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Biomedical subjects

P Hertel

Publications and source records attributed to P Hertel.

At least 37 records · Page 2Linked to original sources
PubMed1997

Femoral insertion of the ACL. Radiographic quadrant method.

The optimal femoral insertion or footprint for an anterior cruciate ligament (ACL) graft is the anatomic site. This study was designed to determine the radiographic localization of the femoral insertion of the ACL on a lateral roentgenogram using a quadrant method. Ten human cadaveric knees with intact ACL were dissected. The most anterior, posterior, proximal, and distal borders of the femoral insertion of the ACL were marked with K-wires that were shortened at the bone level of the intercondylar fossa. A roentgenogram was obtained in the strictly lateral position. The end of the K-wires determined the projection of the femoral ACL insertion on the lateral roentgenogram. The center of the radiographically marked area was defined as point K, then four distances were measured on the lateral roentgenogram: distance t (representing the total sagittal diameter of the lateral condyle measured along Blumensaat's line), distance h (representing the maximum intercondylar notch height), distance a (representing the distance of point K from the most dorsal subchondral contour of the lateral femoral condyle), and distance b (representing the distance of point K from Blumensaat's line). Distance a is a partial distance of t and distance b is a partial distance of h, and distances a and b are expressed as length ratios of t and h. The center of the femoral insertion of the ACL was located at 24.8% of the distance t measured from the most posterior contour of the lateral femoral condyle and at 28.5% of the height h measured from Blumensaat's line. Based on these results, the ACL can be found just inferior to the most superoposterior quadrant, which means in anatomic terms it is localized from the dorsal border of the condyle at approximately a quarter of the whole sagittal diameter of the condyle and from the roof of the notch at approximately a quarter of the notch height. By using this radiographic quadrant method combined with fluoroscopic control during surgery, we were able to reinsert the ACL at its anatomic insertion site. This method is independent of variation in knee size or film-focus distance, easy to handle, and reproducible.

Anterior Cruciate Ligament↗
PubMed1996

The psychotomimetic drugs D-amphetamine and phencyclidine release calcitonin gene-related peptide in the limbic forebrain of the rat.

Calcitonin gene-related peptide (CGRP) is the major product of the calcitonin gene in brain and exerts a number of actions in the central nervous system (CNS). In particular the finding that CGRP affects dopamine (DA) release and metabolism has raised the possibility that it may play a role in several neuropsychiatric disorders. Consequently, we have here studied the effects of two psychotomimetic drugs, namely, d-amphetamine (AMPH) and phencyclidine (PCP), on CGRP concentrations in brain microdialysates from freely moving rats. The animals were stereotaxically implanted with vertical concentric probes in the medial prefrontal cortex (mPFC), the ventral striatum (vSTR), or the hippocampus; and the experiments were performed 48 hr after surgery. The dialysis probes were perfused with a modified Ringer's solution at the rate of 5 microliters/min. AMPH 1.5 mg/kg, PCP 2.5 mg/kg, or NaCl 0.9% were injected s.c.; and the perfusates were collected at 60 min intervals before and after the injections and used for CGRP-like immunoreactivity (-LI) determination by radioimmunoassay (RIA). In separate experiment, KCl (100 mM), veratridine (50 microM), or tetrodotoxin (2 microM), were added to the perfusate and infused in the vSTR. Baseline levels of CGRP-LI were detected in dialysates from all three regions. Both AMPH and PCP caused a significant and sustained increase (maximum about 300%) in CGRP-LI concentrations, in particular from the mPFC and vSTR, while saline had no effect. KCl and veratridine also increased CGRP-LI in dialysates during the first posttreatment period, while tetrodotoxin induced a significant but delayed decrease in CGRP-LI levels. Finally, cervical dislocation also elevated CGRP-LI in dialysates from the mPFC and the vSTR. Our findings demonstrate that 1) CGRP-LI can be measured in vivo in microdialysates from mPFC, vSTR, and hippocampus; 2) the release in vSTR is action potential-dependent; and 3) systemic administration of AMPH or PCP results in a long-lasting release of CGRP-LI in the mPFC and vSTR, thus demonstrating a novel action of these drugs in the brain. Since other studies have shown that major antipsychotic drugs appear to reduce CGRP release in brain, our study provides, in principle, support for a role of CGRP in psychotic disorders.

Analysis of Variance↗
PubMed1996

Prazosin inhibits MK-801-induced hyperlocomotion and dopamine release in the nucleus accumbens.

This study examined the putative inhibitory effect of the alpha 1-adrenoceptor antagonist prazosin (1-(4-amino-6,7-dimethoxy-2-quinazolinyl)-4-(2-furanylcarbonyl)pip erazine) on changes evoked by the psychotomimetic, non-competitive NMDA receptor antagonist, MK-801((+)-5-methyl-10,11-dihydroxy-5H-dibenzo-(a,d)cyclohepten-5, 10-imine), in locomotor activity and extracellular concentrations of dopamine and its metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the nucleus accumbens as assessed by microdialysis in freely moving rats. MK-801 (0.1 and 0.3 mg/kg, s.c.) induced a significant, dose-dependent increase in horizontal locomotor activity but did not affect rearing. Prazosin administration alone (1 mg/kg, s.c.) only slightly reduced horizontal activity during an initial 10 min measurement period, although it consistently reduced rearing. However, pretreatment with prazosin effectively suppressed the locomotor stimulation caused by either dose of MK-801 throughout the whole observation period, i.e. 40 min. Both doses of MK-801 significantly increased extracellular levels of dopamine in the nucleus accumbens up to approximately 90%. In addition, MK-801 dose dependently increased dopamine metabolite concentrations in the nucleus accumbens, but 5-HIAA was significantly increased only by the high dose of MK-801. When given alone, prazosin did not affect either dopamine, DOPAC, HVA or 5-HIAA levels. However, prazosin pretreatment effectively blocked MK-801-evoked increases in dialysate dopamine concentrations. Consequently, the potent and selective alpha 1-adrenoceptor antagonist prazosin was found to specifically suppress MK-801-evoked, but not basal dopamine release in the nucleus accumbens, while effectively blocking MK-801-evoked locomotor stimulation with only negligible effects on basal locomotor activity. Thus, alpha 1-adrenoceptor antagonism may act by reducing the sensitivity of the mesolimbic dopamine system to pharmacological or environmental challenge. Since most antipsychotic drugs exhibit both dopamine D2 receptor and alpha 1-adrenoceptor antagonistic properties, they may alleviate psychosis not only through blockade of postsynaptic dopamine receptors, but also presynaptically on the mesolimbic dopamine system, through their alpha 1-adrenoceptor antagonistic action. This latter action may contribute to reduce evoked dopamine hyperactivity, e.g. in response to stress.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Condition-independent sensitization of locomotor stimulation and mesocortical dopamine release following chronic nicotine treatment in the rat.

Chronic nicotine (NIC) pretreatment has been shown to enhance NIC-induced locomotor stimulation, an effect that seems critically dependent on activation of brain dopamine (DA) systems. In the present study the effects of chronic, intermittent NIC treatment were examined in the rat to establish whether such behavioral sensitization is associated with specific, regional changes in brain dopaminergic activity. Male rats received daily injections in their home cage with either saline (SAL) or NIC (0.5 mg/kg, s.c.) for 12 days. Twenty-four hours later, the locomotor activity of the animals subjected to NIC challenge as well as the functional responsiveness of the mesolimbocortical dopaminergic system were assessed. To this end, microdialysis experiments were performed in awake animals, measuring extracellular concentrations of DA and its metabolites in the prefrontal cortex (PFC) and the nucleus accumbens (NAC). Extracellular single cell recordings from DA neurons in the ventral tegmental area (VTA) were also performed in anesthetized animals. NIC (0.5 mg/kg, s.c.) increased all measured parameters of locomotor activity, with the exception of rearing, in SAL-pretreated animals; these effects were substantially enhanced after pretreatment with NIC. Nicotine (0.5 mg/kg, s.c.) increased DA release in both the PFC and the NAC in SAL-treated animals. Nicotine pretreatment significantly enhanced this effect in the PFC, whereas it did not affect the response in the NAC. Low doses of intravenously administered NIC dose-dependently increased burst activity, starting at 12 micrograms/kg in the SAL pretreated animals and at 6 micrograms/kg in the NIC-pretreated animals, and also dose-dependently increased firing rate in SAL as well as NIC-pretreated animals, although starting at a higher dose level, i.e., 25 micrograms/kg. These results demonstrate that behavioral sensitization after chronic NIC treatment is accompanied by an enhanced dopamine release specifically within the PFC. This phenomenon may be highly significant for the dependence-producing effects of NIC, particularly in association with major psychiatric disorder, such as schizophrenia.

Animals↗
PubMed1996

The 5-HT1A receptor antagonist (S)-UH-301 augments the increase in extracellular concentrations of 5-HT in the frontal cortex produced by both acute and chronic treatment with citalopram.

In a recent study, utilizing single cell recording techniques, we have shown that administration of 5-HT1A receptor antagonists, e.g. (S)-UH-301, to rats concomitantly treated, acute or chronically, with the selective serotonin reuptake inhibitor (SSRI) citalopram significantly increases the activity of 5-hydroxytryptamine (5-HT) containing neurons in the dorsal raphe nucleus (DRN). Here we report correlative experiments using microdialysis in freely moving animals to measure extracellular levels of 5-HT and its metabolite 5-hydroxyindole acetic acid (5-HIAA) in the frontal cortex, a major projection area for DRN-5-HT neurons. Acute administration of (S)-UH-301 (2.5 mg/kg s.c.) or citalopram (2.0 mg/kg s.c.) increased 5-HT concentrations with a maximum of about 70% and 185%, respectively, above baseline. However, when (S)-UH-301 was administered 30 min before citalopram the maximal increase in 5-HT levels was approximately 400%. In rats chronically treated with citalopram (20 mg/kg/day i.p. for 14 days) basal 5-HT concentrations in the frontal cortex were significantly increased and 5-HIAA concentrations were decreased when measured 10-12 h, but not 18-20 h, after the last injection of citalopram, as compared to basal 5-HT and 5-HIAA concentrations in chronic saline-treated rats. When (S)-UH-301 (2.5 mg/kg s.c.) was administered 12 h, but not 20 h, after the last dose of citalopram it produced a significantly larger increase in extracellular concentrations of 5-HT than in control rats. However, in rats pretreated with a single, very high dose of citalopram, 20 mg/kg i.p., administration of (S)-UH-301 at 12 h after citalopram did not increase 5-HT levels. The augmentation by (S)-UH-301 of the increase in brain 5-HT output produced by acute administration of citalopram is probably due to antagonism of the citalopram induced feedback inhibition of 5-HT cells in the DRN, as previously suggested. However, the capacity of (S)-UH-301 to further increase the already elevated extracellular concentrations of 5-HT in brain in animals maintained on a chronic citalopram regimen, in which significant tolerance to the initial feedback inhibition of DRN-5-HT cells and developed, represents a novel finding. Generally, the reduced feedback inhibition of 5-HT neurons obtained with chronic citalopram treatment, and the associated elevation of brain 5-HT concentrations, may be related to functional desensitization of somatodendritic 5-HT1A autoreceptors in the DRN. This phenomenon may also largely explain the larger increase in 5-HT output produced by (S)-UH-301 in chronic citalopram treated animals as compared to its effect in control animals. Yet, a contributory factor may be a slight, remaining feedback inhibition of the 5-HT cells caused by residual citalopram at 12, but not 20 h after its last administration. Previous clinical studies suggest that addition of a 5-HT1A receptor antagonist to an SSRI in the treatment of depression may accelerate the onset of clinical effects. Moreover, in therapy-resistant cases maintained on SSRI treatment, addition of a 5-HT1A receptor antagonist may improve clinical efficacy. Since the therapeutic effect of SSRIs in depression has been found to be critically linked to the availability of 5-HT in brain, our experiments results support, in principle, both of the above clinically based notions.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Risperidone: regional effects in vivo on release and metabolism of dopamine and serotonin in the rat brain.

The antipsychotic drug risperidone shows high affinity for both central serotonin (5-HT)2A and dopamine (DA)-D2 receptors in vivo. By employing microdialysis in freely moving rats, the effects of acute risperidone administration on regional brain DA and 5-HT release and metabolism were compared with the corresponding effects of the atypical antipsychotic drug clozapine as well as amperozide, the selective DA-D2 receptor antagonist raclopride and the selective 5-HT2A/5-HT2C receptor antagonist ritanserin. Risperidone (0.2 or 2.0 mg/kg, SC) was found to increase DA release and metabolism to about the same extent in three major projection areas of the mesotelencephalic dopaminergic system, i.e. the nucleus accumbens (NAC), the medial prefrontal cortex (MPC) and the lateral striatum (STR). In contrast, clozapine and amperozide (both 10.0 mg/kg, SC), as well as raclopride (2.0 mg/kg, SC), were all found differentially to affect DA release and metabolism in the three projections areas. Specifically, clozapine and amperozide enhanced DA release in the MPC to a greater extent than in the NAC or the STR, whereas raclopride instead preferentially increased DA release in the NAC and the STR but not in the MPC. Ritanserin (3.0 mg/kg, SC) did not exert any major effects on DA metabolism in the three areas studied. In contrast to the regionally rather homogenous activation of brain DA systems caused by risperidone, the drug was found to enhance brain 5-HT metabolism preferentially in the MPC, as indicated by the elevated extracellular concentration of 5-hydroxyindoleacetic acid (5-HIAA) in this region. A similar elevation of the 5-HIAA level in the MPC was observed after amperozide and, to some extent, after clozapine and ritanserin administration. The risperidone-induced (2.0 mg/kg, SC) elevation of 5-HIAA concentrations in the frontal cortex was found to be paralleled by an increased 5-HT release in this brain area. Consequently, our findings demonstrate a pharmacological profile of risperidone, as reflected in brain DA metabolism, in between that of clozapine and the DA-D2 antagonists. The preferential activation of 5-HT release and metabolism in frontal cortical areas might be of particular relevance for the ameliorating effect of risperidone on negative symptoms in schizophrenia, especially when associated with depression.

Animals↗
PubMed1996

Reactions of meniscal tissue after arthroscopic laser application: an in vivo study using five different laser systems.

In many clinical and in vitro studies, the effect of laser radiation on meniscal tissue was examined. Clinical studies referred to clinical criteria like swelling, effusion, and pain to evaluate laser effects. In vitro studies showed the laser effect in the moment of cutting the tissue. But the effect of laser radiation on biological tissue also depends on the vital reaction of the tissue. So, the real extent of tissue damage caused by laser irradiation can only be examined in long-term in vivo studies. This was the purpose of this study. Seventy-two knees of pigs underwent arthroscopic meniscal cuts in the anterior horn of the medial meniscus. The pigs were divided into 6 groups: The first 5 groups were operated with 5 different laser systems: Neodym: YAG 1,440-nm wavelength; Nd:YAG 1,064-nm wavelength, Excimer, Holmium:YAG, and CO2. The sixth group was operated with mechanical punches. From each group, the menisci of the pigs were examined macroscopically and by light-microscope after survival periods of 0, 2, 6, 12 weeks. Results were as follows. (1) All laser systems caused greater damage to the meniscal tissue than mechanical instruments. (2) This damage was a biological reaction of the tissue, characterized by a necrotic zone surrounding the meniscus cut. (3) This necrotic zone was not visible intraoperatively but only 2, 6 and 12 weeks after operation. The diameter of the necrotic zone ranged between 1.5 nm and 9 mm. (4) Meniscus cuts with mechanical instruments showed no necrotic zone in the surrounding tissue. (5) Laser cuts in the meniscus caused more extensive healing reaction than cuts with mechanical instruments. (6) The quality of this healing reaction varied with the different laser systems: the Nd:YAG 1,064-nm, Ho:YAG, and CO2 laser caused only an incomplete healing because the tissue repair showed by tissue growing from the synovial edge into the defect only. The Nd:YAG 1,440-nm wavelength and Excimer led to tissue growing from the synovial edge and to remodeling of original meniscal tissue, recognizable by reduction of the necrotic zone. Arthroscopic surgeons should be aware that the damage to meniscus tissue caused by a laser is much greater than can be seen intraoperatively and is much greater than the damage caused by mechanical punches. The healing reaction of the tissue is more extensive after laser application than after use of mechanical instruments. Results of in vitro studies on the tissue damage caused by lasers are insufficient to describe the whole extent of laser effects on living tissue.

Animals↗
PubMed1996

[Intraoperative and postoperative insertion control of anterior cruciate ligament-plasty. A radiologic measuring method (quadrant method)].

The best proximal insertion for an ACL graft is an anatomic insertion. The anatomic landmarks of this insertion area are well known, but it is sometimes difficult to find these anatomic landmarks during the operation. Thus, it is desirable to have an objective method to control the insertion. This study was undertaken because no description is available how you can localize the projection of the anatomic ALC insertion exactly in an X-ray picture. We dissected ten human cadaveric knees with intact ACLs. The most ventral, dorsal, distal and proximal borders of the insertion area were marked with 4 K-wires. The K-wires were shortened exactly on the bone border of the intercondylar space. Then the knees were X-rayed in a strictly lateral position. Thus, the shortened ends of the K-wires determined the projection of the ACL insertion in the X-ray picture. The center of this marked area was called point K. Then we determined 4 distances in the X-ray picture: distance t: the sagittal diameter of the lateral condyle, measured along the Blumensaat line distance h: the maximal height of the notch distance a: the distance between K and the dorsal border of the condyle, measured along t distance b: the distance between t and K, measured on a perpendicular line on t Distance a is a partial distance of t and distance b is a partial distance of h. Because of varying projection factors and varying knee sizes, absolute values of these distances are not helpful. This is the reason why we expressed a and b as a proportion of t and h. Distance a was measured 24.8% of distance t. Distance b was measured 28.5% of distance h. The maximal deviation of a and b was 2.2% and 2.5%. Therefore, you can say: In a strictly lateral X-ray picture the distance of K (midpoint of proximal ACL insertion) from the dorsal border of the condyle is 24.8% of the whole diameter of the condyle, and the distance of K from the roof of the notch is 28.5% of the notch-height. This method does not depend on the size of the knee and the distance between the X-ray unit and the knee. The only condition is that the X-ray of the knee must be strictly lateral. This method is easy to handle and is reproducible. It can be used intraoperatively if the surgeon is not sure about the right insertion or if the anatomic landmarks cannot be seen exactly. It can be used postoperatively for documentation of the right position of the substitute. It can be used to find out the possible reason for rupture of a transplant (insertion too ventral) before the revision operation.

Anterior Cruciate Ligament↗
PubMed1995

Effects of D-amphetamine and phencyclidine on behavior and extracellular concentrations of neurotensin and dopamine in the ventral striatum and the medial prefrontal cortex of the rat.

The effects of systemically administered phencyclidine (PCP; 2.5 mg/kg, s.c.) and D-amphetamine (1.5 mg/kg, s.c.) on the extracellular concentrations of neurotensin-like immunoreactivity (NT-LI) and dopamine (DA) in the ventral striatum (vSTR) and the medial prefrontal cortex (mPFC) were studied in freely moving rats using microdialysis. In separate animals, the effects of PCP and D-amphetamine on open field activity were also analyzed. PCP, but not D-amphetamine, caused a significant increase (156% over baseline) of NT-LI levels in the vSTR which was relatively short lasting, i.e., of less than 2 h duration. In contrast, both drugs significantly increased NT-LI concentrations in the mPFC by almost 100% during the same period. PCP and D-amphetamine also significantly increased extracellular levels of DA in the vSTR by 83 and 364%, respectively. However, the peak effect of PCP on DA appeared later than that of D-amphetamine, i.e., at 150 and 60 min, respectively, after drug administration. Also in the mPFC, both PCP and D-amphetamine significantly increased DA concentrations by 98 and 284%, respectively. Generally, effects on DA levels of both PCP and D-amphetamine were, in contrast to their effects on NT-LI levels, clearly more long-lasting, i.e., of 3-4 h duration. Behaviorally, D-amphetamine produced a more pronounced, general activation than PCP, with a faster onset of activation, i.e. within 30 vs 90 min after administration. However, both drugs produced long-lasting effects on the spatial organization of behavioral activity, which lasted for 3-4 h. In conclusion, the more pronounced behavioral stimulation by D-amphetamine (1.5 mg/kg, s.c.) vs PCP (2.5 mg/kg, s.c.) in the rat may largely be explained by its more potent DA-releasing effect in the brain. Initial behavioral suppression by PCP, e.g., of rearing, as well as its rather poor locomotor stimulant action in general, might relate to release of NT in the vSTR. The long-lasting, behavioral disorganization by both PCP and D-amphetamine may, however, be related to increased release of DA rather than NT in the mesolimbocortical areas.

Animals↗
PubMed1995

Ritanserin potentiates the stimulatory effects of raclopride on neuronal activity and dopamine release selectivity in the mesolimbic dopaminergic system.

The atypical profile of clozapine and some other new antipsychotic drugs has been attributed to a relatively selective effect on the mesolimbic dopaminergic system, as well as to their potent serotonin 5-HT2 receptor antagonism and high ratio of 5-HT2 to dopamine D2 receptor affinities. It is unclear, however, how concurrent 5-HT2 and D2 receptor antagonism specifically affects the mesoaccumbens and the mesocortical dopaminergic systems. The present study examined the effect of pretreatment with the 5-HT2 receptor antagonist, ritanserin, on changes in midbrain dopamine neuronal activity as well as in forebrain, extracellular concentrations of dopamine, induced by relatively low doses of the D2 receptor antagonist raclopride, utilizing in vivo extracellular single cell recording techniques and voltammetry in anesthetized rats, as well as microdialysis in freely moving rats. Raclopride alone (10-2560 microgram/kg, i.v.) induced a dose-dependent increase in three parameters of neuronal activity, i.e. burst firing, firing rate and variation coefficient, of midbrain DA neurons. This effect of raclopride was more pronounced in cells of the ventral tegmental area than in cells of the substantia nigra-zona compacta. Ritanserin alone (1.0 mg/kg, i.v.) also increased all three parameters of neuronal activity in dopamine cells of the ventral tegmental area, but only firing rate in the cells of the substantia nigra. Ritanserin pretreatment (30 min) significantly enhanced the stimulatory effects of low doses of raclopride (10-20 micrograms/kg, s.c.) increased extracellular concentrations of dopamine in the medial prefrontal cortex and the dorsolateral striatum by 75 and 110%, respectively, as measured by microdialysis. Ritanserin alone (1.5 mg/kg, s.c.) did not significantly affect cortical and striatal extracellular dopamine concentrations; however, pretreatment (40 min) with ritanserin elevated the raclopride-induced increase of dopamine concentrations in the medial prefrontal cortex of about 250%, but failed to affect the action of raclopride on striatal dopamine levels. Raclopride alone (10 and 320 micrograms/kg, i.v.) dose-dependently increased extracellular concentrations of dopamine in the nucleus accumbens and the dorsolateral striatum to about 500%, as determined by voltammetry. Ritanserin alone (1.0 mg/kg, i.v.) did not significantly affect the voltammetric dopamine signal in the nucleus accumbens or the dorsolateral striatum; however, ritanserin pretreatment (30 min) enhanced the raclopride-induced increase in accumbal but not striatal dopamine concentrations to about 1600%. The stimulatory effect of the combined ritanserin plus raclopride treatment on neuronal activity and DA release was more pronounced in the mesolimbic than the nigrostriatal dopaminergic system. The present data indicate that concurrent 5-HT2 and D2 receptor antagonism selectively affects the activity of the mesolimbic dopaminergic system. These findings provide an experimental basis for the notion that combined 5-HT2 and D2 receptor antagonism may underlie the limbic mode of action of at least some atypical antipsychotic drugs and consequently contribute to their unique therapeutic effects.

Animals↗
PubMed1995

5-HT1A receptor antagonists increase the activity of serotonergic cells in the dorsal raphe nucleus in rats treated acutely or chronically with citalopram.

In this study we have examined the acute effects of systemic administration of the selective serotonin reuptake inhibitor (SSRI), citalopram, in combination with either of the two selective 5-HT1A receptor antagonists, [(S)-5-fluoro-8-hydroxy-2-(dipropylamino)-tetralin [(S)-UH-301] or (+)-N-tertbutyl 3-(4-(2-methoxyphenyl)piperazin-1-yl)-2-phenyl-propionamide dihydrochloride [(+)-WAY100135], on the activity of single 5-HT neurons in the dorsal raphe nucleus (DRN) of anesthetized rats using extracellular recording techniques. Acute administration of citalopram (0.3 mg/kg i.v.) significantly decreased the firing rate of DRN-5-HT cells most likely as a result of indirect stimulation of inhibitory somatodendritic 5-HT1A autoreceptors located on 5-HT cells in the DRN. This effect of citalopram was completely reversed by (S)-UH-301 (0.5 mg/kg i.v.) and partly by (+)-WAY100135 (0.5 mg/kg i.v.). Furthermore, the inhibitory effect of citalopram on the activity of 5-HT neurons was significantly attenuated by pretreatment with (S)-UH-301 (0.25 mg/kg i.v.) or (+)-WAY100135 (0.25 mg/kg i.v.). We have also studied the effects of (S)-UH-301 (0.03-0.50 mg/kg i.v.) on the firing rate of single DRN-5-HT cells in rats chronically treated with citalopram (20 mg/kg/day i.p. x 14 days). Administration of (S)-UH-301 significantly and dose-dependently increased the activity of 5-HT cells in citalopram-treated rats, but did not affect these neurons in saline-treated (1 ml/kg/day i.p. x 14 days), control rats. Our results thus suggest that 5-HT1A receptor antagonists can augment both the acute and chronic effects of citalopram on central serotonergic neurotransmission.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Neural and vascular complications of arthroscopic meniscal surgery.

Injuries to vessels and nerves are very rare complications of arthroscopic meniscal surgery. The clinical development and diagnosis of such complications are described and illustrated by cases described in the literature and by two of our own cases. Typical patterns of injury are simulated by dissection of cadaver knees. To avoid neural complications in suturing the menisci, on the medial side the joint capsule has to be prepared when using the inside-out or the outside-in technique. On the lateral side of the outside-in technique can be performed by small suture incisions in this area when the lateral knee structures can be palpated. When using the inside-out technique the peroneal nerve must be dissected free. When resecting the posterior horn of the medial meniscus forced external rotation of the knee should be avoided because in this position the popliteal artery and the medial inferior genicular artery lie close to the posterior horn.

Aneurysm, False↗
PubMed1994

[Muscle and tendon injuries in the athlete].

Muscle and tendon injuries are the most common injuries in sports; they are mostly caused by overuse and repetitive strain injuries and require special diagnosis and treatment. Selective examples are given of surgical therapy (when conservative treatment fails) for the most frequent sports injuries (like muscle ruptures, jumper's knee, Achilles tendon ruptures, rotator cuff tears, tendinitis, dislocation of tendons, compartment syndrome).

Athletic Injuries↗
PubMed1993

[Magnetic resonance tomography of new rupture of the anterior talofibular ligament].

Twenty acutely traumatised patients with a rupture of the anterior talofibular ligament were studied by MRI. The results of 3D-studies were correlated with conventional stress x-ray studies. The ruptured ligament was directly visualised in all cases as a thickened structure of high signal intensity. In case of complete ruptured ligaments free flowing ligamentous structures were seen in the signal intense exudation in the ankle joint. MRI can help to decide between surgery or conservative therapy.

Adolescent↗
PubMed1993

[Surgical treatment of panaritium articulare with the external minifixator].

Septic interphalangeal arthritis can cause severe damage to the joint affected. Two patients treated by the appropriate operative procedure are presented. After interphalangeal distraction by external fixation two drains are placed in the joint and saline solution is infused regularly. The distraction improves the catheter irrigation and the prospects of success. At follow-up examination we saw no negative consequences of the joint distraction.

Adult↗
PubMed1993

[Gadolinium-DTPA enhanced MRT in the evaluation of the healing of autologous patellar ligament transplants for anterior cruciate ligament reconstruction].

Eighteen patients with autologous patellar tendon transplant for reconstruction of the anterior cruciate ligament were examined postoperatively. The time between operation and MR study was up to 3 weeks in ten patients, between 3 and 35 weeks in three patients and more than 35 weeks in five patients. In all patients, Gd-DTPA enhancement on the surface of the ligamentous transplant was visualized. This enhancement was between 1 and 10 mm thick. In all patients, complete stability of the knee joint was achieved, postoperatively. In 15 patients flexion and extension were normal at the postoperative investigation. Three patients had a limitation of knee movement. In these MR studies, significant hyperplasia of the synovial membrane of the entire joint was diagnosed, explaining the persisting problems. Gd-DTPA-enhanced MR of the knee joint allows non-invasive documentation of remodelling following a patellar ligament transplant and possible complications.

Adolescent↗