Human immunodeficiency virus infection: in situ polymerase chain reaction localization in human placentas after in utero and in vitro infection.

OBJECTIVE: We compared localization of human immunodeficiency virus type 1 within human placentas infected in utero with localization within human placental explants infected in vitro. STUDY DESIGN: Placental tissues from 3 cases of vertical transmission of human immunodeficiency virus type 1 were studied. Human placental explants from 6 term pregnancies not complicated by human immunodeficiency virus type 1 infection were infected in vitro with human immunodeficiency virus type 1(Ba-L). Sections from each placental explant and each placenta infected in utero were analyzed for human immunodeficiency virus type 1 localization by means of in situ polymerase chain reaction. RESULTS: Human immunodeficiency virus type 1 was primarily localized within syncytiotrophoblast, Hofbauer cells, and extravillous mononuclear cells in placental tissue sections from cases of in utero infection. Within placental explants human immunodeficiency virus type 1 deoxyribonucleic acid was found in syncytiotrophoblast and Hofbauer cells. The distributions of viral localization were similar in placentas infected in utero and placental explants infected in vitro. CONCLUSION: Human immunodeficiency virus type 1 can be localized to specific human placental cells (eg, syncytiotrophoblast) after either in utero or in vitro infection, which demonstrates the specificity and selectivity of human immunodeficiency virus infection in the human placenta.

Effects of chronic infusion of angiotensin II on renin and blood pressure in the late-gestation fetal sheep.

OBJECTIVES: Our purpose was to determine whether chronic physiologic elevations in plasma angiotensin II levels decrease plasma renin concentration, alter the relationship between active renin and prorenin in fetal plasma and kidney, and depress the expression of renal renin messenger ribonucleic acid in the fetus. STUDY DESIGN: Seventeen chronically catheterized ovine fetuses at approximately 130 days' gestation were infused with either angiotensin II (48.9 +/- 3.5 ng/kg x min) or vehicle (5% glucose in water) for 72 hours. RESULTS: Mean arterial pressure increased significantly by 1 hour of infusion and continued to increase throughout the infusion. The plasma active renin concentration was significantly decreased by 1 hour of the infusion, whereas the prorenin concentration was not decreased until 24 hours of the infusion. After 72 hours of angiotensin II infusion the renal tissue prorenin content decreased (21.5 +/- 5.1 ng/mg x hr angiotensin I vs 46.4 +/- 6.6 ng/mg - hr angiotensin I in the control animals, p = 0.01), whereas the active renin concentration did not change (26.6 +/- 5.1 ng/mg x hr angiotensin I vs 35.1 +/- 5.4 ng/mg x hr angiotensin I in the control animals, p = 0.28). The renal renin messenger ribonucleic acid expression tended to be lower in the angiotensin II-treated fetuses (p = 0.10). CONCLUSION: Chronic physiologic increases in fetal plasma angiotensin II suppress the secretion of active and prorenin and alter the relationship between processing and secretion of renin in the fetal kidney.

Hemodynamic and hormonal responses to atrial distension in the ovine fetus.

OBJECTIVE: Our purpose was to evaluate the hemodynamic and endocrine responses to elevations of atrial pressure in fetal sheep. STUDY DESIGN: By use of a randomized block design, 10 ovine fetuses underwent pulmonary artery constriction proximal to the ductus arteriosus with and without propranolol pretreatment. RESULTS: Atrial pressure doubled (p < 0.05), whereas mean arterial pressure remained unchanged (p > 0.05), in response to pulmonary artery constriction in both groups. Atrial natriuretic peptide tripled (p < 0.01), arginine vasopressin tripled (p < 0.05), and plasma renin activity doubled (p < 0.05) in both the constriction and constriction plus propranolol groups. No changes in fetal hematocrit values were demonstrated in any group. CONCLUSIONS: The fetal sheep responds to increased atrial pressure with not only increased levels of atrial natriuretic peptide but also with arginine vasopressin and plasma renin activity over time. These changes occur in spite of increases in both atrial pressure and atrial natriuretic peptide. We speculate that the fetal heart may participate in redistribution of cardiac output by releasing atrial natriuretic peptide and augmenting secretion of arginine vasopressin and plasma renin activity.

Effect of chronic infusion of cortisol on renin gene expression and renin response to hemorrhage in fetal lambs.

In the ovine fetus, plasma renin levels increase close to term, and renin responses to various stimuli are enhanced when compared with responses earlier in gestation. These changes are accompanied by increases in renal renin gene expression and renin content, and they occur in conjunction with elevations in fetal plasma cortisol. Thus, the purpose of this study was to test the hypothesis that a chronic, physiologic elevation in fetal plasma cortisol in early gestation would increase activity in the renin-angiotensin system prematurely. We studied fetuses (control, n = 8; cortisol infused, n = 11) at 94 +/- 2 d of gestation. Fetal vessels were catheterized, and cortisol or saline solution was infused for 6 d. At the end of infusion, fetuses were hemorrhaged approximately 30% of estimated blood volume. Blood samples were collected to measure plasma renin concentration. Then the animals were killed, and kidneys were removed to measure renin mRNA and renin content. Plasma cortisol concentrations in the control and cortisol-treated animals were 7.2 +/- 0.8 and 57.7 +/- 8.6 nmol/L (p < 0.01), respectively. Basal plasma renin concentrations were similar in the two groups 3.2 +/- 0.4 versus 4.4 +/- 1.8 ng of angiotensin I/mL/h, and there was a significant increase after hemorrhage in the cortisol-treated group only. Renal renin content and mRNA levels were similar in the two groups. These data indicate that chronic increases in cortisol in fetal lambs at 0.65 gestation significantly enhance the renin response to hemorrhage but do not alter renal renin gene expression.

Myocardial infarction during pregnancy: management and outcome of two pregnancies.

OBJECTIVE: Each year in the United States approximately 500,000 women die from ischemic heart disease. However, there are < 100 reported cases of myocardial infarction occurring during pregnancy. The current management of these patients is empiric, with pulmonary artery catheterization during labor being frequently reported. STUDY DESIGN: In the past year we have managed and delivered two such patients, including the first reported case of myocardial infarction with a triplet gestation. RESULTS: Both patients had clinical and laboratory signs of myocardial infarction and underwent coronary angiography. They subsequently had preeclampsia and were prematurely delivered of viable fetuses. One patient had angina pectoris during labor and was successfully treated with sublingual nitroglycerin. Neither patient suffered reinfarction or heart failure. Invasive hemodynamic monitoring was not used, and the mode of delivery was determined solely on obstetric indications. CONCLUSION: In pregnant patients with myocardial infarction, invasive central monitoring is unnecessary in patients with good cardiac function and reserve and the mode of delivery should be based on obstetric indications.

Effect of elevated atrial pressure on plasma renin activity in hypotensive fetal lambs.

In adults, renin secretion is stimulated by reductions in arterial pressure and inhibited by increases in atrial pressure. In the late gestation fetus, a fall in arterial pressure stimulates renin secretion, but it is unknown whether elevation of atrial pressure will alter such an increase. Therefore we studied the effect of elevated atrial pressure on renin secretion in the presence of nitroprusside-induced arterial hypotension. Thirteen fetal lambs at 127.9 +/- 0.9 days of gestation were prepared 5 days before study with inflatable pulmonary artery occluders and right atrial, vascular, and amniotic catheters. Each fetus underwent two protocols (hypotension and hypotension with occlusion) using a randomized block design. Nitroprusside reduced arterial pressure by 34% in both groups. Right atrial pressure during the course of hypotension was significantly higher in the occlusion group (F = 14.2, P = 0.001). Plasma renin activity increased similarly in both groups during hypotension (F = 6.0, P = 0.003). Elevated right atrial pressure did not alter hypotension-induced renin secretion in the fetus.

Developmental changes in renin gene expression in ovine kidney cortex.

The ontogeny of renin mRNA and renin content from renal cortical slices was studied in two groups of ovine fetuses at 92-94 days (0.64 gestation) and at 138-142 days (0.96 gestation), newborn lambs (0.4-2 days old), and adult sheep. Renal renin mRNA was identified by hybridization with a 32P-labeled full length rat renin cDNA. Renal renin content was measured as nanograms of angiotensin I generated per hour (active renin). There was a significant age effect on renin mRNA levels (F = 10.0, P < 0.001); values increase significantly between 0.64 and 0.95 g (P < 0.005), remain elevated in the newborns (P < 0.05), and subsequently decline in adulthood (P < 0.005). Likewise, renal renin content was significantly higher in late gestation fetuses and newborn lambs than in early gestation and adults (F = 8.3, P < 0.003). The renal renin content was strongly correlated with renin mRNA levels (R = 0.88, P < 0.0001). These results suggest that 1) the renin gene is developmentally regulated in the ovine kidney and 2) the renal content of active renin in basal conditions is regulated, at least in part, by events at the transcriptional level.

Long-term outcome in fetal hydrops from parvovirus B19 infection.

Parvovirus B19 infection in the fetus is associated with anemia and hydrops and can result in fetal death. Fetal transfusion has been used in an attempt to improve outcome; however, it is associated with its own perinatal morbidity. We report two cases of fetal parvovirus B19 infection that were confirmed by polymerase chain reaction for parvovirus B19 deoxyribonucleic acid in umbilical cord blood. Ultrasonographic signs of compromise were observed at 30 and 24 weeks of gestation. Both fetuses were hydropic and one fetus was also anemic. Serial sonograms demonstrated that the hydrops resolved spontaneously over 3 to 5 weeks after diagnosis. One infant was delivered at 32 weeks of gestation as a result of idiopathic preterm labor. The other infant was delivered at term. Both infants appeared relatively normal at birth and have developed normally in the first year of life. Thus fetal hydrops in association with parvovirus B19 infection does not always lead to poor long-term outcome. A conservative approach without in utero therapy may be appropriate for the management of some of these fetuses.