Acute fetal ductal occlusion in lambs

Tulzer, Gerald; Gudmundsson, Sæmundur; Rotondo, Kathleen M.; Wood, Dennis; Yoon, Grace Y.; Huhta, James C.

doi:10.1016/0002-9378(91)90327-n

Cited by 38 publications

(22 citation statements)

References 8 publications

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“…Increased fetal cardiac afterload may lead to a drop in cardiac output and valve regurgitation. 18 In our series, fetuses with the greatest increase in the afterload had semilunar valve regurgitation, most likely pulmonary valve regurgitation. It is not possible to distinguish between the right and left ventricular inflow and outflow regions in mouse fetuses because of the small cardiac size, but both the ductus arteriosus and the foramen ovale are wide open in the fetal circulation, so that the fetal cardiac ventricles function in parallel and the pressure faced by the ventricles is equal.…”

Section: Discussionmentioning

confidence: 96%

Inactivation of the Lysyl Oxidase Gene Lox Leads to Aortic Aneurysms, Cardiovascular Dysfunction, and Perinatal Death in Mice

et al. 2002

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Background-The lysyl oxidases are extracellular copper enzymes that initiate the crosslinking of collagens and elastin, 5 human isoenzymes having been characterized so far. The crosslinks formed provide the tensile strength and elastic properties for various extracellular matrices, including vascular walls. We studied the role of the first described isoenzyme Lox by inactivating its gene in mice. Methods and Results-Murine Lox gene was disrupted by routine methods. Lox Ϫ/Ϫ mice died at the end of gestation or as neonates, necropsy of the live-born pups revealing large aortic aneurysms. In light microscopy, hazy and unruffled elastic lamellae in the Lox Ϫ/Ϫ aortas were observed, and electron microscopy of the aortic walls of the Lox Ϫ/Ϫ fetuses showed highly fragmented elastic fibers and discontinuity in the smooth muscle cell layers in Lox Ϫ/Ϫ fetuses. The wall of the aorta in the Lox Ϫ/Ϫ fetuses was significantly thicker, and the diameter of the aortic lumen was significantly smaller than that in the Lox ϩ/ϩ aortas. In Lox Ϫ/Ϫ fetuses, Doppler ultrasonography revealed increased impedance in the umbilical artery, descending aorta, and intracranial artery blood velocity waveforms, decreased mean velocities across cardiac inflow and outflow regions, and increased pulsatility in ductus venosus blood velocity waveforms. Conclusions-Lox

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Section: Discussionmentioning

confidence: 96%

Inactivation of the Lysyl Oxidase Gene Lox Leads to Aortic Aneurysms, Cardiovascular Dysfunction, and Perinatal Death in Mice

et al. 2002

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“…All these changes resolved after ductal occlusion was released. 22 It has also been shown that in human fetuses with increased vascular impedance in the descending aorta, RVFS is decreased with no change in the left ventricle. 23 An abnormal fractional shortening could reflect myocardial compromise or an increase in the fetal ventricular workload.…”

Section: Discussionmentioning

confidence: 99%

Ultrasonographic and Biochemical Markers of Human Fetal Cardiac Dysfunction in Placental Insufficiency

et al. 2002

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Background-Placental insufficiency may lead to fetal cardiovascular compromise. We sought to determine whether ultrasonographic parameters of fetal cardiovascular function correlate with umbilical arterial levels of biochemical markers of myocardial dysfunction and damage in placental insufficiency. Methods and Results-In 48 fetuses with placental insufficiency, umbilical artery blood was obtained at delivery for assessment of N-terminal peptide of proatrial natriuretic peptide (NT-proANP) and cardiac troponin-T (cTnT). Group 1 fetuses (nϭ12) had normal NT-proANP and cTnT serum concentrations. Group 2 fetuses (nϭ25) showed increased NT-proANP (Ͼ1145 pmol/L) and normal cTnT values. Group 3 fetuses (nϭ11) had increased NT-proANP and cTnT (Ͼ0.10 ng/mL) levels. The ultrasonographic parameters of fetal cardiovascular function were compared between the groups. Pulsatility indices for veins of the ductus venosus, left hepatic vein, and inferior vena cava correlated significantly with NT-proANP levels. In group 3, ductus venosus, left hepatic vein, and inferior vena cava pulsatility indices for veins were higher (PϽ0.01) than in groups 1 and 2. The proportion of left ventricular cardiac output of combined cardiac output was greater (PϽ0.05) and that of right ventricle was smaller (PϽ0.05) in group 3 than in group 2. In group 3, tricuspid regurgitation was noted most often (PϽ0.05), and right ventricular fractional shortening was less (PϽ0.01) than in group 2. Conclusions-Pulsatility in human fetal systemic veins correlated significantly with the cardiac secretion of ANP. Fetuses with myocardial damage demonstrate increased systemic venous pressure, a change in the distribution of cardiac output toward the left ventricle, and a rise in right ventricular afterload.

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“…An acute increase in the afterload has been shown to induce tricuspid regurgitation in sheep fetuses with ductal closure and in human pregnancies with ductal constriction. 35 The presence of atrioventricular valve regurgitation in this setting shows that the fetal myocardium was still able to generate pressure. This is noteworthy, as in our previous study with intra-amniotically administered LPS, valve leaks were not present, and the time intervals describing cardiac systolic and diastolic functions were abnormal.…”

Section: Discussionmentioning

confidence: 88%

Mechanism of Acute Fetal Cardiovascular Depression after Maternal Inflammatory Challenge in Mouse

Rounioja

Räsänen

Ojaniemi

et al. 2005

The American Journal of Pathology

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Acute fetal ductal occlusion in lambs

Cited by 38 publications

References 8 publications

Inactivation of the Lysyl Oxidase Gene Lox Leads to Aortic Aneurysms, Cardiovascular Dysfunction, and Perinatal Death in Mice

Inactivation of the Lysyl Oxidase Gene Lox Leads to Aortic Aneurysms, Cardiovascular Dysfunction, and Perinatal Death in Mice

Ultrasonographic and Biochemical Markers of Human Fetal Cardiac Dysfunction in Placental Insufficiency

Mechanism of Acute Fetal Cardiovascular Depression after Maternal Inflammatory Challenge in Mouse

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