We investigated the basic characteristics of the rat embryonic circulation and also looked at the hemodynamic effects of a-and P-agonists, digitalis, and atrial natriuretic peptide, using a modified organ culture system in which the embryo was placed in oxygenated Hanks' balanced salt solution, blood pressure was measured by a servo-null micropressure system, and blood flow pattern was obtained by a 20-MHz pulsed Doppler velocity meter. The peak pressure was 0.5 ? 0.04 (SEM) mm Hg at the atrium (n = 6), 2.3 + 0.10 mm Hg at the ventricle (n = 15), 1.6 ? 0.03 mm Hg at the truncus (n = 7), and 1.0 ? 0.05 mm Hg at the umbilical artery (n = 21). There was a pressure drop from the I ventricle to the truncus and then a smaller pressure decrease to I the umbilical artery. The atrial a-wave was 20% of ventricular I pressure and ventricular inflow blood flow pattern showed very low early-to-late filling ratio, indicating that the ventricle was stiff. These findings were essentially the same as in the chick embryo. We recorded the ventricular image by using a highspeed video system with a frame rate of 200/s, and the ventricular pressure-area loop showed a triangular shape with short isovolumetric phases, which was different from that of the chick embryo at a similar stage. Isoproterenol increased ventricular pressure from 2.3 ? 0.1 to 2.6 2 0.1 mm Hg (n = 7, p < 0.05) and decreased umbilical blood pressure from 0.68 -C 0.05 to 0.61 + 0.04 mm Hg (n = 7, p < 0.05), suggesting contraction of the outflow tract, although positive change in pressure per unit time of ventricular pressure did not change. Ventricular negative change in pressure per unit time was increased with isoproterenol from 40 + 4 to 51 + 6 mm Hg/s (n = 7, p < 0.05), implicating improvement of diastolic function. Atrial natriuretic peptide and norepinephrine did not exert any significant responses, which was in contrast to the marked effects of these drugs seen in chick embryos. Acetylstrophanthidin, a rapid-acting digitalis, slowed the heart rate from 184 + 4 to 171 t 3 bpm (n = 6, p < 0.05) but did not change other parameters. In conclusion, basic characteristics of the circulation of the mammalian embryo are similar to those of the avian embryo, but responses to various cardiovascular agents known in the chick embryo cannot be extrapolated to the mammalian embryo. Previous studies have shown that basic cardiovascular function becomes established at very early stages of cardiovascular morphogenesis and the embryonic circulation is crucial to ensure normal organogenesis (1-3). The critical role of the embryonic circulation was shown by studies in which altered hemodynamics had adverse effects on the normal growth of the embryo (4-6); thus, stability of embryonic circulation is very important for the normal development and growth of the embryo. Inasmuch as the heart and vessels are not innervated during the early and critically important period of organogen-
ABSTRACT. Effects of hyperthermia on the cardiovascular function of the mammalian embryo have not been well defined. The effect of hyperthermia on the blood flow and umbilical artery blood pressure was studied in rat embryos at gestational d 12 by using a method developed in our laboratory. When the temperature was changed from 37 to 42"C, the heart rate increased by 15% (n = 33). Mean umbilical artery blood pressure, measured by a servo-null micropressure system, decreased from 0.64 + 0.05 to 0.53 f 0.04 mm Hg (n = 11), whereas blood flow velocity at the conotruncus, a measure of cardiac output, obtained by a 20-MHz pulsed Doppler ultrasound flowmeter, increased by 36 f 11% (n = 11). Mean umbilical artery blood flow increased by 66 f 13% (n = 11) and its vascular resistance, calculated by ratio analysis, decreased from 3.7 (median) to 1.8 units. These changes returned to baseline values when the temperature was returned to 37°C. The change in blood pressure was different from that seen in the chick embryo, indicating that there is species difference in the hemodynamic effect. (Pediatr Res 30: 505-508, 1991) Hyperthermia is an environmental hazard to the mammalian embryo and is reported to be a teratogen, although this is not unanimously accepted (1-3). We previously found that hyperthermia increased blood pressure and cardiac output in chick embryos (4), which was considered to be causally related to the cardiovascular pathogenesis, at least in part. The effects of high temperature on cardiovascular function of the mammalian embryo, however, have not been studied. We have found that various interventions have different hemodynamic effects in chick and rat embryos (5). Therefore, the purpose of the present study was to investigate the hemodynamic effect of high temperature in the rat embryo and to compare the results with those in the chick embryo. MATERIALS AND METHODSisolated and put into a bath of Hanks' solution. Then, a part of the uterus wall was pinned down on the rubber sheet at the bottom of the bath and the yolk sac was opened to expose the embryo and umbilical vessels (5, 6). In the modified system, the perfusate was bubbled with 100% oxygen gas in a glass flask, which was warmed to 37°C on an electric heating pan, and a constant flow through the bath was maintained by a roller pump (5) (Fig. 1). The Poz of perfusate in the bath ranged from 60 to 67 kPa. The hemodynamic condition was stable for at least 30 min in this system.The umbilical artery blood pressure was measured with a servo-null micro-pressure system (model 900; WP Instruments, Inc., Sarasota, FL) by inserting a micro-glass pipette into the umbilical artery. The blood flow velocity at the conotruncal region was obtained with a 20-MHz pulsed Doppler velocity meter (University of Iowa) by placing a piezoelectric crystal as the Doppler beam passed through the axis of the outflow tract of the embryo heart. Although cardiac output could not be obtained because simultaneous measurement of the diameter of that portion was not feasible, any cha...
ABSTRACT. Atrial natriuretic peptide (ANP) is important in the modulation of hemodynamics and fluid balance in the mature subject, but its hemodynamic effects at early stages of morphogenesis are not defined. We studied the effect of rat atriopeptin 111 on hemodynamics in chick embryos at Hamburger-Hamilton stage 21. The cardiovascular system is not yet innervated, nor is the kidney formed in these embryos. The vitelline arterial and venous blood pressures were measured with a servo-null, micro-pressure system and the dorsal aortic blood flow was measured with a 20 M H z pulsed Doppler velocity meter. The peptide was infused into the vitelline vein with a microinjector at doses of 0.1, 1.0, and 10 ng. Doses normalized by body wt of embryos averaged 0.003, 0.035, and 0.32 ng/mg (n = 61), respectively. Vitelline arterial blood pressure decreased in a dose dependent manner [y = 55.8 -9 . 9~; r = -0.49; p < 0.01 (y = % of baseline, x = log ng/mg)], and dorsal aortic blood flow, a measure of cardiac output, decreased similarly (y = 39.6 -1 6 . 2~; r = -0.47; p < 0.01). Heart rate did not change. Ten ng of ANP increased the vitelline venous diameter, determined directly under a microscope, from 125 + 47 (SD) pm to 139 f 49 pm (n = 11; p < 0.01), and decreased vitelline venous pressure from 0.34 f 0.05 mm Hg to 0.10 + 0.07 mm Hg (n = 5). We conclude that ANP exerts its hemodynamic effect by direct venodilation in the noninnervated and anephric circulation. We speculate that ANP modulation of vascular tone and volume could be a mechanism for the regulation of the preinnervated embryonic cardiovascular system. (Pediatr Res 27: 557-560,1990) Abbreviations ANP, atrial natriuretic peptide ANP is important in the regulation of hemodynamics and fluid balance (1-3). In mature subjects, the hemodynamic actions of ANP can be influenced by both neurohumoral reflexes and diuresis (4-7); therefore, its precise mechanism of action has not been completely defined. During the early stages of development, the cardiovascular system is not innervated (8) and the kidneys are not developed (9). Thus, an investigation of the effect of ANP in this unique model would provide information on the direct vascular effects of this cardiovascular peptide. In addition, it is not known whether the cardiovascular system responds to this potent vasoactive substance during the early period of morpho- genesis. Therefore, we studied the effect of ANP on blood pressure and cardiac output in chick embryos at early developmental stages. We found that the atrial natriuretic factor had a dose dependent effect on embryonic hemodynamics, decreasing cardiac output and arterial blood pressure through direct venodilation and venous pooling. MATERIALS AND METHODSA total of 84 white Leghorn chick embryos at HamburgerHamilton stage 21 (10) were used. Hemodynamic parameters were obtained by the method reported by Clark and Hu (1 I). Briefly, the vitelline artery or vein was punctured with a microglass pipette that was connected to a servo-null micro-pressure system (W-P...
Endothelin-1 is a very potent vasoconstrictor, but its function has not yet been investigated in the early stage of cardiovascular development. The purpose of the present study was to clarify whether endothelin-1 exerts a hemodynamic effect in stage 21 chick embryos. We measured vitelline artery blood pressure with a servo-null micropressure system and blood flow velocity at the dorsal aorta with a 20 MHz pulsed Doppler velocity meter. The vitelline vessels were directly measured with a microscope video system. While monitoring these parameters, endothelin-1 was infused into a vein by a microinjector and data were collected. Endothelin-1 increased the blood pressure and heart rate, but decreased the dorsal aortic blood flow. Only the vitelline veins with a diameter of between 100 and 200 microm constricted after endothelin infusion, but smaller or larger veins and the arteries did not show any significant change in size, although the resistant arteries could not be measured by this method. In conclusion, endothelin-1 has apparent constrictive effects in the selected vessel in the early stages of cardiovascular development when the endocrine and autonomic nervous systems have not yet developed.
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