Prevalence of chronic thromboembolic pulmonary hypertension after acute pulmonary embolism. Prevalence of CTEPH after pulmonary embolism.

Chronic thromboembolic pulmonary hypertension (CTEPH) has been estimated to occur in 0.1-0.5% of patients who survive a pulmonary embolism (PE), but more recent prospective studies suggest that its incidence may be much higher. The absence of initial haemodynamic evaluation at the time of PE should explain this discrepancy. We performed a prospective multicentre study including patients with PE in order to assess the prevalence and to describe risk factors of CTEPH. Follow-up every year included an evaluation of dyspnea and echocardiography using a predefined algorithm. In case of suspected CTEPH, the diagnosis was confirmed using right heart catheterisation (RHC). Signs of CTEPH were searched on the multidetector computed tomography (CT) and echocardiography performed at the time of PE. Of the 146 patients analysed, eight patients (5.4%) had suspected CTEPH during a median follow-up of 26 months. CTEPH was confirmed using RHC in seven cases (4.8%; 95%CI, 2.3 - 9.6) and ruled-out in one. Patients with CTEPH were older, had more frequently previous venous thromboembolic events and more proximal PE than those without CTEPH. At the time of PE diagnosis, patients with CTEPH had a higher systolic pulmonary artery pressure and at least two signs of CTEPH on the initial CT. After acute PE, the prevalence of CTEPH appears high. However, initial echocardiography and CT data at the time of the index PE suggest that a majority of patients with CTEPH had previously unknown pulmonary hypertension, indicating that a first clinical presentation of CTEPH may mimic acute PE.

Upregulation of Calbindin-D-28k immunoreactivity by excitatory amino acids.

Excessive or prolonged exposure to excitatory amino acids (EAA) are thought to be neurotoxic by altering calcium homeostasis. A protective role of Calbindin-D-28 k (Calbindin) has been postulated due to its capacity to buffer calcium. Calbindin is highly expressed in the Purkinje cells (PCs), of the cerebellar cortex. Changes of the Calbindin immunoreactivity (IR) by the EAA has been here investigated in cerebellar slices maintained in vitro. It was found that at low temperature, PCs are very slightly immunoreactive and therefore the experiments were done at 22 degrees C. The results show that Calbindin-IR increases in PCs exposed to the neurotoxic agonists, Kainic acid (KA) and AMPA as well as to glutamate (Glu), the endogenous EAA. The increase is very rapid and slowly reversible; is induced by excitatory and excitotoxic concentrations of the agonists; is independent of the calcium influx. While KA- and AMPA-induced Calbindin-IR is blocked by CNQX, the KA/AMPA receptor antagonist, Glu-induced Calbindin-IR is only slightly decreased by CNQX and AP5, the NMDA receptor antagonist. It is concluded that Calbindin-containing neurons can increase their calcium buffering capacity in response to EAA binding to specific receptors, the response being independent of, but concomitant to calcium influx.

Glutamate, GABA, calbindin-D28k and parvalbumin immunoreactivity in the pulvinar-lateralis posterior complex of the cat: relation to the projection to the Clare-Bishop area.

Neurons of the pulvinar-lateralis posterior complex (Pul-LP) containing glutamate (Glu) and GABA, as presumed neurotransmitters, and calbindin- D28k (calbindin) and parvalbumin (PV), as Ca-binding proteins, were identified in the cat by using immunohistochemical methods. In vibratome sections, neurons immunoreactive (IR) to each of the four antibodies were observed throughout the Pul-LP. In semithin sections, GABA-IR neurons were also PV-IR but not calbindin-IR and some of them also co-localized Glu. The Glu-IR neurons which were negative for GABA co-localized calbindin but not PV. The neurons of the Pul-LP projecting to the Clare-Bishop area (CB) in the suprasylvian gyrus were identified with a retrogradely transported tracer and the sections were then immunostained for Glu, GABA, calbindin and PV. Only Glu- and calbindin-IR neurons were retrogradely labeled. These results show that, if calbindin and PV have a Ca-binding role, the presumably excitatory Glu-IR neurons projecting to the CB are use calbindin whereas the presumably inhibitory GABA-IR neurons are intrinsic and use PV. This relationship implies that these proteins probably have other roles specifically related to the kind of agonist to be released at the neuron.

Cerebellar nuclei and the nucleocortical projections in the rat: retrograde tracing coupled to GABA and glutamate immunohistochemistry.

The amino acids GABA and glutamate (Glu) are thought to be the principal substances in the central nervous system responsible for neuronal inhibition and excitation. Their distributions among the different neurons in a defined pathway may thus be indicative of the contributions of the cells to pathway function. Examples of such neurons are those of the cerebellar nuclei which, while regulating output from the Purkinje cells of the cerebellar cortex, are also found to project back to the cerebellar cortex. Immunohistochemical experiments were done to identify GABA and glutamate (Glu) containing cells in the adult rat cerebellar nuclei. Consecutive semithin and serial vibratome sections were incubated with antisera raised in rabbit against GABA and Glu. In semithin sections, only small neurons were intensely GABA immunoreactive (GABA-IR) (31.7%), and the majority (80.5%) were Glu immunoreactive (Glu-IR) of different sizes. Consistent with Glu being a metabolic precursor for GABA, 75.4% of the GABA-IR population colocalized Glu. In vibratome sections GABA-IR neurons showed some local differences in number, whereas the Glu-IR were uniformly distributed in the three nuclei studied. Measured mean diameters for these neurons showed a distinct size difference for the GABA- and Glu-IR with little overlap. Cerebellar nuclei neurons projecting to the cortex (nucleocortical neurons, NCN) were identified by locally preinjecting the retrograde transported WGA-apoHRP-colloidal gold complex in the cerebellar cortex. Vibratome sections of these cerebellar were silver intensified for the retrograde tracer and double labeled for GABA and Glu. Of the total number of identified NCN, 8.7% were GABA-IR (10 animals) and 47.7% Glu-IR (5 animals). Many retrograde labeled NCN in the core of the thick sections were immunonegative for both amino acids due to poor antibody penetration, thus underestimating the proportions of cells containing GABA and Glu. The size distributions for the GABA-IR and Glu-IR NCN were similar to those measured in non-retrograde labeled nuclei in thick sections. The conclusions reached are that GABA-IR neurons of the cerebellar nuclei, including the NCN, use GABA as the presumed inhibitory neurotransmitter and that Glu-IR neurons may use Glu or another excitatory neurotransmitter.

The immunocytochemical distribution of calbindin-D28k and parvalbumin in identified neurons of the pulvinar-lateralis posterior complex of the cat.

The calbindin-D28k and parvalbumin immunoreactivities of the neurons of the pulvinar-lateral posterior complex (Pul-LP) were studied in the cat. The neurons of the Pul-LP projecting to the cerebral cortex were identified by a retrogradely transported tracer injected in the suprasylvian gyrus. Two populations of cells were found, a calbindin-D28k-immunoreactive, large-diameter population and a parvalbumin-immunoreactive, small-diameter group. The two kinds of cells are closely intermingled. The former includes the neurons retrogradely marked, and therefore projecting to the suprasylvian gyrus. The latter includes neurons which were not retrogradely marked, and therefore presumably intrinsic elements.

Colocalization of calbindin and GABA in medial nucleus of the trapezoid body of the rat.

Using immunocytochemical methods, both calbindin and GABA were found to be colocalized in the somas of all the cells of the medial nucleus of the trapezoid body (NMTB) of the rat auditory system. In the lateral superior olive (LSO), calbindin was also found in the terminals but not in the cells. Some terminal labelling was found in the medial superior olive (MSO). GABA was also found in the somas of some cells in both LSO and MSO, but most of the labelling was in terminals. In the rat, calbindin appears to be more involved in a pathway that detects interaural intensity differences.

Anterograde tracing of the rat olivocerebellar system with Phaseolus vulgaris leucoagglutinin (PHA-L). Demonstration of climbing fiber collateral innervation of the cerebellar nuclei.

The olivocerebellar climbing fiber system was investigated in the rat with anterograde Phaseolus vulgaris leucoagglutinin (PHA-L) tracing. The specific objective of the study was to find morphological evidence of climbing fiber collaterals innervating the cerebellar nuclei. Small iontophoretic injections of PHA-L were placed in different parts of the inferior olivary complex, and labelled olivocerebellar fibers could be traced to their termination as climbing fibers in sagittal zones of the contralateral cerebellar cortex. Reaching the cerebellum via the restiform body, the labelled olivocerebellar axons entered the deep cerebellar white matter anterior to the cerebellar nuclei. Most of these thicker, nonterminal axons continued dorsally around the nuclei, but some ran through them. Bundles of fibers could be followed into the folial white matter toward their cortical zones of termination. Depending on which part of the olivary complex that was injected with PHA-L, labelled axons were seen to converge on different regions of the cerebellar nuclei, where dense plexuses of thin varicose terminal fibers appeared. Quantitative estimates of the innervation ranged from 1.7 to 4.3 million boutons per mm3 in the fastigial (FN), interposed, and main parts of the lateral cerebellar (LCN) nuclei, whereas the parvicellular portion of LCN demonstrated 15-20 million varicosities per mm3. Frequently, thicker olivocerebellar axons, which seemed directed toward the cerebellar cortex, were seen to send a fine collateral branch toward these areas of nuclear innervation. As controls, PHA-L was injected into the degenerated olivary complex of 3-acetylpyridine-treated rats. Neither cortical climbing fiber terminals nor nerve terminal plexuses in the nuclei appeared in these experiments. In cases with injection sites extending into the reticular formation, substantial mossy fiber labelling was present bilaterally in the cortex, but the cerebellar nuclei were devoid of labelled innervation or demonstrated only a few larger diameter fibers. The projection of the inferior olivary complex to the cerebellar nuclei was strictly topographically organized and agreed in principle with the organization described in the cat by Groenewegen et al. ('79). The caudal medial accessory olive (MAO) projected to FN, the rostral MAO to the posterior interposed nucleus (NIP), the rostral part of the dorsal accessory olive (DAO) to the anterior interposed nucleus (NIA), and the principal olive (PO) to LCN.(ABSTRACT TRUNCATED AT 400 WORDS)

Reflex control of the retractor bulbi muscle in the cat.

The effects of vestibular and trigeminal stimulation on reflex responses of each slip of the retractor bulbi muscle were tested by recording the electromyogram. 1. In "encéphale isolé" cat, phasic electrical stimulation of the horizontal canal induced no response in the RB slips. Repetitive vestibular stimulation did not produce nystagmus in the RB muscle while strong muscular discharges were observed in the nystagmus lateral rectus muscle. 2. In anaesthetized cats, three trigeminal inputs elicited strong reflex responses in each slip of the RB muscle. Electrical stimulation of the vibrissae or the infra-orbital nerve evoked a two component reflex response (latencies: 5 ms +/- 0.5 and 14 ms +/- 2). Electrical stimulation of the supraorbital nerve elicited a single component reflex response (latency: 6 ms +/- 0.5). Electrical stimulation of the long ciliary nerves evoked a complex response with four components (latencies: 7.5 ms +/- 0.5, 10 ms +/- 2, 15 ms +/- 2,20 ms +/- 2). 3. Pentobarbital and morphine produced lasting depression of the reflex responses of the RB muscle. The depressive effect of morphine was reversed by naloxone.

[Localization of motoneurones of retractor bulbi muscles by retrograde transport of exogenous peroxidase in cats]. / Localisation des motoneurones du muscle retractor bulbi par transport rétrograde de peroxydase exogène chez le Chat.

Retrograde transport of exogene horseradish peroxidase has been used to localize the retractor bulbi muscle motoneurones. These motoneurones are located ventro-laterally in the tegmental reticular field; they are grouped in a rostro-caudal column above the superior olive. They correspond to the accessory nucleus of the VIe nerve described by old anatomists.