Clinical anatomy of the popliteal blood vessels.

The surgical management of venous injuries in the popliteal fossa is a contested issue. The basic options are ligation or repair. Most anatomy textbooks briefly describe a single popliteal vein, and the literature contains few references on venous patterns in this region. Although the primary objective of this study was to analyze venous variability in 52 dissected cadaveric popliteal fossae and 63 venograms, data were also collected on the popliteal artery. Nine groups (A-I) were designated regarding the manner of formation of the popliteal vein. These groupings were based primarily on differences in the union of the anterior tibial, posterior tibial, and fibular (peroneal) veins to form medial and lateral (popliteal) veins, and whether these two veins fused to form a singular popliteal vein proximal or distal to the transverse plane at the level of the distal edge of the femoral condyles (FC). In the majority of the dissections and venograms, multiple veins crossed the FC, and the medial vein was larger in diameter than the lateral vein. Two patterns of popliteal artery termination were observed based on differences in the site of origin of the fibular artery. The results were compared with anatomy and vascular surgery textbook descriptions and sparse literature reports on vascular variations in the popliteal fossa. It is hoped that these data will benefit surgeons performing procedures in this region.

Absence of correlation between transient cranial hemorrhages and congenital malformations following neural crest ablation in chicks.

Ablation of premigratory cardiac neural crest has been used to produce and study extensively a model of abnormal cardiovascular dysmorphology. Previous and continuing research in this laboratory concerns different aspects of the involvement of cranial neural crest in the development of cranial, cervical and cardiac tissues in chick embryos. Recently, we detected the occurrence of transient cranial hemorrhages 24-48 hr after the ablation of selected segments of premigratory cranial neural crest. Since one possible mechanism of action for certain teratogens involves nonreparable damage to a primordial embryonic tissue by an antecedent hemorrhage, the objective of this study was to determine which of three different neural crest ablations is associated with hemorrhages and whether subsequent congenital abnormalities were correlated with the ablation procedure and/or hemorrhage. Premigratory neural crest was ablated from 3 different sites, designated cardiac, mesencephalic and trunk crest, respectively, of stage 8-10 chick embryos. Sham-operated embryos were controls. At 24, 30, and 48 hr after ablation, each embryo was observed for the presence of hemorrhages. On incubation day 11 all the living embryos were killed, fixed, weighed, and analyzed for selected length measurements, developmental stage, and the types and rates of congenital abnormalities. Cardiac and mesencephalic ablation group embryos exhibited significant incidences of cranial hemorrhages and changes in many of the parameters analyzed. It was concluded that the cardiac and mesencephalic, but not the trunk neural crest ablations, produced significant changes in incubation day 11 embryos. However, there was no correlation between the abnormalities and the prior occurrence of the transient cranial hemorrhages.

Effects of in vivo exposure of pregnant hamsters to glucose. 1. Abnormalities in LVG strain fetuses following intermittent multiple treatments with two isomers.

The increased frequency of congenital malformations including caudal regression syndrome, in infants of women with insulin-dependent diabetes mellitus is well documented. Most of the related animal research has involved the in vitro embryo culturing methodology. This study involved the alternative in vivo approach in order to determine the effects of treatment of pregnant hamsters with the D- and L-isomers of glucose at five times just before and during the period of embryonic organogenesis on maternal blood glucose levels and the rates and types of fetal abnormalities. One group of animals was injected with 5 doses (4 g/kg each) of D-glucose, i.e., on gestation day (D) 6, 3 PM; D7, 8 AM and 3 PM; D8, 8 AM and 3 PM. Two other groups were treated the same way but with L-glucose (4 g/kg per dose) and water (10 ml/kg per dose), respectively. The D-glucose treatment produced alternating periods of hyperglycemia and normoglycemia in the pregnant hamsters, enlarged placentae and fetuses with small urinary bladders, microphthalmia and skeletal abnormalities of the sternum, caudal vertebrae, pelvic bones, and femora. The L-glucose treatment did not produce changes in maternal blood D-glucose levels but did produce fetuses with small urinary bladders, microphthalmia and abnormal ossification limited to the manubrium. Several interpretations of the D-glucose-induced fetal abnormalities involving the vertebrae, proximal hindlimb bones and urinary bladders are discussed, including the consideration that this cluster has interesting similarities to the spectrum of skeletal and soft tissue abnormalities of human diabetes-related caudal regression syndrome.

The effect of cadmium on the development of the facial prominences: surface area measurements of day 10-8 a.m. hamster embryos.

The environmental contaminant cadmium (Cd) is a proven teratogenic agent in rodents. In hamsters, it causes craniofacial dysmorphogenesis. The underlying mechanism for this damage is unknown. Early facial development in hamsters occurs during gestation days 9-11 and involves the formation and appropriate fusion of several prominences surrounding the stomodeum. The hypothesis for this study is that the occurrence of Cd-induced facial defects involves a disruption of the normal formation and/or fusion of one or more of the facial prominences. Pregnant hamsters were treated with Cd (2 mg/kg) or water intravenously on gestation day 8 (8 A.M.). On gestation day 10 (8 A.M.) surviving embryos were processed to obtain scanning electron micrographs of the frontal view of the face. Measurements of the surface areas of 15 different portions of the face were obtained using a microcomputer equipped with a digitizer. Both qualitative and quantitative differences in the faces were detected upon comparing the Cd-exposed and control embryos. The surface areas of the prominences measured were significantly smaller in the Cd-exposed embryos. However the sizes of the other regions of the Cd-exposed faces were either little affected (nasal pit areas) or markedly increased (the interval of the face between the medial nasal prominences). Two possible explanations for these data are discussed.

The effect of mercuric acetate on selected enzymes of maternal and fetal hamsters at different gestational ages.

This study establishes levels of activity of glucose-6-phosphate dehydrogenase (G6PD), glycogen phosphorylase (GP), and cytochrome c oxidase (cyt c ox) in maternal, placental, and fetal tissues at Days 9, 12, and 15 in the 16-day gestation period of the hamster, and following a single dose of either 8 or 15 mg/kg mercuric acetate on the eighth gestational day. Mercury significantly elevated maternal kidney G6PD activity and decreased GP activity. The increase in kidney G6PD strongly correlated with observed urine and kidney abnormalities.

The amelioration of mercury-induced embryotoxic effects by simultaneous treatment with zinc.

Prior work has demonstrated that inorganic mercury produces a number of toxic effects in embryos when this metal is administered to pregnant hamsters subcutaneously on the eighth gestation day. Also, treatment of various pregnant animals with zinc produces little evidence of embryotoxicity. The literature reveals that the simultaneous exposure of pregnant animals to different combinations of teratogenic and nonteratogenic agents produces variable responses which can be characterized as either protective or synergistic types of interactions. The purpose of this study was to determine the effect of subcutaneously injected combinations of zinc and mercury on the developing hamster embryo. The major conclusion drawn from this work is that the simultaneous maternal treatment with zinc and mercury ameliorates the harmful effects produced by treatment with mercury alone.

Neural crest cells contribute to normal aorticopulmonary septation.

By analyzing the hearts of quail-chick chimeras, it was found that neural crest cells at the level of occipital somites 1 to 3 migrate to the region of the aorticopulmonary septum. Bilateral removal of this neural crest population prior to migration causes malformation of the aorticopulmonary septum resulting in common arterial outflow channels or transposition of the great vessels.

The susceptibility of inbred strains of hamsters to cadmium-induced embryotoxicity.

Prior-research has involved several aspects of cadmium-induced embryotoxicity in non-inbred hamsters, mice, and rats. This study compares the embryotoxic profile of cadmium in one non-inbred (LVG) and five inbred (CB, LHC, LSH, MHA, PD4) strains of hamsters. A single IV dose (2 mg/kg) of cadmium sulfate was injected into pregnant hamsters early on the 8th gestation day. Fifteenth gestation day fetuses from treated, and control animals were studied for the kinds and incidence of external, internal, and skeletal malformations, as well as the frequency of resorptions. All six hamster strains developed significant resorption rates and external, internal, and skeletal abnormalities, e.g., exencephaly, microphthalmia, cleft lip, cleft palate, renal agenesis, rib fusions, etc. Significant interstrain differences were detected in only three categories of embryonic damage, i.e., resorptions, microphthalmia, and renal agenesis. The data of this study was compared with that of another study in which the same hamster strains were exposed to the metallic teratogen, lead. While the manner by which cadmium damages the mammalian embryo is unknown at this time, several possibilities are presented.

The effect of the time of administration of chromium trioxide on the embryotoxic response in hamsters.

Prior work has demonstrated that chromium trioxide is embryotoxic in hamsters if administered to pregnant animals early on the eighth gestation day. The major manifestations are cleft palate and an increased frequency of resorptions. In the present study a single iv dose (8 mg/kg) of chromium trioxide was injected into pregnant hamsters at 8 A.M. on either day 7, 8, 9, 10 or 11 of gestation in order to determine the effect of altering the time of treatment on embryotoxicity. Fetuses from females treated with chromium or demineralized-distilled water were collected on day 15 of gestation and were examined for the types and frequency of external and internal malformations. The number of resorption sites was recorded. Cleft palate, the major malformation detected, was produced only when chromium was administered on days 7, 8, or 9 of gestation. Since the frequency of resorptions and the incidence of cleft palate varied with the time of treatment it is concluded that the time at which chromium trioxide is injected into the pregnant hamster does influence embryotoxicity. The results suggest that an interference with embryonic growth may be an important factor in chromium-induced cleft palate in hamsters.

A variable embryotoxic response to lead in different strains of hamsters.

Lead nitrate was administered intravenously at 50 mg/kg to five inbred strains (MHA, LSH, LHC, CB, and P)4) and the non-inbred LVG strain of pregnant hamsters early on the 8th gestation day. All fetuses from treated and control hamsters were collected on the 15th gestation day and examined for the frequency and kinds of external, internal, and skeletal abnormalities. The major embryotoxic effects included resorptions, tail bud abnormalities, hydrocephalus, and skeletal defects. It is concluded that the LSH, LHC, LVG, and PD4 strains are susceptible while the MHA and CB strains are relatively resistant to the lead exposure.

The embryotoxicity of ytterbium chloride in golden hamsters.

Two experiments were performed to assess the embryotoxicity of intravenously administered ytterbium chloride in golden hamsters: (1) 50, 75, 100, or 150 mg/kg ytterbium chloride were injected early on the 8th gestation day; (2) 100 mg/kg ytterbium chloride were administered at 4 different times during the critical period of organogenesis in this species (7th day, 4 PM; 8th day, 8 AM or 4 PM; 9th day, 8 AM). The pregnant females were killed on the 12th, 14th, or 15th gestation day and the frequency of resorptions was determined, and surviving offspring were studied for the presence of external and internal malformations as well as skeletal damage. Relatively few externally visible malformations and no significant internal malformations were produced. Damage to the skeletal system included fused and supernumerary ribs, and many different sites of poor ossification. Maximal susceptibility to these effects occurred on the 8th day.