Urban eddy covariance measurements reveal significant missing NOx emissions in Central Europe.

Nitrogen oxide (NOx) pollution is emerging as a primary environmental concern across Europe. While some large European metropolitan areas are already in breach of EU safety limits for NO2, this phenomenon does not seem to be only restricted to large industrialized areas anymore. Many smaller scale populated agglomerations including their surrounding rural areas are seeing frequent NO2 concentration violations. The question of a quantitative understanding of different NOx emission sources is therefore of immanent relevance for climate and air chemistry models as well as air pollution management and health. Here we report simultaneous eddy covariance flux measurements of NOx, CO2, CO and non methane volatile organic compound tracers in a city that might be considered representative for Central Europe and the greater Alpine region. Our data show that NOx fluxes are largely at variance with modelled emission projections, suggesting an appreciable underestimation of the traffic related atmospheric NOx input in Europe, comparable to the weekend-weekday effect, which locally changes ozone production rates by 40%.

Congenital heart surgery: expected versus observed surgical performance according to the Aristotle complexity score.

BACKGROUND: The Aristotle score quantifies the complexity involved in congenital heart surgery. It defines surgical performance as complexity score times hospital survival. We studied how expected and observed surgical performance evolved over time. METHODS: 2312 main procedures carried out between 2006 and 2010 were analyzed. The Aristotle basic score, corresponding hospital survival and related observed surgical performance were estimated. Expected survival was based on the mortality risks published by O'Brien and coauthors. Observed performance divided by expected performance was called the standardized ratio of performance. This should trend towards a figure above 100%. Survival rates and performance are given with 95% confidence intervals. RESULTS: The mean Aristotle basic score was 7.88 ± 2.68. 51 patients died: observed hospital survival was 97.8 % (97.1 %-98.3%). 115 deaths were anticipated: expected survival was 95.2% (93.5%-96.3%). Observed and expected surgical performance reached 7.71 (7.65-7.75) and 7.49 (7.37-7.59), respectively. Therefore the overall standardized ratio of performance was 102.94%. The ratio increased from 2006 (ratio = 101.60%) to 2009 (103.92%) and was 103.42% in 2010. Performance was high for the repair of congenital corrected transposition of the great arteries and ventricular septal defect (VSD) by atrial switch and Rastelli procedure, the Norwood procedure, repair of truncus arteriosus, aortic arch repair and VSD closure, and the Ross-Konno procedure, with corresponding standardized ratios of 123.30%, 116.83%, 112.99%, 110.86% and 110.38%, respectively. With a ratio of 82.87%, performance was low for repair of Ebstein's anomaly. CONCLUSION: The standardized ratio of surgical performance integrates three factors into a single value: procedure complexity, postoperative observed survival, and comparison with expected survival. It constitutes an excellent instrument for quality monitoring of congenital heart surgery programs over time. It allows an accurate comparison of surgical performance across institutions with different case mixes.

Surgical management of congenital heart disease: correlation between hospital costs and the Aristotle complexity score.

BACKGROUND: Hospital costs are expected to correlate with clinical complexity. Do costs for congenital heart surgery correlate with Aristotle complexity scores? METHODS: 442 inpatient stays in 2008 were evaluated. Aristotle scores and levels were determined. Costs were estimated according to the German Institute for Hospital Reimbursement system. Pearson and Spearman R correlation coefficients and corresponding goodness-of-fit regression coefficients R2 were calculated. RESULTS: Mean basic and comprehensive Aristotle scores were 7.60 +/- 2.74 and 9.23 +/- 2.94 points, respectively. Mean expenses per hospital stay amounted to 29,369 +/- 30,823 Euros. Aristotle basic and comprehensive scores and levels were positively correlated with hospital costs. With a Spearman R of 1 and related R2 of 0.9436, scores of the 6 Aristotle comprehensive levels correlated best. Mean hospital reimbursement was 26,412 +/- 17,962 Euros. Compensation was higher than expenses for patients in comprehensive levels 1 to 3, but much lower for those in levels 4 to 6. CONCLUSIONS: Aristotle comprehensive complexity scores were highly correlated with hospital costs. The Aristotle score could be used as a scale to establish the correct reimbursement after congenital heart surgery.

The Norwood procedure - does the type of shunt determine outcome?

BACKGROUND: Stage I palliation of hypoplastic left heart syndrome (HLHS) and its variants is usually performed by a Norwood operation. The management of pulmonary blood flow during this procedure remains controversial. The RV-to-PA conduit (RVPAC) has been proposed as the better alternative compared to a systemic-to-pulmonary shunt (SPS). METHODS: A retrospective single center chart review of consecutive patients who underwent a Norwood I procedure between 01/1997 and 09/2006 was performed. All patients were operated in deep hypothermia, with or without circulatory arrest, using different shunt modifications according to surgeon's preference. Patients were divided into two groups depending on surgical management for pulmonary blood flow (modified BT shunt [BT] and non-valved RVPAC [Sano]). RESULTS: Fifty-four patients were included in the study (BT: 31 patients vs. Sano: 23 patients). Diastolic blood pressure during the first 24 hours postoperatively was significantly lower in the BT group (BT: 38.6 +/- 6.9 mmHg vs. Sano: 42.4 +/- 7.2 mmHg; P < 0.01) with a trend towards a higher systolic blood pressure (BT: 74.1 +/- 13.5 mmHg vs. Sano: 69.8 +/- 12.1 mmHg; P = 0.08). Mean circulatory arrest time in the BT group was significantly longer compared to the Sano patients (BT: 41 +/- 21 min vs. Sano: 25 +/- 23 min; P < 0.01). The mean hospital stay was 18.5 days for BT patients and 20 days for Sano patients ( P = 0.45). Early mortality for the total cohort was 14.8 % (n = 8) (BT 19.4 % [n = 6] vs. Sano 8.7 % [n = 2]; P = 0.12). There was no significant difference in inter-stage mortality between the two groups (BT: 18.2 % vs. Sano: 21.1 %; P = 0.47). CONCLUSION: The results for both established surgical methods (BT and Sano) for the palliation of HLHS and its variants have improved over time and are reaching acceptable early mortality rates. There was a trend towards a favorable early outcome for Sano patients, which did not reach statistical significance in this study due to the low patient numbers.

A musculo-skeletal model of rat ankle motion and its experimental test on rat.

A biomechanical musculo-skeletal model of functional electrical stimulation (FES)-induced rat ankle motion was implemented and tested in rat experiments. The muscle model is a new Hill-based model which includes established physiological relations of force-velocity and force-length-frequency. However, the series-elastic component and the activation component of previous Hill-based models are replaced by a new component which accounts for dynamic time delays and recruitment that occur in real muscle force generation during limb movements. The skeletal model includes gravity and dynamic forces that occur in real rat ankle motions. In computer simulations, various FES patterns were applied to the tibialis anterior (TA) and soleus (SO) model muscles to produce walk-like ankle motions. In lab experiments, the same stimulation patterns were applied by epimysial electrodes implanted in the TA and SO muscles of live rats cordotomized at level T7. The resulting rat motions were recorded by video camera. Video data was converted to ankle angle-vs-time files for comparison with corresponding model angle-vs-time files. Over a physiologically significant range of ankle motions, model parameters were adjustable to yield model motions that agreed with rat motions to within 2 degrees (root mean square differences of rat and model ankle angles). This is shown in plots of model and rat motions presented here for representative cases of FES. The accuracy of our model in reproducing real ankle motions supports the hypothesis that our new muscle model generates correct muscle forces over a useful range of limb motions. It suggests that the model may be useful in the design of FES neural prostheses.

Utility of N-terminal brain natriuretic peptide plasma concentrations in comparison to lactate and troponin in children with congenital heart disease following open-heart surgery.

We conducted a prospective study in a pediatric cardiac intensive care unit in order to determine the diagnostic value of N-terminal brain natriuretic peptide (N-BNP) plasma concentration in the perioperative care of children with congenital heart disease (CHD). N-BNP plasma concentrations were determined by using a validated enzyme immunoassay. We measured N-BNP the day before surgery and up to 15 days postoperatively in 23 children (age range, 0.25-11 years) undergoing cardiac surgery due to various CHDs. Supply and duration of catecholamines, vasodilators, and respiratory therapy were determined and correlated to N-BNP. In addition, troponin T (TnT) and arterial Lactat (aL) concentrations were measured simultaneously. We found a significant correlation between preoperative and maximal N-BNP levels and dosage of vasodilators (r = 0.41, p < 0.02 and r = 0.83, p < 0.01, respectively). Maximal TnT and aL levels were not correlated to dosage of vasodilators. The dosage and duration of catecholamines, the duration of respiratory therapy, and the plasma concentration of TnT and aL were not correlated to pre- or perioperative N-BNP. Maximal TnT and aL levels were correlated to duration (r = 0.53, p < 0.01 and r = 0.48, p < 0.02) and dosage (r = 0.52, p < 0.02 and r = 0.60, p < 0.01) of catecholamines and duration of respiratory therapy (r = 0.57, p < 0.01 and r = 0.50, p < 0.02). As recent studies show, N-BNP appears to be a powerful neurohumoral indicator of ventricular function and prognosis for guiding therapy in the outpatient department or for discriminating cardiac from noncardiac symptoms. In contrast, the value of N-BNP for guiding perioperative therapy in pediatric cardiac intensive care units is limited.

Biventricular repair of double outlet right ventricle with non-committed ventricular septal defect (VSD) by VSD rerouting to the pulmonary artery and arterial switch.

OBJECTIVES: Biventricular repair of double outlet right ventricle non-committed ventricular septal defect (DORVncVSD) is usually achieved by a VSD rerouting to the aorta. This technique can be limited by the presence of tricuspid chordae and by the pulmonary artery to tricuspid valve distance. Furthermore, there is an important risk of late subaortic obstruction related to the long patch required that creates a potential akinetic septal area. Presented here is another technique; by VSD rerouting to the pulmonary infundibulum and arterial switch. METHODS: Ten patients, with DORVncVSD, underwent a VSD rerouting to the pulmonary infundibulum followed by arterial switch. Seven had a previous pulmonary artery banding and one a moderate infundibular stenosis. The median age at surgery was 16 months (range 3 weeks to 4.5 years). All patients had a bilateral infundibulum, with a large persistent subaortic conus, D malposition of the aorta, side-by-side vessels and double loop coronary patterns. The VSD was perimembranous with inlet or trabecular extension. Subaortic obstruction was constant. The VSD was severely distant from both the aortic and the pulmonary annulus. The operation was conducted through a combined approach. The VSD was constantly enlarged superiorly. The almost permanent subaortic obstruction was released. The VSD was always found quite close to the pulmonary infundibular ostium. The arterial switch technique was adapted to the complex coronary anatomy. RESULTS: There was one non-cardiac death. At a mean follow-up of 20 months, all nine survivors are in NYHA class I, in sinus rhythm, and have no subaortic gradient greater than 15 mm. CONCLUSION: This technique of VSD rerouting to the pulmonary artery and arterial switch limits greatly the size of the rerouting patch, respects the tricuspid chordae and is independent of the pulmonary artery-tricuspid valve distance. In this early series of biventricular repair of DORVncVSD, the VSDs were always found close to the pulmonary artery, allowing this new type of repair.

The Caenorhabditis elegans peb-1 gene encodes a novel DNA-binding protein involved in morphogenesis of the pharynx, vulva, and hindgut.

Gene expression in the Caenorhabditis elegans pharynx is regulated in part by organ-specific signals, which in the myo-2 gene target a regulatory sequence called the C sub-element. C sub-element activity requires the organ specification factor PHA-4, a winged-helix transcription factor expressed in all pharyngeal cells. To identify additional factors involved in pharyngeal organogenesis, we performed a yeast one-hybrid screen for C sub-element binding proteins. Here we describe the novel factor PEB-1, which is coexpressed with PHA-4 in many pharyngeal cell types, including muscles, epithelial cells, marginal cells, and glands, but is undetectable in the pharyngeal nervous system. PEB-1 is also detected outside the pharynx in cells surrounding the rectum and vulva, as well as in the germ line. Reduction of peb-1 function using RNAi results in morphological defects in the somatic tissues in which peb-1 is expressed. We have mapped the PEB-1 DNA-binding domain to a 158-residue region, which is unrelated to known DNA-binding proteins but shares some sequence similarity to the Drosophila Mod(mdg4) proteins. PEB-1 specifically recognizes a site in the C subelement that partially overlaps the PHA-4 binding site. Both the PEB-1 and the PHA-4 binding sites are necessary for strong C sub-element enhancer activity in some cells in which these factors are coexpressed. In contrast the PEB-1 site is dispensable for C sub-element activity in pharyngeal neurons. We propose that PEB-1 functions with PHA-4 to activate target gene expression in cells in which they are coexpressed.

Nosocomial outbreak of vancomycin-resistant Enterococcus faecium at a German university pediatric hospital.

Nosocomial Infections caused by vancomycin-resistant enterococci (VRE) are an emerging threat to critically ill patients. At the University Hospital Eppendorf, VRE were isolated from 38 patients between August 1993 and April 1997, of whom 32 were hospitalized at the Department of Pediatrics. Pulsed-field gel electrophoresis revealed that 26 Enterococcus faecium isolates from patients of the Department of Pediatrics were identical or closely related, and that isolates from three additional patients of the same department were possibly related. All of these isolates were of vanA genotype. They were resistant to glycopeptides, ampicillin, ciprofloxacin, clindamycin, and erythromycin. Most isolates displayed high-level resistance to gentamicin, but all remained susceptible to quinupristin/dalfopristin. Implementation of stringent hand disinfection and environmental disinfection policies, as well as measures for patient isolation contained this first outbreak of VRE at a German Children's hospital, which emphasizes the importance of hygienic measures for the control of nosocomial spread of these organisms.

The DAF-3 Smad binds DNA and represses gene expression in the Caenorhabditis elegans pharynx.

Gene expression in the pharyngeal muscles of Caenorhabditis elegans is controlled in part by organ-specific signals, which in the myo-2 gene target a short DNA sequence termed the C subelement. To identify genes contributing to these signals, we performed a yeast one-hybrid screen for cDNAs encoding factors that bind the C subelement. One clone recovered was from daf-3, which encodes a Smad most closely related to vertebrate Smad4. We demonstrated that DAF-3 binds C subelement DNA directly and specifically using gel mobility shift and DNase1 protection assays. Mutation of any base in the sequence GTCTG interfered with binding in the gel mobility shift assay, demonstrating that this pentanucleotide is a core recognition sequence for DAF-3 binding. daf-3 is known to promote formation of dauer larvae and this activity is negatively regulated by TGFbeta-like signaling. To determine how daf-3 affects C subelement enhancer activity in vivo, we examined expression a gfp reporter controlled by a concatenated C subelement oligonucleotide in daf-3 mutants and other mutants affecting the TGFbeta-like signaling pathway controlling dauer formation. Our results demonstrate that wild-type daf-3 can repress C subelement enhancer activity during larval development and, like its dauer-promoting activity, daf-3's repressor activity is negatively regulated by TGFbeta-like signaling. We have examined expression of this gfp reporter in dauer larvae and have observed no daf-3-dependent repression of C activity. These results suggest daf-3 directly regulates pharyngeal gene expression during non-dauer development.

Rescue of Caenorhabditis elegans pharyngeal development by a vertebrate heart specification gene.

Development of pharyngeal muscle in nematodes and cardiac muscle in vertebrates and insects involves the related homeobox genes ceh-22, nkx2.5, and tinman, respectively. To determine whether the nematode and vertebrate genes perform similar functions, we examined activity of the zebrafish nkx2.5 gene in transgenic Caenorhabditis elegans. Here, we report that ectopic expression of nkx2.5 in C. elegans body wall muscle can directly activate expression of both the endogenous myo-2 gene, a ceh-22 target normally expressed only in pharyngeal muscle, and a synthetic reporter construct controlled by a multimerized CEH-22 binding site. nkx2.5 also efficiently rescues a ceh-22 mutant when expressed in pharyngeal muscle. Together, these results indicate that nkx2.5 and ceh-22 provide a single conserved molecular function. Further, they suggest that an evolutionarily conserved mechanism underlies heart development in vertebrates and insects and pharyngeal development in nematodes.

Immunolocalization of nitric oxide synthases at the postsynaptic domain of human and rat neuromuscular junctions--light and electron microscopic studies.

Neuronal (n) and inducible (i) nitric oxide synthase (NOS) were immunolocalized at the postsynaptic domain of human and rat neuromuscular junctions (NMJs) by light and electron microscopy. We applied polyclonal and monoclonal antibodies for colocalization with three other synaptic proteins, utilizing double and triple fluorescence labeling, and gold and peroxidase for immunoelectron microscopy. By light microscopy, nNOS and iNOS colocalized with desmin and dystrophin, known postsynaptic components, but not with neurofilament protein, a presynaptic component. By electronmicroscopy, nNOS, but not iNOS, colocalized postsynaptically on the same structures as desmin; iNOS was also postsynaptic, but did not colocalize with desmin immunoreactivity. At the NMJs of Duchenne muscular dystrophy patients, both nNOS and iNOS were strongly immunoreactive. At the NMJs of a patient with myasthenia gravis, nNOS was weaker than in controls. Total denervation of rat sciatic nerve did not cause any decrease of nNOS or iNOS immunoreactivity 7 days thereafter. At 15 days after denervation, there was a gradual decrease of immunoreactivity, and immunoreactivity disappeared 30 days after denervation, corresponding to the ultrastructurally detectable disorganization of the postsynaptic region. This seems to be the first combined light and electron microscopic description of the postsynaptic localization of nNOS and iNOS at human and rat NMJs.

The Caenorhabditis elegans NK-2 homeobox gene ceh-22 activates pharyngeal muscle gene expression in combination with pha-1 and is required for normal pharyngeal development.

Pharyngeal muscle development in the nematode Caenorhabditis elegans appears to share similarities with cardiac muscle development in other species. We have previously described CEH-22, an NK-2 class homeodomain transcription factor similar to Drosophila tinman and vertebrate Nkx2-5, which is expressed exclusively in the pharyngeal muscles. In vitro, CEH-22 binds the enhancer from myo-2, a pharyngeal muscle-specific myosin heavy chain gene. In this paper, we examine the role CEH-22 plays in pharyngeal muscle development and gene activation by (a) ectopically expressing ceh-22 in transgenic C. elegans and (b) examining the phenotype of a ceh-22 loss-of-function mutant. These experiments indicate that CEH-22 is an activator of myo-2 expression and that it is required for normal pharyngeal muscle development. However, ceh-22 is necessary for neither formation of the pharyngeal muscles, nor for myo-2 expression. Our data suggest parallel and potentially compensating pathways contribute to pharyngeal muscle differentiation. We also examine the relationship between ceh-22 and the pharyngeal organ-specific differentiation gene pha-1. Mutations in ceh-22 and pha-1 have strongly synergistic effects on pharyngeal muscle gene expression; in addition, a pha-1 mutation enhances the lethal phenotype caused by a mutation in ceh-22. Wild-type pha-1 is not required for the onset of ceh-22 expression but it appears necessary for maintained expression of ceh-22.

Localization of Activin and Activin Receptors in Rat Spinal Motoneurons.

The purpose of this experiment was to determine whether rat spinal motoneurons (a) produce activin protein and (b) transcribe mRNAs coding for the betaA-subunit of activin and activin receptors II and IIB. The production of activin was determined by immunocytochemistry. The expression and localization of the mRNAs were elucidated by the reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization techniques. We have observed that activin A protein was produced and mRNAs encoding activin betaA-subunit and activin receptors II and IIB were expressed by motoneurons of the rat spinal cord. Furthermore, the identity of RT-PCR products was confirmed by DNA sequencing. It is concluded that activin may have a functional role in the maintenance of rat spinal motoneurons. Copyright 1996 S. Karger AG, Basel

Oncogenic potential of inhaled hydrazine in the nose of rats and hamsters after 1 or 10 1-hr exposures.

Hydrazine (N2H4) is used as a fuel for missiles and standby power systems of operational military aircraft. Maintenance of missiles and aircraft may result in accidental human exposure to high concentrations for brief periods of time. The purposes of this study were to assess the oncogenic potential of N2H4 in rats and male hamsters exposed to a high concentration of N2H4 for repeated short exposures and to investigate the relationships of acute and subchronic effects of N2H4 to nasal tumorigenesis. In phase 1 (acute and subchronic) and Phase 2 (lifetime experiments, groups of male and female Fischer 344 rats and male Syrian golden hamsters were exposed by inhalation to 0, 75 (Phase 2 only), or 750 ppm N2H4 for 1 (acute) or 10 (subchronic) 1-hr weekly exposures. Rodents were euthanized 24 hr after exposures 1 and 10 and 24 to 30 months poststudy initiation. Significant reductions in body weight were observed in N2H4-treated rodents compared to controls during the exposure interval. No hydrazine-induced mortality was detected. Histopathologic examination after the acute and subchronic exposures revealed degeneration and necrosis of transitional, respiratory, and olfactory epithelia in the anterior nose and, in rats exposed subchronically, squamous metaplasia of the transitional epithelium. Minimal to mild rhinitis resulted from N2H4 exposures. Apoptosis was observed in olfactory and squamous metaplastic transitional epithelium. Lesions occurred at sites reportedly having high air-flow and generally appeared to be more severe in the anterior portion of the nose. By 24 months, the squamous metaplastic transitional epithelium reverted back to normal-appearing transitional epithelium. By 24+ months, low incidences (sexes combined) of hyperplasia (5/194, 2.6%) and neoplasia (11/194, 5.7%) were detected, principally in the transitional epithelium of the 750 ppm N2H4-treated rats. A similar incidence of hyperplasia (2/94, 2%) and neoplasia (5/94, 5.3%) was detected in the high-exposure group of hamsters. The location and type of N2H4-induced proliferative lesions were similar to those reported in a chronic N2H4-exposure study (5.0 ppm x 6 hr/day x 5 days/week for 1 year) conducted in our laboratory, but the chronic study had much higher incidences (rats, sexes combined: hyperplasia 15.5% vs 2.6% and polypoid adenoma 44.6% vs 5.2%). The product (CD) of concentration + time was the same (750 ppm hours) for the high-dose groups for both studies, but the duration of exposure was 150 x longer and the concentration was 150 x lower in the chronic study.(ABSTRACT TRUNCATED AT 400 WORDS)

Down-regulation of thyrotropin-releasing hormone (TRH) receptors in spinal cord after transection as revealed by quantitative autoradiography.

The autoradiographic localization of thyrotropin-releasing hormone (TRH) receptors was investigated in the rat spinal cord after transection at the level of T8-T9. The discrete distribution of [3H]-MeTRH binding was measured with a computerized image analyzer at the cervical (C6-C7) and lumbar (L2-L3) level, one week and three weeks after injury. The TRH receptor density was expressed in fmol/mg protein. There was no significant change in the density of TRH receptors below the injury site. In the cervical region, TRH receptor concentration in the dorsal gray matter did not differ from normal controls; in contrast we found a time dependent change in lamina 10 and in the ventral gray, with a significant decrease (25% and 19%, respectively) of TRH receptor binding sites one week after transection and a return to control levels by three weeks. From these data and the known increase of TRH immunoreactivity above a spinal injury, a down-regulation of spinal cord TRH receptors in response to elevated levels of TRH is suggested.

Effects of experimental spinal cord transection on substance P receptors: a quantitative autoradiography study.

The autoradiographic localisation of Substance P (SP) receptors was investigated in the rat spinal cord following cordotomy at the thoracic 8-9 level. The binding of [125I]-BH-SP was measured in discrete gray matter structures above (C6-C7 level) and below (L2-L3 level) the injury site, and expressed in fmol/mg protein. There was a statistically significant increase in SP receptor density 1 week after cordotomy in the dorsal horn and in the central canal of lumbar region, in laminae 3-4-5 and also in the ventral horn of cervical spinal cord. Elevated SP receptor density was also noted in cervical ventral horn at 3 weeks after thoracic cordotomy, whereas the increase seen at 1 week was normalized at 3 weeks everywhere else. Since SP concentration has been reported to show a similar localized increase below a spinal transection, the present results are consistent with an up-regulation of SP receptors. A similar direct relationship between SP receptors and SP content appears to occur also in the ventral horn above the injury site.

Response to deep hypoglycemia does not involve glucoreceptors in carotid perfused tissue.

In the present study we examined whether the magnified hormonal counter-regulatory response seen during deep hypoglycemia (40 mg/dl) could be attenuated by supplying the forebrain with glucose furnished through carotid infusion. Two protocols were performed in conscious dogs. In the first protocol we infused glucose bilaterally into the carotid circulation to produce a forebrain glycemia of 55 +/- 1 mg/dl (as reflected in the jugular vein), whereas systemic glycemia declined to 39 +/- 2 mg/dl. In the second protocol as a control we infused glucose into the systemic circulation at a rate matched to protocol 1 so that both systemic and jugular plasma glucose concentrations were equivalent to the systemic glucose concentrations in protocol 1 (jugular, 41 +/- 3 mg/dl; systemic, 40 +/- 2 mg/dl; P greater than 0.9). In spite of a substantial difference in forebrain glycemia (55 mg/dl compared with 41 mg/dl) there were no differences in the counter-regulatory responses of catecholamines or glucagon. In addition, through the use of radiolabeled microspheres, we defined the precise regions of the forebrain irrigated during bilateral intracarotid glucose infusions. The concentration of microspheres was high in the forebrain but very low in the hindbrain. Our results indicate that glucoreceptor cells in tissues perfused by carotid arteries may play a tautological role in the sympathetic response to hypoglycemia and imply that glucose-sensitive receptors must also be located elsewhere in the central nervous system or in the periphery.

Sinoaortic denervation changes catecholamines in caudate-putamen of rats.

The 3-day sinoaortic-denervated (SAD) rat has a reduced concentration of dopamine (DA) in caudate-putamen (CP) (Brain Research, 299 (1984) 380-383). This suggested that the nigrostriatal system processes input from the cardiovascular system via arterial baroreceptor pathways. In this study we compared regional DA levels in CP of SAD and sham-operated (SO) rats 3 and 7 days after surgery. Bilateral CP samples were obtained by micropunch from consecutive frozen brain sections. Samples were taken throughout the entire length of CP from dorsal, lateral and ventral areas. Punches of two consecutive sections were pooled and assayed for DA and norepinephrine (NE). SO rats showed a rostro-caudal gradient of DA in all 3 areas. Three-day SAD rats had significantly lower cumulative DA concentrations in each of the 3 CP areas. The concentrations in each region of the 3 areas were also reduced and about half of them achieved statistical significance. SO rats did not show a gradient of NE. Cumulative NE was significantly lower in dorsal and ventral areas of SAD rats. In 7 days SAD rats, DA values were no longer reduced, but were significantly elevated in dorsal but unchanged in ventral areas. These data support evidence of nigrostriatal interaction with baroreceptor pathways.

Autoradiographic localization of substance P receptors in rat spinal cord: effects of experimental spinal transection.

The autoradiographic localization of Substance P (SP) receptors was studied in the rat spinal cord following thoracic cordotomy. The binding of [125I]-BH-SP was measured in discrete gray matter structures above and below the injury site. There was a significant increase in SP receptor density 1 week after cordotomy in the dorsal horn and in the central canal of lumbar region, and in laminae 3-4-5 and also in the ventral horn of cervical spinal cord. Elevated SP receptor density was noted only in cervical ventral horn at 3 weeks after cordotomy. Since SP concentration has been reported to show similar localized increases, the present results are consistent with an up-regulation of SP receptors.