Hemodynamic analysis of Hyrtl anastomosis in human placenta

The Hyrtl anastomosis is a common connection between the umbilical arteries near the cord insertion in most human placentas. It has been speculated that it equalizes the blood pressure between the territories supplied by the umbilical arteries. However, its functional role in the regulation and distribution of fetal blood flow to the placenta has not yet been explored. A computational model has been developed for quantitative analysis of hemodynamic characteristic of the Hyrtl anastomosis in cases of discordant blood flow in the umbilical arteries. Simulations were performed for cases of either increased placental resistance at the downstream end or reduced arterial blood flow due to some pathologies upstream of one of the arteries. The results indicate that when placental territories of one artery impose increased resistance to fetal blood flow, the Hyrtl anastomosis redistributes the blood flow into the second artery to reduce the large pressure gradients that are developed in the affected artery. When one of the arteries conducts a smaller blood flow into the placenta and a relatively smaller pressure gradient is developed, the Hyrtl anastomosis rebuilds the pressure gradients in the affected artery and redistributes blood flow from the unaffected artery to the affected one to improve placental perfusion. In conclusion, the Hyrtl anastomosis plays the role of either a safety valve or a pressure stabilizer between the umbilical arteries at the placental insertion.

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Abstract P308: Rgs2 Promotes Uterine Blood Flow During Pregnancy

Hypertension ◽

10.1161/hyp.70.suppl_1.p308 ◽

2017 ◽

Vol 70 (suppl_1) ◽

Author(s):

Jennifer N Koch ◽

Elizabeth A Owens ◽

Shelby Dahlen ◽

Jie Li ◽

Patrick Osei Owusu

Keyword(s):

Gene Expression ◽

Blood Pressure ◽

Blood Flow ◽

G Protein ◽

Arterial Blood Flow ◽

G Protein Signaling ◽

Protein Signaling ◽

Uterine Blood Flow ◽

Placental Perfusion ◽

Arterial Blood

Regulators of G protein signaling (RGS) proteins are crucial in mediating vascular smooth muscle contraction via the regulation of heterotrimeric G proteins, affecting blood pressure and arterial blood flow. Previous studies by others and us showed that RGS2 deficiency augments vascular tone and impairs uterine blood flow (UBF) in non-pregnant mice, and that an Rgs2 loss-of-function mutation is linked to preeclampsia in humans; however, the mechanisms are unclear. Here, we tested the hypothesis that increased RGS2 expression and/or function facilitates placental perfusion by promoting vasodilation and UBF. We determined gene expression throughout pregnancy and post-partum period by real-time qPCR, while uterine blood flow and blood pressure were examined by ultrasound and carotid artery catheterization, respectively, under anesthesia. RGS2 expression decreased markedly by pregnancy day 10 (0.049 ± 0.013 vs. 0.023 ± 0.017) but returned to non-pregnancy level by day 15 (0.049 ± 0.013 vs. 0.041 ± 0.008,) in wild type mice. The pattern of changes in impedance to UBF mimicked gene expression profile in WT mice; in contrast, impedance remained elevated in Rgs2-/- mice at pregnancy day 15 (RI; WT: 0.516 ± 0.027, vs. RGS2-/-: 0.714 ± 0.020). Systemic blood pressure was similar between WT and Rgst2-/- mice at all stages of pregnancy. The results together indicate that RGS2 promotes uterine perfusion during pregnancy independently of its blood pressure effects. These findings are clinically relevant as selective targeting of G protein signaling could improve utero-placental hypoperfusion during pregnancy and prevent the development of pregnancy complications such as preeclampsia.

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Role of glucagon in splanchnic hyperemia of chronic portal hypertension

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.251.5.g674 ◽

1986 ◽

Vol 251 (5) ◽

pp. G674-G677 ◽

Cited By ~ 7

Author(s):

J. N. Benoit ◽

B. Zimmerman ◽

A. J. Premen ◽

V. L. Go ◽

D. N. Granger

Keyword(s):

Blood Flow ◽

Portal Hypertension ◽

Venous Blood ◽

Reference Sample ◽

Venous Hypertension ◽

Arterial Blood Flow ◽

Venous Blood Flow ◽

Portal Vein Stenosis ◽

Arterial Blood

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.

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