Control of negative inotropic vagal preganglionic neurons in the dog: synaptic interactions with substance P afferent terminals in the nucleus ambiguus?

Previous research from this laboratory has shown that substance P-immunoreactive (SP) terminals synapse upon negative chronotropic vagal preganglionic neurons (VPNs), but not upon negative dromotropic VPNs, of the ventrolateral nucleus ambiguus (NA-VL). Moreover, SP agonists injected into NA-VL cause bradycardia without decreasing AV conduction. In the current study, we have: (1) defined the electron microscopic characteristics of the SP neurons of NA-VL in dog; and (2) tested the hypothesis that SP nerve terminals synapse upon negative inotropic VPNs of NA-VL, retrogradely labeled from the cranial medial ventricular (CMV) ganglion. Numerous SP terminals and a few SP neurons were observed in the vicinity of retrogradely labeled neurons. SP terminals were observed forming synapses with unlabeled dendrites and with SP dendrites, but never with the retrogradely labeled neurons. Together, these results and earlier findings suggest that SP agonists may be able to induce bradycardia without decreasing AV conduction or ventricular contractility.     

Atrophy of the supraspinatus belly Assessment by MRI in 55 patients with rotator cuff pathology

A study of 5 fresh cadaveric shoulders demonstrated that an oblique-sagittal plane which crosses the scapula through the medial border of the coracoid process offers a view of the supraspinatus fossa mostly limited by bone.This view could easily be reproduced by MRI and we called it the Y-shaped view. It allowed a reliable measurement of supraspinatus muscle atrophy by the calculation of the occupation ratio (R) which is the ratio between the surface of the cross-section of the muscle belly and that of the fossa.This ratio was calculated in a prospective study based on 55 shoulders divided into 3 groups with different rotator cuff status: group I, 15 controls; group II, 10 degenerative cuffs, without tears; group III, 30 operated tears. There was no difference between groups I (mean ratio 0.7) and II (mean ratio 0.62), but the ratio was decreased in group III (mean ratio 0.44), in which the extent of the tear in both the sagittal and coronal planes aggravated the muscle atrophy. We propose a three-stage classification to improve indications for rotator cuff tear treatment.     

Effects of α2-Adrenoceptor Agonists on Perinatal Excitotoxic Brain Injury: Comparison of Clonidine and Dexmedetomidine

Background: A growing number of children have severe neurologic impairment related to very premature birth. Experimental data suggest that overstimulation of cerebral N-methyl-d-aspartate (NMDA) receptors caused by excessive glutamate release may be involved in the genesis of perinatal hypoxic-ischemic brain injury. [alpha]2-Adrenoceptor agonists are protective in models of brain ischemia in adults. The authors sought to determine whether they prevent perinatal excitotoxic neuronal damage.

Methods: Five-day-old mice were allocated at random to clonidine (4-400 [mu]g/kg), dexmedetomidine (1-30 [mu]g/kg), or saline injected intraperitoneally before an intracerebral stereotactic injection of the NMDA receptor agonist ibotenate; cortical and white matter lesions were quantified 5 days later by histopathologic examination. Cortical neuron cultures exposed to 300 [mu]m NMDA were used to evaluate the effects of clonidine or dexmedetomidine on neuronal death assessed by counting the number of pycnotic nuclei after fluorescent chromatin staining.

Results: In vivo, both clonidine and dexmedetomidine induced significant concentration-dependent reductions in the size of ibotenate-induced lesions in the cortex and white matter. In vitro, the number of neurons damaged by NMDA exposure was significantly decreased by both dexmedetomidine (-28 +/- 12% at 10 [mu]m;P < 0.01) and clonidine (-37 +/- 19% at 100 [mu]m;P < 0.01) as compared with controls. In both models, the selective [alpha]2-adrenoceptor antagonist yohimbine abolished the neuroprotective effect of clonidine and dexmedetomidine.     

Peak systolic over protodiastolic ratio as an objective substitute for the uterine artery notch

Objective To measure the inter-rater agreement for the identification of a uterine artery notch, as well as the association between an observed notch and the peak systolic over protodiastolic (A/C) ratio.
Design Cohort study.
Setting Tertiary care university hospital.
Population and methods Six hundred and sixty-five nulliparous women in whom 1022 examinations of uterine artery velocity waveforms were performed by pulsed Doppler at 18 and at 26 weeks of gestation. Agreement between two independent raters was analysed using Cohen's kappa statistics. A/C ratios of flow velocity waveforms with or without a notch were compared. The agreement between A/C values and the presence of a notch was estimated by measuring the surface under the receiver operating characteristic (ROC) curve.
Results Inter-rater agreement for the identification of a notch was 074 (95% CI 0.64–0.83) at 18 weeks and 0.72 (95% CI 0.64–0.80) at 26 weeks. NC ratios were higher when a notch was present (   P < 0.0001  ). The area under the ROC curve was 0.86 (95% CI 0.81491) for the placental uterine artery and 0.93 (95% CI 0.90–0.96) for the nonplacental artery. An A/C value 2.5 in any uterine artery had a sensitivity of 88% and a specificity of 86% to detect a notch.
Conclusion Although there is no definitive definition of the notch, its detection is reproducible within a center. However, published prevalences between centers in unselected populations vary. The measure of the NC ratio can serve as an objective substitute.     

Évolution inhabituellement prolongée d’une dactylite tuberculeuse avec atteinte osseuseUnusually prolonged course of tuberculous dactylitis with osteitis

We report a case of tuberculous dactylitis that was unusual in 2 regards: the bone was infected, and the course was prolonged and atypical, with a spontaneous clinical remission followed by a recurrence that led to the diagnosis.     

Number processing after stroke: anatomoclinical correlations in oral and written codes.

Calculation and number-processing abilities were studied in 49 patients with chronic single vascular brain lesions by means of a standardized multitask assessment battery (EC301), as well as through other tasks, testing functions thought to be implicated in calculation such as language, visuo-perceptive abilities, verbal and spatial working memory, planning, and attention. The results show that (1) lesions involving parietal areas-particularly left parietal lesions-are prone to alter calculation processing. A more detailed analysis showed that patients with lesions involving left parietal areas were impaired in both digital (i.e., comprehension and production of numbers written in Arabic code) and oral (i.e., comprehension and production of numbers heard or expressed orally) processing while lesions involving right parietal areas lead to an impairment in digital processing only. However, linguistically related alphanumerical processing (i.e., comprehension and production of numbers written orthographically) was not influenced by parietal lesions. (2) Semantic representations (knowledge of the magnitude related to a given number) as well as rote arithmetical knowledge are also impaired following damage to parietal and particularly left parietal lesions, suggesting that these areas are also implicated in magnitude comparisons and in the retrieval of arithmetical facts. (3) Performance in calculation is highly correlated with language. (4) Moreover, we found a highly significant correlation between performances in oral calculation and verbal working memory, and between written-digit calculation and visuospatial working memory. Performances in regard to visuo-perceptive abilities, planning, and attention were less consistently correlated with calculation. These results stress the close correlation, but relative independence between calculation and language, as well as a dissociated sensitivity of oral and digital processing to brain lesions.     

Anesthetics Affect the Uptake but Not the Depolarization-evoked Release of GABA in Rat Striatal Synaptosomes

Background: Numerous classes of anesthetic agents have been shown to enhance the effects mediated by the postsynaptic gamma-aminobutyric acid A (GABAA) receptor-coupled chloride channel in the mammalian central nervous system. However, presynaptic actions of anesthetics potentially relevant to clinical anesthesia remain to be clarified. Therefore, in this study, the effects of intravenous and volatile anesthetics on both the uptake and the depolarization-evoked release of GABA in the rat stratum were investigated.

Methods: Assay for specific GABA uptake was performed by measuring the radioactivity incorporated in purified striatal synaptosomes incubated with3 H-GABA (20 nM, 5 min, 37 degrees Celsius) and increasing concentrations of anesthetics in either the presence or the absence of nipecotic acid (1 mM, a specific GABA uptake inhibitor). Assay for GABA release consisted of superfusing3 H-GABA preloaded synaptosomes with artificial cerebrospinal fluid (0.5 ml *symbol* min sup 1, 37 degrees Celsius) and measuring the radioactivity obtained from 0.5 ml fractions over 18 min, first in the absence of any treatment (spontaneous release, 8 min), then in the presence of either KCl alone (9 mM, 15 mM) or with various concentrations of anesthetics (5 min), and finally, with no pharmacologic stimulation (5 min). The following anesthetic agents were tested: propofol, etomidate, thiopental, ketamine, halothane, enflurane, isoflurane, and clonidine.

Results: More than 95% of3 H-GABA uptake was blocked by a 10 sup 3 -M concentration of nipecotic acid. Propofol, etomidate, thiopental, and ketamine induced a dose-related, reversible, noncompetitive, inhibition of3 H-GABA uptake: IC50 = 4.6 plus/minus 0.3 x 105 M, 5.8 plus/minus 0.3 x 10 sup -5 M, 2.1 plus/minus 0.4 x 10 sup -3 M, and 4.9 plus/minus 0.5 x 10 sup -4 M for propofol, etomidate, thiopental, and ketamine, respectively. Volatile agents and clonidine had no significant effect, even when used at concentrations greater than those used clinically. KCl application induced a significant, calcium-dependent, concentration-related, increase from basal3 H-GABA release, +34 + 10% (P < 0.01) and +61 plus/minus 13% (P < 0.001), respectively, for 9 mM and 15 mM KCl. The release of3 H-GABA elicited by KCl was not affected by any of the anesthetic agents tested.     

Effects of Ketamine on Ventricular Conduction, Refractoriness, and Wavelength: Potential Antiarrhythmic Effects: A High-resolution Epicardial Mapping in Rabbit Hearts

Background: The aims of the study were to verify the effects of ketamine on ventricular conduction velocity and on the ventricular effective refractory period, to determine its effects on anisotropy and on homogeneity of refractoriness, and to use wavelength to determine whether ketamine has antiarrhythmic or arrhythmogenic properties.

Methods: A high-resolution epicardial mapping system was used to study the effects of 50, 100, 150, and 200 micro Meter racemic ketamine in 15 isolated, Langendorff-perfused rabbit hearts. Five hearts were kept intact to study the effects of ketamine on spontaneous sinus cycle length (RR) interval and its putative arrhythmogenic effects. In 10 other hearts, a thin epicardial layer was obtained by an endocardial cryoprocedure (frozen hearts) to study ventricular conduction velocity, ventricular effective refractory periods (five sites), and ventricular wavelength.

Results: Ketamine induced a concentration-dependent lengthening of the RR interval. Ketamine slowed longitudinal and transverse ventricular conduction velocity with no anisotropic change, and it prolonged the ventricular effective refractory period with no significant increase in dispersion. Ventricular longitudinal and transverse wavelengths tend to increase, but this was not statistically significant. Finally, no arrhythmia could be induced regardless of the ketamine concentration.     

Budd-Chiari syndrome secondary to carcinoma: Report of two cases

In two patients who had Budd-Chiari syndrome secondary to carcinoma, the diagnosis was made intraoperatively at the time of emergency right atrial clearance required for severe cardiovascular distress. Curative resection was not possible and both patients died. As previously noted in the literature, it is extremely difficult to relate carcinoma to the origin of Budd-Chiari syndrome. Retro- and suprahepatic involvement of the vena cava is associated with a very poor prognosis. Complete resection of these tumors is the only potentially curative treatment. We suggest ways to obtain a simple and early histologic diagnosis before initiating appropriate and radical surgical treatment.     

Magnetization transfer on in vitro circulating blood: Implications for time-of-flight MR angiography

Effects of magnetization transfer were evaluated In vitro on circulating blood. Various velocities were tested from 0 to 72 cm/second. Decrease signal intensity caused by magnetization transfer effects was inversely proportional to inflow velocity. It reached 10% at very low velocities and disappeared at velocities higher than 30 cm/second.