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PubMed1990

NMDA receptor antagonists reduce medial, but not lateral, perforant path-evoked EPSPs in dentate gyrus of rat hippocampal slice.

NMDA receptor antagonists produced differential effects on medial and lateral perforant path-evoked excitatory postsynaptic potentials (EPSPs) recorded in the dentate gyrus molecular layer of hippocampal slices. D-(-)-2-amino-5-phosphonovaleric acid (D(-)-APV) and 3[(+/-)-2-carboxypiperazin-4-yl]-propyl-1-phosphonic acid (CPP) significantly reduced the peak amplitude and total area, but not the initial negative slope, of the medial perforant path-evoked EPSP. Neither antagonist affected any component of the lateral perforant path-evoked EPSP. In contrast, population spikes evoked by stimulation of either pathway were depressed.

2-Amino-5-phosphonovalerate↗
PubMed1978

Synaptic enhancement in fascia dentata: cooperativity among coactive afferents.

Evidence is presented that long-lasting enhancement of perforant path synapses following high-frequency activity is a cooperative process requiring coactivity of a considerable number of fibers. This was demonstrated in two ways: (1) A threshold stimulus intensity during high-frequency stimulation was required before any enhancement was observed. This threshold was considerably above the stimulus threshold for observing a minimal synaptic response in the fascia dentata. Above the enhancement threshold, the amount of enhancement increased as the intensity of high-frequency stimulation increased. (2) Concurrent high-frequency activation of fibres of the medial and lateral perforant path produced enhancement at intensities where identical but independent stimulation of the two pathways either failed or was less effective. Discharge of the granule cells during the high-frequency stimulation was independently manipulated and found not to be physically coupled to the enhancement generating mechanism.

Afferent Pathways↗
PubMed1992

Carcinomas of the nasal cavity.

Between 1969 and 1985, 45 patients with carcinomas of the nasal cavity proper received curative treatment. Thirty patients had squamous cell carcinoma, one had undifferentiated carcinoma, 9 had adenocarcinoma, and 5 had adenoid cystic carcinoma. Eighteen patients were treated with definitive radiotherapy (interstitial brachytherapy in 5 and external beam therapy in 13 patients), and 27 received surgery and radiotherapy. The median length of follow-up was 11 years (range: 2.8-16.8 years). Thirty-six patients had no evidence of disease at the last follow-up visit. All 14 patients with carcinoma of the nasal septum had the disease controlled. Nine of 31 patients with lesions of the lateral wall and floor died of the disease, 5 of uncontrolled local disease, 2 of distant metastases, and 2 of both. The disease-specific survival rates at 5 and 10 years were 83 and 80%, respectively, and the corresponding overall survival rates were 75 and 60%, respectively. Blindness occurred in 4 patients, 2 due to orbital exenteration and 2 to radiation injury to the cornea and optic pathway. Other infrequent side effects were bone necrosis, dental decay, nasal stenosis, and septal perforation. This study indicated that the prognosis of patients with nasal cavity carcinoma was better than that of patients with maxillary sinus cancer treated during the same era. In addition, the study showed that carcinomas of the nasal septum were smaller than those of lateral wall and floor at diagnosis, so that excellent control could be achieved by definitive radiotherapy; when accessible, interstitial brachytherapy might be the treatment of choice in such patients.

Adenocarcinoma↗
PubMed1985

"Epileptic" brain damage is replicated qualitatively in the rat hippocampus by central injection of glutamate or aspartate but not by GABA or acetylcholine.

Repeated intraventricular injection of the excitatory amino acids glutamate and aspartate for one hour produced morphologic changes in the hippocampus that were qualitatively identical to the acute and chronic changes seen in the brains of human epileptics and in experimental animals in which hippocampal seizure activity was induced by kainic acid or electrical stimulation of the perforant path. Light and electron microscopy revealed acute effects of glutamate and aspartate consisting of glial and dendritic swelling and neuronal soma necrosis ("dark cell degeneration"). Electron microscopy showed the focal dendritic swelling induced by glutamate or aspartate to be of the axon-sparing type with presynaptic terminals relatively unaffected. Four weeks after injection, irreversible neuron loss and reactive gliosis had occurred. The inhibitory amino acid gamma-aminobutyric acid caused acute glial swelling similar to that caused by glutamate and aspartate but did not produce neurotoxic effects, indicating that glial swelling may not be causally related to neuronal death but may be the result of amino acid uptake. The excitatory non-amino acid acetylcholine produced no direct, periventricular hippocampal damage or glial swelling but did produce dendritic swelling in the CA3 region innervated by the perforant path, presumably as a result of acetylcholine-induced seizure activity in this pathway. Glutamate and aspartate also caused glial and neuronal changes in other periventricular structures, e.g., septum, hypothalamus, caudate and habenula, as well as in the most dorsal portion of the cerebellum. Dendritic swelling induced by glutamate and aspartate in the cerebellar molecular layer was accompanied by acute necrosis of Purkinje cell somata. These results suggest that seizure-associated brain damage is initiated by excessive endogenous excitatory amino acid receptor activation.

Acetylcholine↗
PubMed2004

Immediate vulvar and vaginal reconstruction using the gluteal-fold flap: long-term results.

The gluteal-fold flap was used to reconstruct vulvar and posterior vaginal wall defects in 40 patients. This is a fasciocutaneous, islanded flap based on the internal pudendal artery and vein perforators. The flap is robust and has the advantage of being away from the pathway of carcinoma spread. In addition it has minimal donor-site morbidity as the scar is hidden in a natural crease.

Aged↗
PubMed2004

[Guidelines for surgery in the treatment of rhegmatogenous detachments (buckle, pneumatic retinopexy, endosurgery)].

In view of diverging opinions for retinal detachment surgery (pneumatic retinopexy or buckling procedure with or without drainage versus primary vitrectomy without external buckling) pneumatic retinopexy, orbital balloon, buckling procedures (sponge, encircling band) are discussed with a short historical background and a brief description of current technology. Pros and cons of the individual technique are discussed on the basis of monographs and articles. From the repertoire of a retinal surgeon typical case examples are presented, different operation methods discussed, advantages and disadvantages of each individual technique emphasized. A goal of the work is to provide a practicable manual for the less experienced surgeon and the expert, who experiences an increasing trend to vitrectomy techniques instead of the conventional buckling procedures.

Catheterization↗
PubMed2004

Decreased aortic smooth muscle contraction in a rat model of multibacterial sepsis.

We investigated whether blockade of the smooth muscle cell (SMC) inducible nitric oxide synthase (iNOS)-soluble guanylyl cyclase (sGC) vasodilator pathway would restore the fall in vasoreactivity produced by sepsis following cecal ligation and perforation (CLP) in rats. Contraction of adjacent aortic rings paired for the presence or absence of endothelial cells (EC) was recorded following high [K(+)](e) (40 mm) or norepinephrine (NE, 10(-8) to 10(-5) m) in the presence of the nitric oxide synthase inhibitor (NOS), N(G)-nitro-l-arginine methyl ester (l-NAME, 0.3 mm) or the sGC inhibitor, 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (ODQ, 5 mum). In EC-denuded rings, sepsis halved SMC contraction induced by high [K(+)](e) or NE; neither l-NAME nor ODQ produced an increase in NE E(max) or high [K(+)](e)-evoked contraction. In conclusion, SMC contractility is globally reduced in CLP; this reduction does not appear to be explained by induction of SMC NOS in this CLP model.

Animals↗
PubMed1989

Transcatheter radiofrequency ablation of atrial tissue using a suction catheter.

Closed chest ablative technique that avoid barotrauma would be attractive for ablation at thin walled cardiac structures, such as the atrial free wall or coronary sinus. Transcatheter radiofrequency (RF) currents produce tissue necrosis the size of which is dependent on the contact between the tissue and the electrode. In order to assess the effects of transvenous RF ablation of atrial free wall using a suction electrode catheter, we delivered in ten dogs, one single unmodulated RF pulse 1.2 MHz, in a unipolar mode, through the distal electrode of a lumen catheter (USCI 8F) (USCI, Billerica, MA USA) located in the right appendage. During the pulse an 80 KPa vacuum depression was applied to the lumen of the catheter. Each pulse had a 10 seconds duration and the mean delivered power was 4.3 +/- 1.4 W. Aortic pressure and electrocardiogram were monitored during the procedure. A right atrial electrophysiological study was performed at the ablated site, at control, after suction application and after RF pulse delivery. The animals were sacrificed after 14 or 21 days. Atrial pacing threshold values decreased after suction application in comparison to control values after the pulse (0.42 +/- 0.06 vs 0.60 +/- 0.23 mA, P less than O.05) but increased after the pulse delivery (2.60 +/- 1.85 mA, P less than 0.01). In contrast, the atrial effective refractory period did not significantly change after suction, nor after RF pulse delivery. Aortic pressure remained unchanged throughout the procedure. Complex arrhythmias were not observed during or after RF pulse delivery. One dog died suddenly at the first day after ablation, but this death was most probably unrelated to RF ablation. Anatomic lesions had a length of 8.8 +/- 3.3 mm, a width of 4.6 +/- 2.5 mm and a depth of 3.6 +/- 1.1 mm. They were transmural in nine of the ten dogs but without atrial wall perforation in any case. Lesions suggesting tissue volatilization were present in four dogs. These results demonstrate that low energy RF currents delivered with a suction electrode catheter can produce transmural necrosis of free wall, without risk of perforation. Such ablative technique would be of interest for ablation of right sided accessory pathways or atrial ectopic foci. Further experimental data are required in order to define the optimal energy level required to avoid tissue volatilization.

Animals↗
PubMed2005

Spatial navigation and causal analysis in a brain-based device modeling cortical-hippocampal interactions.

We describe Darwin X, a physical device that interacts with a real environment, whose behavior is guided by a simulated nervous system incorporating aspects of the detailed anatomy and physiology of the hippocampus and its surrounding regions. This brain-based device integrates cues from its environment and solves a spatial memory task. The responses of simulated neuronal units in the hippocampal areas during its exploratory behavior are comparable to place cells in the rodent hippocampus and emerged by associating sensory cues during exploration. To identify different functional hippocampal pathways and their influence on behavior, we employed a time series analysis that distinguishes causal interactions within and between simulated hippocampal and neocortical regions while the device is engaged in a spatial memory task. Our analysis identified different functional pathways within the neural simulation and prompts novel predictions about the influence of the perforant path, the trisynaptic loop and hippocampal-cortical interactions on place cell activity and behavior during navigation. Moreover, this causal time series analysis may be useful in analyzing networks in general.

Animals↗
PubMed1990

Subcutaneous emphysema of the lower extremity of abdominal origin.

Three cases of subcutaneous emphysema of the lower extremity due to abdominal disease are reported. These were due to (a) perforation of the sigmoid, (b) perirectal abscess, and (c) non-traumatic metastatic gas gangrene due to emphysematous cholecystitis. The mechanisms and anatomical pathways are discussed.

Abscess↗
PubMedDate not supplied

Effect of the vascular endothelium on contractions induced by noradrenaline and phenylephrine in perforating branch of the human internal mammary artery.

The effects of noradrenaline (Nor) and phenylephrine (Phe) on the isolated, non-precontracted perforating branch of the human internal mammary artery (HIMA) were investigated. Nor and Phe induced concentration-dependent contractions of intact and endothelium-denuded arterial rings with no statistically significant differences between the pEC(30) and maximal response values. The pretreatment of arterial rings with indomethacin had no effect on Nor- and Phe-induced contractions of both, intact and endothelium-denuded preparations. The pre-addition of L-NMMA did not affect contractions of perforating branch of the HIMA evoked by Nor, but provoked significant potentiation of Phe-induced contractions of perforating branch of the HIMA both intact and denuded of endothelium only at Phe concentration higher than 3 x 10(-6)M. The effects of selective alpha1-adrenoceptor antagonist, prazosin and selective alpha2-adrenoceptor antagonist, rauwolscine were concentration-dependent, and they induced a significant shift to the right (for both studied antagonists) of the concentration-response curves for Nor in both preparations with or without endothelium. The effects of prazosin and rauwolscine on the concentration-response curves for Phe were similar. In conclusion, this study has shown that Nor and Phe induce concentration-dependent contractions of the perforating branch of the HIMA. Removal of the endothelium did not modify this effect. Products of cyclooxygenase pathway had no influence on Nor and Phe action. Endothelium derived nitric oxide (NO) had no modulatory effect of Nor-induced contractions, but inhibition of NO synthesis provoked potentiation of Phe-induced contractions either in intact or endothelium-denuded preparations. The mechanism of this effect remains still unclear. On the basis of differential affinity of the antagonists and affinities of Nor and Phe themselves, we suggest that alpha1-adrenoceptor subtype is probably involved in the Nor- and Phe-induced contraction of the perforating branch of the HIMA both intact or denuded of endothelium.

Adrenergic alpha-Antagonists↗
PubMed1993

Hip sepsis from retroperitoneal rupture of diverticular disease.

Retroperitoneal perforation of diverticular disease is very uncommon and can be difficult to diagnose because of possible pathways of communication between the retroperitoneal space and the thigh. An iliopsoas abscess from a ruptured diverticulum may drain into the hip joint if the capsule has been violated. Cases of abscesses or gas in the thigh have been reported in which thigh pain was the predominant symptom, overshadowing any abdominal signs. We report a case in which hip sepsis due to a ruptured diverticulum was the presenting feature.

Aged↗
PubMed1979

Neurogenic gastroduodenal ulceration and bleeding associated with spinal cord injuries.

Twenty-four of 576 consecutive patients with spinal cord injuries developed acute gastroduodenal ulceration and hemorrhage. Twenty-two were males and two were females: 88% were 12 to 25 years old. Seventeen patients sustained injuries to the spinal cord in sports and recreation related activities. Twenty-three patients had lesions of the spinal cord above the sympathetic outflow. Twenty patients developed gastroduodenal perforation or bleeding within 4 weeks following the injury. Ten patients developed perforation of gastric or duodenal ulcer and "shoulder tip" pain was a symptom of perforation in six patients. Six patients of seven who had gastroscopy and upper GI series were found at laparotomy to have ulcers. Gastric (nine) and duodenal (seven) ulcers were evenly distributed. There were no deaths due to gastroduodenal hemorrhage in the present series. A single cause for the pathogenesis of gastroduodenal ulceration and hemorrhage cannot be pinpointed. However, ischemia of gastric mucosa produced in various ways and altered equilibrium between the parasympathetic and sympathetic neural pathways following trauma to the spinal cord seem to be important in initiating the process.

Acute Disease↗
PubMed2005

Signal transduction pathways of group I metabotropic glutamate receptor-induced long-term depression at sensory spinal synapses.

Activation of spinal group I metabotropic glutamate receptors (mGluRs) may have antinociceptive or pro-nociceptive effects in different pain models. Pharmacological activation of group I mGluRs leads to long-term depression (LTD) of synaptic strength between Adelta-fibers and neurons in lamina II of spinal dorsal horn of the rat. Here, we studied the signal transduction pathways involved. Synaptic strength between Adelta-fibers and lamina II neurons was assessed by perforated whole-cell patch-clamp recordings in a spinal cord-dorsal root slice preparation of young rats. Bath application of the specific group I mGluR agonist (S)-3,5-dihydroxyphenylglycine [(S)-3,5-DHPG] produced an LTD of Adelta-fiber-evoked responses. LTD induction by (S)-3,5-DHPG was prevented, when intracellular Ca(2+) stores were depleted by thapsigargin or cyclopiazonic acid (CPA). Preincubation with ryanodine to inhibit Ca(2+)-induced Ca(2+) release had no effect on LTD-induction by (S)-3,5-DHPG. In contrast, pretreatment with 2-aminoethoxydiphenyl borate (2-APB), an inhibitor of inositol-1,4,5-trisphosphate (IP(3))-sensitive Ca(2+) stores prevented LTD induction. Preincubation with the specific protein kinase C (PKC) inhibitors bisindolylmaleimide I (BIM) or chelerythrine, respectively, had no effect. Inhibition of L-type VDCCs by verapamil or nifedipine prevented LTD-induction by (S)-3,5-DHPG. The presently identified signal transduction cascade may be relevant to the long-term depression of sensory information in the spinal cord, including nociception.

Animals↗
PubMed2003

Mu-opioid receptors facilitate the propagation of excitatory activity in rat hippocampal area CA1 by disinhibition of all anatomical layers.

Hippocampal mu-opioid receptors (MORs) have been implicated in memory formation associated with opiate drug abuse. MORs modulate hippocampal synaptic plasticity acutely, when chronically activated, and during drug withdrawal. At the network level, MORs increase excitability in area CA1 by disinhibiting pyramidal cells. The precise inhibitory interneuron subtypes affected by MOR activation are unknown; however, not all subtypes are inhibited, and specific interneuron subtypes have been shown to preferentially express MORs. Here we investigate, using voltage-sensitive dye imaging in brain slices, the effect of MOR activation on the patterns of inhibition and on the propagation of excitatory activity in rat hippocampal CA1. MOR activation augments excitatory activity evoked by stimulating inputs in stratum oriens [i.e., Schaffer collateral and commissural pathway (SCC) and antidromic], stratum radiatum (i.e., SCC), and stratum lacunosum-moleculare (SLM; i.e., perforant path and thalamus). The augmented excitatory activity is further facilitated as it propagates through the CA1 network. This was observed as a proportionately larger increase in amplitudes of excitatory activity at sites distal from where the activity was evoked. This facilitation was observed for excitatory activity propagating from all three stimulation sites. The augmentation and facilitation were prevented by GABAA receptor antagonists (bicuculline, 30 microM), but not by GABAB receptor antagonists (CGP 55845, 10 microM). Furthermore, MOR activation inhibited IPSPs in all layers of area CA1. These findings suggest that MOR-induced suppression of GABA release onto GABAA receptors augments all inputs to CA1 pyramidal cells and facilitates the propagation of excitatory activity through the network of area CA1.

Animals↗
PubMed1998

Perforating branches: important contribution to the formation of the dorsal metacarpal arteries.

The perforating branches that originate from the deep palmar arch of the hand have been studied to provide a complete anatomical description of these vessels and assess their importance in the blood collateral pathway of the hand. We injected latex into the arteries of 50 cadaveric hands of 25 adults, of both sexes, all of Brazilian origin. These were dissected under a stereoscopic microscope. The perforating branch of the second interosseous space originated from the deep palmar arch in 80% of the cases, and it corresponded to the radial artery passing through the second space in 16%; the one of the third interosseous space originated from the deep palmar arch in 76% of the cases and from the palmar metacarpal artery of the third interosseous space in 16%; the one of the fourth interosseous space originated from the deep palmar arch in half the cases, from the deep palmar branch of the ulnar artery in 14%, and from the palmar metacarpal artery of this space in 18%. The perforating branch of the second space anastomosed with the second dorsal metacarpal artery (DMA) in 60% of the cases and formed it in 10%; the one of the third space anastomosed with the third DMA in 20% and formed it in 64%; the one of the fourth space anastomosed with the fourth DMA in 8% and formed it in 78%. These vessels are an important anastomotic pathway between the dorsal carpal network and the deep arteries of the hand and are important in the supply to the dorsum.

Adult↗
PubMed1996

Activation of corticostriatal pathway leads to similar morphological changes observed following haloperidol treatment.

Treatment with haloperidol, a dopamine receptor D-2 antagonist, for one month resulted in an increase in the mean percentage of asymmetric synapses containing a discontinuous, or perforated, postsynaptic density (PSD) [Meshul et al. (1994) Brain Res., 648:181-195] and a change in the density of striatal glutamate immunoreactivity within those presynaptic terminals [Meshul and Tan (1994) Synapse, 18:205-217]. We speculated that this haloperidol-induced change in glutamate density might be due to an activation of the corticostriatal pathway. To determine if activation of this pathway leads to similar morphological changes previously described following haloperidol treatment, GABA (10(-5) M, 0.5 microliters) was injected into the thalamic motor (VL/VM) nuclei daily for 3 weeks. This treatment resulted in an increase in the mean percentage of striatal asymmetric synapses containing a perforated PSD and an increase in the density of glutamate immunoreactivity within nerve terminals of asymmetric synapses containing a perforated or non-perforated PSD. Subchronic injections of GABA into the thalamic somatosensory nuclei (VPM/VPL) had no effect on the mean percentage of synapses with perforated PSDs but resulted in a small, but significant, increase in density of glutamate immunoreactivity. Using in vivo microdialysis, an acute injection of GABA (10(-5) M, 15 microliters) into VL/VM resulted in a prolonged rise in the extracellular level of striatal glutamate. The increase in asymmetric synapses with perforated PSDs and in glutamate immunoreactivity within nerve terminals of the striatum following either subchronic haloperidol treatment or GABA injections into VL/VM suggest that an increase in glutamate release may be a common factor in these two experiments. It is possible that the extrapyramidal side effects associated with haloperidol treatment may be due, in part, to an increase in release of glutamate within the corticostriatal pathway.

Animals↗