SUMMARY A noninvasive method is described for measuring the pressure drop across the mitral valve in mitral stenosis by Doppler ultrasound. A maximum frequency estimator was used to record maximum velocity in the Doppler signal from the mitral jet. Provided the angle between the ultrasound beam and the maximum velocity is close to zero the pressure drop can be calculated directly.Good correlation was found between Doppler measurements and simultaneous pressure recordings during heart catheterisation in 10 patients. No false negative or false positive diagnoses ofmitral stenosis were made among 55 patients (35 patients with mitral stenosis and 20 patients with other valve lesions). The measurements were easy to perform in most patients and the method seems well suited both to diagnose and to follow patients with mitral stenosis. Holen et al. (1976) have shown that the pressure drop across a stenotic mitral valve may be calculated from transcutaneous Doppler ultrasonic measurements of the blood velocity in the mitral jet. A pressure difference across the valve is necessary both to accelerate the blood through the valve constriction and to overcome the viscous resistance. The work of Holen et al. indicates that viscous resistance may be neglected for the blood with the highest velocity in the jet. The pressure drop across the valve may then be calculated from the maximum velocity in the jet using the Bernoulli equation.The ultrasound reflected from a small blood sample will undergo a change in frequency (Doppler effect) which is proportional to the velocity of the blood and to the cosine of the angle between this velocity and the ultrasonic beam. This angle can be approximated to zero for measurements of mitral jet velocity from the chest. The maximum velocity in the jet can, therefore, be calculated from the maximum frequency shift in the Doppler signal. Holen et al. used a complete spectral analysis to obtain the maximum frequency shift in the Doppler signal. In the present study a simple maximum frequency estimator is used (Brubakk et al., 1977), and the time variation of the frequency shift can be recorded on an ordinary paper recorder.

A dults born very preterm (VP; <32 weeks of gestation) or at very low birth weight (VLBW; <1500 g) have higher blood pressure than their peers born at term.1-10 A recent meta-analysis showed that VLBW or VP adults have on average 3.3 mm Hg higher systolic pressure than controls. 7 Another meta-analysis, including studies in adults born at any degree of prematurity, concluded that the mean difference between adults born preterm and controls was 4.2 mm Hg for systolic and 2.6 mm Hg for diastolic blood pressure. 8 These differences were more pronounced among women (systolic/diastolic 4.9/2.9 mm Hg) but clearly present among men as well (2.0/1.3 mm Hg). 8 These differences are considerable given that, at the population level, a 2 mm Hg reduction in diastolic pressure is estimated to result in a 7% to 14% reduction in mortality from ischemic heart disease and 9% to 19% from stroke with greatest reductions in the youngest age groups. 11Although these meta-analyses have been important in confirming the association between very preterm birth and adult blood pressure, they have, apart from sex, not been able to assess any other risk factors or protective factors for high blood pressure among adults born very preterm. This would be a crucial step in identifying underlying mechanisms, which then could serve as targets for prevention.The higher blood pressure among adults born VLBW/VP could arise from dissimilar conditions that lead to preterm birth or Abstract-Adults born preterm at very low birth weight (VLBW; <1500 g) have higher blood pressure than those born at term.It is not known whether all VLBW adults are at risk or whether higher blood pressure could be attributed to some of the specific conditions underlying or accompanying preterm birth. To identify possible risk or protective factors, we combined individual-level data from 9 cohorts that measured blood pressure in young adults born at VLBW or with a more stringent birth weight criterion. In the absence of major heterogeneity, we performed linear regression analysis in our pooled sample of 1571 adults born at VLBW and 777 controls. Adults born at VLBW had 3.4 mm Hg (95% confidence interval, 2.2-4.6) higher systolic and 2.1 mm Hg (95% confidence interval, 1.3-3.0) higher diastolic pressure, with adjustment for age, sex, and cohort. The difference in systolic pressure was present in men (1.8 mm Hg; 95% confidence interval, 0.1-3.5) but was stronger in women (4.7 mm Hg; 95% confidence interval, 3.2-6.3). Among the VLBW group, blood pressure was unrelated to gestational age, maternal smoking, multiple pregnancy, retinopathy of prematurity, or bronchopulmonary dysplasia. Blood pressure was higher than that of controls among VLBW adults unexposed to maternal preeclampsia. Among those exposed, it was even higher, especially if born appropriate for gestational age. In conclusion, although female sex and maternal preeclampsia are additional risk factors, the risk of higher blood pressure is not limited to any etiologic subgroup of VLBW adults, arguing for vigilance in...

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The assumption that the lung is an effective filter for gas bubbles is of importance for certain occupations (e.g., divers, astronauts) as well as in the accomplishment of several medical procedures. The filtering capacity was tested in pigs by use of continuous air infusion into the right ventricle and a transesophageal echocardiographic transducer for detection of air in the left atrium. Twenty pigs, anesthetized with pentobarbital sodium and mechanically ventilated, were divided into groups that received air at infusion rates of 0.05 (group 1a, n = 7), 0.10 (group 2, n = 6), and 0.20 (group 3, n = 5) ml.kg-1.min-1. Two pigs served as controls. The breakthrough incidence was 0, 67, and 100%, respectively. Group 1a received a second infusion of 0.10 ml.kg-1.min-1 (group 1b, n = 7), and spillover of bubbles occurred in only 14% of these pigs. Infusion of gas caused a maximum increase in mean pulmonary arterial pressure (PAP) of 129 +/- 9% to 39.2 +/- 1.3 (SE) mmHg, with no significant difference between the groups. Breakthrough was observed only in animals with a dramatic reduction in mean arterial pressure and a PAP that returned to almost-normal values at spillover time. Our results suggest that the threshold value for breakthrough of air bubbles in pigs is reduced compared with that in dogs. The hemodynamic consequences at a given infusion rate are, however, greatly enhanced.

Glucose and acetate metabolism and the synthesis of amino acid neurotransmitters, anaplerosis, glutamate-glutamine cycling and the pentose phosphate pathway (PPP) have been extensively investigated in the adult, but not the neonatal rat brain. To do this, 7 day postnatal (P7) rats were injected with [1-C]glucose and [1,2-C]acetate and sacrificed 5, 10, 15, 30 and 45 min later. Adult rats were injected and sacrificed after 15 min. To analyse pyruvate carboxylation and PPP activity during development, P7 rats received [1,2-C]glucose and were sacrificed 30 min later. Brain extracts were analysed using Hand C-NMR spectroscopy. The neonatal brain contained lower levels of glutamate, aspartate and N-acetylaspartate but similar levels of GABA and glutamine compared to adults. Metabolism of [1-C]glucose at the acetyl CoA stage was reduced much more than that of [1,2-C]acetate. The transfer of glutamate from neurons to astrocytes was greatly reduced while transfer of glutamine from astrocytes to glutamatergic neurons was relatively higher compared to adults. However, transport of glutamine from astrocytes to GABAergic neurons was lower. Using [1,2-C]glucose it could be shown that despite much lower pyruvate carboxylation, relatively more pyruvate from glycolysis was directed towards anaplerosis than pyruvate dehydrogenation in astrocytes compared to reports from the adult brain. Moreover, the ratio of PPP/glucose metabolism was higher in P7 compared to adult brain. Our findings indicate that only the part of the glutamateglutamine cycle that transfers glutamine from astrocytes to neurons is operating in the After uptake into the cell, glucose (via pyruvate from glycolysis) and acetate can be converted to the TCA cycle substrate acetyl CoA. It has been reported that glucose oxidation is lower and that the average time the metabolites stay in the TCA cycle before conversion to substances such as neurotransmitters glutamate and thereafter γ-amino butyric acid (GABA) is longer in the neonatal compared to the adult brain [7]. This is in part attributed to the low levels of enzymes for pyruvate metabolism and oxidative glucose metabolism in the postnatal period [8].Pyruvate carboxylase, the brain's exclusive anaplerotic enzyme [9], is present in astrocytes only [10], and is of major importance for glial metabolic support of neurotransmission. Pyruvate carboxylase content is low in the neonatal period and increases 15-fold up to young adult age (postnatal day 30-40) when the level reaches a plateau [8].Most of the glutamate in the brain is found in neurons and is released into the synapse after depolarisation [11]. The ability of astrocytes to take up glutamate from the synapse and convert it into glutamine by the astrocyte specific enzyme glutamine synthetase [12] is vital for normal metabolic homeostasis and as a defence mechanism against excitotoxicity [13]. The subsequent transfer of glutamine from astrocytes to neurons for deamidation to glutamate closes the glutamate-