Tissue Doppler gated (TDOG) dynamic three-dimensional ultrasound imaging of the fetal heart.

Dynamic three-dimensional (3D) ultrasound imaging of the fetal heart is difficult due to the absence of an electrocardiogram (ECG) signal for synchronization between loops. In this study we introduce tissue Doppler gating (TDOG), a technique in which tissue Doppler data are used to calculate a gating signal. We have applied this cardiac gating method to dynamic 3D reconstructions of the heart of eight fetuses aged 20-24 weeks.The gating signal was derived from the amplitude and frequency contents of the tissue Doppler signal. We used this signal as a replacement for ECG in a 3D-volume reconstruction and visualization, utilizing techniques established in ECG-gated 3D echocardiography.The reliability of the TDOG signal for fetal cardiac cycle detection was experimentally investigated. Simultaneous recordings of tissue Doppler of the heart and continuous wave (CW) spectral Doppler of the umbilical artery (UA) were performed using two independent ultrasound systems, and the TDOG signal from one system was compared to the Doppler spectrum data from the other system. Each recording consisted of a two-dimensional (2D) sector scan, transabdominally and slowly tilted by the operator, covering the fetal heart over approximately 40 cardiac cycles. The total angle of the sweep was estimated by recording a separate loop through the center of the heart, in the elevation direction of the sweep.3D reconstruction and visualization were performed with the EchoPAC-3D software (GE Medical Systems). The 3D data were visualized by showing simultaneous cineloops of three 2D slices, as well as by volume projections running in cineloop.Synchronization of B-mode cineloops with the TDOG signal proved to be sufficiently accurate for reconstruction of high-quality dynamic 3D data. We show one example of a B-mode recording with a frame rate of 96 frames/s over 20 seconds. The reconstruction consists of 31 volumes, each with 49 tilted frames. With the fetal heart positioned 5-8 cm from the transducer, the sampling distances were approximately 0.15 mm in the beam direction, 0.33 degrees approximately 0.37 mm azimuth and 0.45 degrees approximately 0.51 mm elevation. From this single dataset we were able to generate a complete set of classical 2D views (such as four-chamber, three-vessel and short-axis views as well as those of the ascending aorta, aortic and ductal arches and inferior and superior venae cavae) with high image quality adequate for clinical use.     

Ischemic disruption of glutamate homeostasis in brain: quantitative immunocytochemical analyses

More than 10 years ago, it was shown by microdialysis that the excitatory transmitter glutamate accumulates in the interstitial space of brain subjected to ischemic insult. This was one of the key observations leading to the formulation of the `glutamate hypothesis' of ischemic cell death. It is now assumed that even a transient glutamate overflow may set in motion a number of events that ultimately cause cell loss in vulnerable neuronal populations. The aim of the present review is to discuss the intracellular changes that underlie the dysregulation of extracellular glutamate during and after ischemia, with emphasis on data obtained by postembedding, electron microscopic immunogold cytochemistry. While the time resolution of this approach is necessarily limited, it can reveal, quantitatively and at a high level of spatial resolution, how the intracellular pools of glutamate and metabolically related amino acids are perturbed during and after an ischemic insult. Moreover, this can be done in animals whose extracellular amino acid levels are monitored by microdialysis, allowing a direct correlation of extra- and intracellular changes. Immunogold analyses of brains subjected to ischemia have identified dendrites and neuronal somata as likely sources of glutamate efflux, probably mediated by reversal of glutamate uptake. The vesicular glutamate pool has been found to be largely unchanged after 20 min of ischemia. Ischemia causes an increased glutamate content and an increased glutamate/glutamine ratio in glial cells, as revealed by double immunogold labelling. This argues against the idea that glial cells contribute to the extracellular overflow of glutamate in the ischemic brain.     

Nitrous oxide fraction in the carbon dioxide pneumoperitoneum during laparoscopy under general inhaled anesthesia in pigs

During prolonged laparoscopy, the diffusion of other gases in the carbon dioxide (CO(2)) pneumoperitoneum may lessen its safety. Nitrous oxide (N(2)O)/CO(2) gas mixtures may become hazardous with regard to gas embolization and fire risk. We therefore evaluated the kinetics of pneumoperitoneal intrusion of N(2)O. In five anesthetized domestic pigs, controlled ventilation, with an initial fraction of inspired oxygen = 1.0, was adjusted to keep ETCO(2) pressure between 35 and 45 mm Hg. The peritoneum was insufflated with CO(2) to a pressure of 12 mm Hg, which was maintained throughout the procedure. T0 was defined as the time when N(2)O was introduced in the breathing circuit (N(2)O end-tidal fraction = 66%). Gas samples (10 mL) from the pneumoperitoneum were analyzed every 10 min after T0. The N(2)O concentration was measured by using capillary gas chromatography coupled with mass spectrometry. Percentages of N(2)O in the CO(2) increased with time (t) according to the ideal equation: N(2)O((t)) = 66 (1 - exp(-0.005t)). In the peritoneal cavity, <2 h were required for the N(2)O to reach the concentration of 29%, which can support combustion. Eight hours to 10 h after T0, the intraperitoneal N(2)O fraction approaches the level of the N(2)O end-tidal fraction. Options to prevent accumulation of N(2)O are suggested. IMPLICATIONS: Pig models were used to evaluate the time course of nitrous oxide (N(2)O) diffusion in the pneumoperitoneum during nitrous oxide/oxygen anesthesia. Although peritoneal N(2)O concentration approaches the end-expiratory value after 8-10 h, it reaches 29% within 2 h. At this level, N(2)O is known to support combustion. This N(2)O pollution should be prevented.     

Prematurity Reduces Functional Adaptation to Intestinal Resection in Piglets

Background: Necrotizing enterocolitis and congenital gastrointestinal malformations in infants often require intestinal resection, with a subsequent risk of short bowel syndrome (SBS). We hypothesized that immediate intestinal adaptation following resection of the distal intestine with placement of a jejunostomy differs between preterm and term neonates. Methods: Preterm or term piglets were born by cesarean section and fed enterally for 2 days. On day 2, piglets were subjected to 50% distal intestinal resection with placement of a jejunostomy. On the following 4–5 days, piglets received parenteral nutrition with gradually increasing doses of enteral nutrition (bovine colostrum). Intestinal tissue samples were collected at delivery and 2 and 6–7 days after birth for histological examination and assessment of digestive enzyme activities. Results: Preterm and term piglets showed similar increases in intestinal weight and digestive enzyme activities from birth to 2 days. On days 6–7 after birth, the remnant intestine showed a similar density (g/cm) and mucosal mass in term and preterm piglets, but villus height, crypt depth, enzyme activities (sucrase, maltase, dipeptidyl peptidase IV [DPPIV]), and hexose uptake capacity were significantly higher in term piglets (P < .05). Preterm piglets were more prone to develop hypoglycemia, respiratory distress syndrome, dehydration, and circulatory instability after surgery compared with term piglets. Conclusion: Studies on intestinal adaptation after resection are feasible in both preterm and term piglets, but intensive clinical support is required when rearing preterm piglets with SBS. Physiological instability and immaturity of the intestine may explain the fact that immediate adaptation after resection is reduced in preterm vs term neonates.     

Transient plasma cobalamin elevation in patients with pneumonia – two case reports

We report two cases of transient significantly elevated plasma cobalamin (B12) in geriatric patients acutely admitted with fever, increased C-reactive protein and X-ray verified pneumonia. Extensive diagnostic workup did not reveal kidney or liver disease, neither any signs of cancer. Furthermore, none of the patients had received therapeutic B12 supplementation prior to admission. In both cases, plasma B12 normalized at an out-patient control few months later. We were not able to identify the reason for the initial B12 elevation in any of the patients, since none of the usually recognized causes were evident. Since both patients had an infection and temporarily elevated B12, we suggest a possible inflammatory response or a vitamin B12 production by the infectious agents as the cause. Both suggestions, however, need further exploration.     

Value and limitations of human myocardial biopsy.

Twenty-three myocardial biopsies from 22 patients with various cardiological diseases were examined by light and electron microscopy. The amount of fibrosis, endocardial thickening, “whorling of myofibers”, “irregular running of myofibers”, fat infiltration and lipofuscein granules were compared to cardiological parameters such as the function group of the patients, cardiac index, stroke index and the pulmonary capillary wedge pressure. The histological grading showed a weak correlation to the function group of the patients and the pulmonary capillary wedge pressure, but not to the cardiac index or stroke index. While patients with an almost normal heart function had a normal histology, both normal and abnormal histology were seen in patiens with severe heart disease. It was not possible to relate any morphological changes in the myocardium, neither at the light microscopical nor at the ultrastructural level to specific heart diseases as for example primary or alcoholic cardiomyopathy. However, severe contraction artefacts disturbed both the light microscopical and especially the ultrastructural evaluation of the specimens.This problem is discussed and in order to diminish the risk of misinterpretation of myocardial biopsy specimens, recommendations are given with regard to fixation, mincing and embedding of the specimens as well as to the evaluation of both the light microscopic slides and the ultrathin sections.     

Simulated dive in rats lead to acute changes in cerebral blood flow on MRI, but no cerebral injuries to grey or white matter

In this study, the effect of a simulated dive on rat brain was investigated using several magnetic resonance imaging (MRI)-methods and immunohistochemistry. Rats were randomly assigned to a dive- or a control group. The dive group was exposed to a simulated air dive to 600 kPa for 45 min. Pulmonary artery was monitored for vascular gas bubbles by ultrasound. MRI was performed 1 h after decompression and at one and 2 weeks after the dive with a different combination of MRI sequences at each time point. Two weeks after decompression, rats were sacrificed and brains were prepared for histology. Dived rats had a different time-curve for the dynamic contrast-enhanced MRI signal than controls with higher relative signal intensity, a tendency towards longer time to peak and a larger area under the curve for the whole brain on the acute MRI scan. On MRI, 1 and 2 weeks after dive, T₂-maps showed no signal abnormalities or morphological changes. However, region of interest based measurements of T₂ showed higher T₂ in the brain stem among decompressed animals than controls after one and 2 weeks. Microscopical examination including immunohistochemistry did not reveal apparent structural or cellular injuries in any part of the rat brains. These observations indicate that severe decompression does not seem to cause any structural or cellular injury to the brain tissue of the rat, but may cause circulatory changes in the brain perfusion in the acute phase.     

Employment status at time of first hospitalization for heart failure is associated with a higher risk of death and rehospitalization for heart failure

Aims

Employment status at time of first heart failure (HF) hospitalization may be an indicator of both self‐perceived and objective health status. In this study, we examined the association between employment status and the risk of all‐cause mortality and recurrent HF hospitalization in a nationwide cohort of patients with HF.

Methods and results

We identified all patients of working age (18–60 years) with a first HF hospitalization in the period 1997–2015 in Denmark, categorized according to whether or not they were part of the workforce at time of the index admission. The primary outcome was death from any cause and the secondary outcome was readmission for HF. Cumulative incidence curves, binomial regression and Cox regression models were used to assess outcomes. Of 25 571 patients with a first hospitalization for HF, 15 428 (60%) were part of the workforce at baseline. Patients in the workforce were significantly younger (53 vs. 55 years) more likely to be male (75% vs 64%) and less likely to have diabetes (13% vs 22%) and chronic obstructive pulmonary disease (5% vs 10%) (all P < 0.0001). Not being part of the workforce was associated with a significantly higher risk of death [hazard ratio (HR) 1.59; 95% confidence interval (CI) 1.50–1.68] and rehospitalization for HF (HR 1.09; 95% CI 1.05–1.14), in analyses adjusted for age, sex, co‐morbidities, education level, calendar time, and duration of first HF hospitalization.

Conclusion

Not being part of the workforce at time of first HF hospitalization was independently associated with increased mortality and recurrent HF hospitalization.