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BACKGROUND: Offspring of women with gestational diabetes (OGD) have greater risk for obesity and impaired metabolic health. Whether impaired metabolic health occurs in the absence of obesity is not clear. OBJECTIVE: The purpose of this study was to investigate the independent and interactive effects of intrauterine exposure to gestational diabetes and of children's current weight status on their metabolic health. METHODS: Children aged 5­10 years (n = 51) with and without intrauterine exposure to gestational diabetes (OGD vs. offspring of non-diabetic women [CTRL]) were grouped into normal weight (body mass index [BMI] < 85th %) and overweight (BMI > 85th %) according to Centers for Disease Control growth curves. Lipid profile was obtained by fasting blood draw, insulin sensitivity (SI) and secretion by liquid meal tolerance test, and body composition by dual-energy X-ray absorptiometry. RESULTS: Despite similar average BMI percentiles among normal weight OGD versus CTRL, and overweight OGD vs. CTRL, OGD had greater total %fat and trunk fat adjusted for leg fat compared with CTRL (P < 0.05). Overweight children had lower SI (P < 0.05) and greater basal, static, and total insulin secretion independent of SI (P < 0.05). OGD was independently associated with greater static insulin secretion (P < 0.05) and the interaction between OGD and overweight was associated with greater basal insulin secretion independent of SI (P < 0.01). OGD and overweight were each associated with lower high-density lipoprotein-cholesterol (HDL-C) (P < 0.05). CONCLUSION: Intrauterine exposure to gestational diabetes was associated with greater central adiposity and insulin secretion, and lower HDL-C, irrespective of current weight status. Future research should examine respective contributions of the intrauterine environment and of underlying genotype on children's metabolic health.

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An assumption of the classical three-compartment lung model is that the physiologic shunt fraction (Qs/Qt) remains constant with changes in cardiac output (Qt). As a result, when Qt decreases, both the arterial O2 tension (PaO2) and the mixed venous O2 tension (PvO2) must also decrease. Yet observations in intact dogs with pulmonary edema and humans with the adult respiratory distress syndrome (ARDS) indicate that as Qt decreases, Qs/Qt occasionally declines while the PaO2 increases. The present study was conducted to examine these discordant observations using a computer model of pulmonary gas exchange with a diffusion impairment. A computer model of gas exchange was developed to specifically analyze the effect of changing Qt upon PaO2 and Qs/Qt in the presence of diffusion impairment. Using the classical three-compartment model of gas exchange, a diffusion impairment was inserted by a MIMIC subroutine. The results of this computer simulation indicated that in the presence of a diffusion impairment, lowering Qt caused PaO2 to increase while Qs/Qt and PvO2 decreased. These changes indicated that a diffusion impairment might account for the experimental observations of the effects of Qt on PaO2 in ARDS.

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The effect of increased arterial pressure (Pa) on microvessel pressure (Pc) and edema following microvascular obstruction (100-micron glass spheres) was examined in the isolated ventilated dog lung lobe pump perfused with blood. Lobar vascular resistance (PVR) increased 2- to 10-fold following emboli when either Pa or flow was held constant. Microbead obstruction increased the ratio of precapillary to total PVR from 0.60 +/- 0.05 to 0.84 +/- 0.02 (SE) or to 0.75 +/- 0.06 (n = 6), as determined by the venous occlusion and the isogravimetric capillary pressure techniques, respectively. Isogravimetric Pc (5.0 +/- 0.7) did not differ from Pc obtained by venous occlusion (3.8 +/- 0.2 Torr, n = 6). After embolism, Pc in constant Pa decreased from 6.2 +/- 0.3 to 4.4 +/- 0.3 Torr (n = 16). In the constant-flow group, embolism doubled Pa while Pc increased only 40% (6.7 +/- 0.6 to 9.2 +/- 1.4 Torr, n = 6) with no greater edema formation than in the constant Pa groups. These data indicate poor transmission of Pa to filtering capillaries. Microembolism, even when accompanied by elevated Pa and increased flow velocity of anticoagulated blood of low leukocyte and platelet counts, caused little edema. Our results suggest that mechanical effects alone of lung microvascular obstruction cause minimal pulmonary edema.

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Oleic acid (OA) administered to experimental animals increases pulmonary vascular permeability and produces a condition that pathophysiologically resembles adult respiratory distress syndrome (ARDS) in humans. The present study examined the sequence of cardiorespiratory changes after OA infusion and their similarity to ARDS. After a baseline period, mechanically ventilated and anesthetized dogs were administered 0.18 ml/kg body weight OA into the pulmonary artery while hemodynamic and respiratory changes were monitored. After OA infusion, cardiac output fell by 39%, paralleling a 26% decrease in heart rate. Pulmonary vascular resistance (PVR) increased over 200% without a change in pulmonary capillary wedge pressure and initially without an increase in pulmonary artery pressure (PAP). Within 30 min after OA infusion, dynamic pulmonary compliance (Cdyn) was reduced 32% from baseline values, with a coincident increase in the alveolar-arterial PO2 gradient (P[A-a]O2) but without a significant change in the pulmonary shunt fraction (Qsp/Qt). This was followed in 30 min by a further 27% decrease in Cdyn, with a Qsp/Qt in excess of 50%. Both the hematocrit and hemoglobin concentration increased progressively after OA infusion, without a change in plasma protein concentration. The results suggest that the sequence of cardiopulmonary changes after OA injury are initially marked by a decrease in Cdyn and an increase in PVR and P(A-a)O2. This is followed by an increase in Qsp/Qt, PAP, hemoglobin concentration and PCO2. The changes appear related to progressive flooding of the alveolar air space with edema fluid. These findings parallel the sequential cardiorespiratory changes reported to occur in ARDS.

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The base-line capillary filtration coefficient (Kf) obtained from rates of lobe weight gain during stepwise vascular pressure elevation is reported to be threefold greater in isolated than in intact dog lung. To further evaluate the stepwise pressure elevation technique, we obtained Kf in control and oleic acid-injured isolated lung. The left lower lung lobe was removed, placed on a balance, ventilated, and pump perfused with autogenous blood. Saline (n = 6) or oleic acid (n = 6) was infused, and rate of lobe weight gain was obtained during stepwise pressure elevation. Kf averaged 0.071 +/- 0.012 and 0.243 +/- 0.027 ml X min-1 X Torr-1 X 100 g-1 in the control and injured lobes, respectively. Stepwise pressure elevation can yield a base-line Kf in isolated lung similar to Kf's obtained from this and other gravimetric methods in intact and isolated lung. Furthermore, Kf increased severalfold following lung injury with oleic acid. The stepwise pressure elevation technique for Kf determination in isolated lung can be a useful tool for quantitating changes in vascular permeability.

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