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Placentas of anesthetized rats were perfused in situ on the fetal side to study mechanisms of Mg2+ transport. The perfusate was a Mg(2+)-free Krebs-Ringer, and the unidirectional transfer of Mg2+ from maternal plasma to this Ringer was compared with that of 45Ca and 51Cr-EDTA, the latter being employed as a paracellular diffusional marker. Placental perfusion with amiloride (0.5 mM) or ouabain (1 mM) both rapidly (4 min) reduced maternal-fetal clearance (Kmf) for Mg2+ but had no effect on Kmf for 45Ca. In contrast, perfusion of the carbonic anhydrase inhibitor acetazolamide (1 mM) did not affect Kmf for Mg2+ or 45Ca. Placental perfusion with a Na+-free Ringer reduced Kmf for both Mg2+ and 45Ca, although the latter response was delayed. Kmf for 51Cr-EDTA was increased by amiloride and was unaffected by perfusion of ouabain, acetazolamide, or Na+-free Ringer, indicating that the effects of these treatments on Kmf of Mg2+ do not reflect nonspecific effects on placental permeability. These data suggest that maternal-fetal transfer of Mg2+ across the perfused rat placenta is Na+ dependent.

Two human parathyroid hormone-related protein (hPTHrP) fragments were tested for effects on maternofetal transfer of 45Ca and Mg across the in-situ perfused rat placenta at 21 days of gestation (term = 23 days). The fetal placental circulation was perfused with a Mg-free Krebs-Ringer solution and the unidirectional maternofetal clearance (Kmf) of 45Ca and Mg compared with that of 51Cr-EDTA, the latter being employed as a paracellular diffusional marker. Placental perfusion with hPTHrP(1-34) (100 ng/ml) or hPTHrP(75-86)amide (50 ng/ml) did not significantly alter the Kmf of 45Ca or that of Mg. In separate rats, however, hPTHrP(1-34) but not hPTHrP(75-86)amide stimulated marked placental cyclic AMP (cAMP) release, the peak response of 63 +/- 7 pmol/min occurring 10 min after the beginning of the peptide perfusion. A lower dose of hPTHrP(1-34) (4 ng/ml) produced a similar peak release of cAMP, as did [Nle8,21, Tyr34]-rPTH(1-34)amide (4 ng/ml) and the adenylate cyclase agonist forskolin (17 mumol/l). Forskolin also rapidly increased the Kmf of 45Ca but not that of Mg or 51Cr-EDTA. The present study indicates that hPTHrP does not acutely affect maternofetal transfer of Ca or Mg across the perfused rat placenta. The data also question the role played by cAMP in the stimulatory actions of forskolin on placental Ca transport.

Objective: To study the need for and effectiveness of a ward based opportunistic immunisation policy., Design: A six month prospective study., Setting: An acute medical paediatric ward of an inner city teaching hospital., Subjects: 296 children admitted to the ward who lived within Central Manchester Health Authority boundaries and were aged from 5 months to 6 years., Main Outcome Measures: Completion of immunisation schedule appropriate for age., Results: 56 children were three or more months behind with immunisations. The parent's history was not reliable for 18 children. Accessing health authority immunisation records was not difficult. The main reasons for falling behind were the mobility of the families (15 children), lack of motivation (14), and frequent minor illnesses (9). 40 children were immunised before discharge, but three could not be because of valid contraindications. Of the 16 children requiring more immunisations after discharge, only four obtained them at the correct time and five children not at all., Conclusion: An opportunistic immunisation policy is an important means of immunising a vulnerable group of children who would often default on routine immunisations, and such policies should operate whenever possible. Our ward based policy can achieve immunisation of three quarters of possible children without change or inconvenience to the daily ward work, but efficacy relies on adequate levels of enthusiastic staff. The system can be improved by having accurate and updated immunisation records available in the hospital, and by encouraging nursing staff to participate.

Mechanisms of maternofetal Mg transfer have been investigated across the in situ perfused rat placenta at 21 d gestation (term = 23 d). The fetal placental circulation was perfused with Mg-free Krebs-Ringer solution and clearance of Mg from maternal plasma across the placenta [unidirectional maternofetal clearance (Kmf) Mg] compared with that for 45Ca and 51Cr-EDTA, the latter being used as a diffusional marker. Because diffusion coefficients determined for these solutes were similar (6.8-7.6 X 10(-6) cm2.sec-1), greater Kmf values determined for Mg and 45Ca (mean +/- SD: 26.7 +/- 9.2 and 93.1 +/- 29.8 microL.min-1.g-1 placenta, respectively) compared to 51Cr-EDTA (3.2 +/- 0.9 microL.min-1.g-1) suggest that maternofetal transfer of these cations occurs by mechanisms in addition to diffusion. Kmf Mg was also greater than Kmf 51Cr-EDTA when measured across the dually perfused rat placenta, in which the maternal uterine artery was additionally perfused with Mg-containing (0.5 mmol.L-1) Krebs-Ringer solution. Decreasing the Mg concentration in the maternal perfusate by 90% reduced Mg appearance in the fetal perfusate by 87% within 8 min; this suggests that Kmf Mg across the in situ perfused placenta largely reflects Mg transfer from maternal plasma and not simply elution of a placental Mg pool. Addition of KCN (1 mmol.L-1) to the fetal perfusate or lowering perfusate temperature from 37 to 26 degrees C significantly reduced Kmf Mg and Kmf 45Ca across the in situ perfused placenta. In contrast, Kmf 51Cr-EDTA was increased by KCN and unaffected by temperature.(ABSTRACT TRUNCATED AT 250 WORDS)

Control of maternofetal calcium transfer across the in situ perfused rat placenta at day 21 of gestation (term 23 d) was investigated in both intact fetuses and those parathyroidectomized by decapitation on day 19. Decapitation resulted in significant fetal hypocalcemia. Injection of fetuses subcutaneously through the uterine wall with 0.43 micrograms bovine (b) PTH(1-84), 20 ng 1,25(OH)2D3 or 10 microL of the appropriate diluent resulted 2 h later in a raised fetal blood ionized Ca concentration only with bPTH(1-84) in both normal and decapitated fetuses. Fetal decapitation caused a significant (p less than 0.001) fall in the clearance of 45Ca across the placenta (Kmf45Ca), which was significantly (p less than 0.05) reversed after fetal bPTH(1-84) and 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) injection, but not back to normal levels. There was no effect of either hormone on Kmf45Ca in placentas from intact fetuses, or on Kmf51Cr-EDTA (used as an extracellular marker) in either group. When 4 ng/mL r[Nle8,21, Tyr34] PTH(1-34), 50 pg/mL 1,25(OH)2D3 or the appropriate diluent was perfused through placentas the only response observed was a significant (p less than 0.05) increase in Kmf45Ca with 1,25(OH)2D3 perfusion in placentas from decapitated fetuses, Kmf51Cr-EDTA being unchanged. Finally, perfusion with 10(-5) M forskolin (an activator of adenylate cyclase) stimulated Kmf45Ca in placentas from both normal and decapitated fetuses. Although there was also some effect on Kmf51Cr-EDTA in the latter, there was none in the placentas from normal fetuses, and here the effect on Kmf45Ca was dose dependent with an initial response at 10(-6) M.(ABSTRACT TRUNCATED AT 250 WORDS)

Maternofetal clearance of 45Ca and 51Cr-EDTA (diffusional marker) were simultaneously measured across in situ perfused placentas of intrauterine growth-retarded (IUGR) and control rat fetuses on d 20 of gestation. IUGR was induced by uterine artery and vein ligation on d 17 of gestation. Control fetuses and their placentas were taken from sham-operated dams. We hypothesized that calcium transfer would be impaired across placentas of IUGR fetuses. The mean body wt of IUGR fetuses was 42% lower, and the mean nose-anus length was 16% lower than those of control fetuses. The mean total calcium content of IUGR fetuses was significantly lower than that of control fetuses, but not when it was normalized to body wt. The mean maternal whole blood ionized calcium concentration was not significantly different in the two groups. The materno-fetal clearance of 45Ca across IUGR placentas was significantly lower than that across control placentas (IUGR = 35.2 +/- 1.9 micro L/min/g placenta, mean +/- SEM; control = 93.1 +/- 12 microliters/min/g placenta, p less than 0.002). In contrast, the maternofetal clearance of 51Cr-EDTA, the reference diffusional marker, was not significantly different across IUGR and control placentas. We conclude that maternofetal transfer of calcium is reduced across placentas of IUGR rat fetuses.

Pulmonary fat embolism in a preterm infant receiving Intralipid intravenously is described. Serum obtained at the time of clinical deterioration agglutinated Intralipid. This coincided with the onset of septicaemia and with a raised serum C reactive protein concentration. Subsequent clinical improvement was associated with reduction in the C reactive protein concentration and nonagglutination of Intralipid.