Role of decreased cardiac output in isoproterenol‐induced cardiovascular teratogenesis in chick embryos

Gilbert, Enid F.; Bruyere, Harold J.; Ishikawa, Shizen; Foulke, Laura M.; Heimann, Sandra R.

doi:10.1002/tera.1420210305

Cited by 28 publications

(3 citation statements)

References 12 publications

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“…One way is the pulsed Doppler tech-nique10"11; the other is microcinephotography. [12][13][14][15] We chose microcinephotography as the least invasive of the techniques available to study ventricular function because our aim was to reincubate embryos for detailed morphological study of the heart and great arteries after the major events of cardiogenesis. This has proven to be a good choice, as shown by the fact that there was no difference in the survival rates between filmed and nonfilmed embryos.…”

Section: Discussionmentioning

confidence: 99%

Relation of early hemodynamic changes to final cardiac phenotype and survival after neural crest ablation in chick embryos.

et al. 1991

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Section: Discussionmentioning

confidence: 99%

Relation of early hemodynamic changes to final cardiac phenotype and survival after neural crest ablation in chick embryos.

et al. 1991

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“…Herein we indicate that measurement of blood pressure in the rat embryo is feasible, but with some limitations, and that there may be qualitative hemodynamic differences between the rat and chick embryos. (Pediatr Res 23: 200-205,1988) While searching for the basic mechanism of normal and abnormal morphogenesis of the cardiovascular system, several investigators have been trying to correlate the change of hemodynamics or rheology of the cardiovascular system to morphogenesis (1)(2)(3)(4)(5). These studies have revealed that several teratogenic factors alter the hemodynamics (6-12).…”

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confidence: 99%

Developmental Hemodynamic Changes in Rat Embryos at 11 to 15 Days of Gestation: Normal Data of Blood Pressure and the Effect of Caffeine Compared to Data from Chick Embryo

et al. 1988

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ABSTRACT. We attempted to measure arterial blood pressure of the rat embryo. The embryo was excised within the uterus and immersed in Hanks' solution at 37" C. The uterus wall and yolk sac were opened to expose the umbilical vessels. The umbilical artery was punctured with a glass micro-pipette, and blood pressure was measured by using a servo-null micro-pressure system. The mean blood pressure was 0.27 + 0.05 mm Hg in the embryo at the 11th day of gestation (n = 7), 0.48 f 0.03 mm Hg in the 12-day embryos (n = 19), 1.3 + 0.08 mm Hg in the 13-day (n = ll), and 2.6 -1-0.1 mm Hg in the 15-day embryos (n = 10). Heart rate was 84 + 11 in 11-day, 122 -1-3 in 12-day, 192 f 7 in 13-day, and 198 f 5 in 15-day embryos.These parameters were stable within 10 min after the excision. A comparison of the data with those of the chick embryo of comparable developmental stages revealed that the blood pressure was lower in 11-and 12-day rat embryos than in the chick embryo of Hamburger-Hamilton stages 18 and 21, but this was reversed in the later stages. In the stage 21 chick embryo, intravenous administration of caffeine (60 f 9 mglkg embryo weight) induced an increase in blood pressure by 11 + 3% (n = 8), but did not result in a significant increase in dorsal aortic blood flow (6 -1-6%, n = 9) or in heart rate. In contrast, caffeine (62 + 3 mg/kg) increased the heart rate by 8 f 2% (n = 10) without changing the blood pressure in the rat embryo of day 12. The velocity of blood flow in the truncus was measured by a pulsed Doppler flowmeter. Caffeine injection increased the mean velocity by 21 -1-8% (n = 8). Herein we indicate that measurement of blood pressure in the rat embryo is feasible, but with some limitations, and that there may be qualitative hemodynamic differences between the rat and chick embryos. (Pediatr Res 23: 200-205,1988) While searching for the basic mechanism of normal and abnormal morphogenesis of the cardiovascular system, several investigators have been trying to correlate the change of hemodynamics or rheology of the cardiovascular system to morphogenesis (1-5). These studies have revealed that several teratogenic factors alter the hemodynamics (6-12). However, it is known that caffeine induces aortic aneurysm in the chick (1 3), whereas in the rat it induces ventricular septa1 defect (14, 15). This indicates that there is a species difference in the teratogenecity of a single intervention. Previous hemodynamic studies, however, have only used the chick embryo, and very few have been done in the mammalian embryo. The ultimate goal of investigation in this field is an understanding of human cardiac morphogenesis. Experiments using any mammalian species may be better for this purpose than those using other species. Therefore, we attempted to measure the blood pressure and blood flow parameters in the rat embryo, and looked at whether there was any difference in the hemodynamic effect of caffeine in the chick and rat embryo. MATERIALS AND METHODSThe Wistar rat was used and pregnancy was confirmed by vaginal...

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“…In view of this, it is of great interest to note that abnormalities of the great vessels have been induced experimentally by modifying the normal blood flow pattern [66,67] or by production of episodes of embryonic bradycardia, ventricular arrhythmia and temporary cardiac arrest [68]. A wide variation of vessel defects, including the malposition of the great vessels, can be induced by selectively increasing, decreasing, or misdirecting blood flow in the developing cardiovascular system by mechanical methods or by cardioactive substances [69,70]. Lack of sufficient blood flow and pressure changes have been related to the induction of abnormally absent vessels.…”

Section: Hypoxia-reoxygenation Damagementioning

confidence: 99%

Class III Antiarrhythmics and Phenytoin: Teratogenicity Due to Embryonic Cardiac Dysrhythmia and Reoxygenation Damage

Danielsson¹,

Sköld²,

Azarbayjani³

2001

CPD

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Class III antiarrhythmic drugs, like almokalant, dofetilide and ibutilide, cause a spectrum of malformations in experimental teratology studies. The pattern of developmental toxic effects is very similar to those reported for phenytoin, which is an established human and animal teratogen. The toxic effects are characterised by embryonic death, decreased fetal weights, and stage specific malformations, such as distal digital reductions, orofacial clefts and cardiovascular defects. Class III antiarrhythmics decrease the excitability of cardiac cells by selectively blocking the rapid component of the delayed rectified potassium channel (IKr), resulting in prolongation of the repolarisation phase of the action potential. Phenytoin, which decrease the excitability of neurones, has recently also been shown to block IKr, in addition to its known blockade of sodium channels. Animal studies indicate that IKr is expressed in the embryo and that the embryonic heart is extremely susceptible to IKr-blockers during a restricted period in early development. At concentrations not affecting the maternal heart, the embryonic heart reacts with bradycardia, arrhythmia and cardiac arrest when exposed to such drugs. Available studies strongly support the idea that birth defects after in utero exposure to both selective and non-selective IKr-blockers (like phenytoin) are initiated by concentration dependent embryonic bradycardia/arrhythmia resulting in 1) hypoxia; explaining embryonic death and growth retardation, 2) episodes of severe hypoxia, followed by generation of reactive oxygen species within the embryo during reoxygenation, causing orofacial clefts and distal digital reductions, and 3) alterations in embryonic blood flow and blood pressure, inducing cardiovascular defects.

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Role of decreased cardiac output in isoproterenol‐induced cardiovascular teratogenesis in chick embryos

Cited by 28 publications

References 12 publications

Relation of early hemodynamic changes to final cardiac phenotype and survival after neural crest ablation in chick embryos.

Relation of early hemodynamic changes to final cardiac phenotype and survival after neural crest ablation in chick embryos.

Developmental Hemodynamic Changes in Rat Embryos at 11 to 15 Days of Gestation: Normal Data of Blood Pressure and the Effect of Caffeine Compared to Data from Chick Embryo

Class III Antiarrhythmics and Phenytoin: Teratogenicity Due to Embryonic Cardiac Dysrhythmia and Reoxygenation Damage

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