liver and least blood supply to left lobe of liver have caused the hypoplasia of gall bladder as well as right lobe of liver and fibrosis of left lobe of liver.

Although the mechanism by which greater arterial blood supply to developing stomach caused gastric hyperplasia is not studied in the present work but it must be related with gastric over-nutrition and gastric hyperoxia which is just reverse to foetal hypoxia described by Leist and Grauwiler (1974). Cystohepatic hypoplasia due to lesser arterial blood supply to developing liver and gall bladder supports hypoxia hypothesis and gastric hyperplasia due to greater arterial blood supply to developing stomach creates "Hyperoxia Hypothesis" which is not available in literature as yet and is being put forth by the author for the first time.

References:

  1. Brent, R.L., and Franklin, J.B. (1960): Uterine vascular clamping : New procedure for the study of congenital malformations. Science, 132: 89-91.
  2. Caplan, A.I., and Koutroupas, S. (1973): The control of muscle and cartilage development in the chick limb. The role of differential vascularization. Journal of Embryology & Experimental Morphology. 29 : 571-583.
  3. Danielsson, B.R.G., Reiland, S., Rundgvist, E., and Danielsson, M. (1989): Digital defects induced by vasodilating agents. Relationship to decreased uteroplacental blood flow. Teratology. 40: 351-358.
  4. Danielsson, B.R.G., Daneilsson, M., Reiland, S; Eva Rundgvist, Lennart Denker and Carl Gunnar Regard (1990): Histological and in vitro studies supporting decreased uteroplacental blood flow as explanation for digital defects after administration of vasodilators. Teratology. 41: 185-193.
  5. Franklin, J.B., and Brent, R.L. (1964): The effect of uterine vascular clamping on the development of rat embryos three to fourteen days old. Journal of Morphology 115: 273-290.
  6. Grabowski, C.J.: Embryonic oxygen deficiency – a physiological approach to analysis of teratological mechanism. In : Advances in Teratology. D.H.M. Woolam, ed. Logos Press Ltd., London, Vol. 9 pp. 125-169. (1970).
  7. Leist, K.H., and Grauwiler, J. (1972): Influence on the developmental stage on embryotoxicity following uterine vessel clamping in the rat. 2nd Conference, European Teratology Society, Prague, 23-26 May.
  8. Leist, K.H. and Grauwiler, J. (1974): Fetal pathology in rats following uterine vessel clamping on day 14 of gestation. Teratology. 10: 55-56.

Missing Image

(Gastric Hypoplasia With Cystohepatic hypoplasia)

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