Biomedical subjects

T Kauppila

Publications and source records attributed to T Kauppila.

34 records · Page 2Linked to original sources

PubMed1993

A laminin graft replaces neurorrhaphy in the restorative surgery of the rat sciatic nerve.

We investigated the role of laminin in functional recovery of a peripheral nerve injury using electrophysiological and behavioral approaches on the rat sciatic nerve in vivo. These studies were complemented by neurofilament protein immunocytochemistry on the sciatic nerve 20 days after an operation, in which an 8-mm piece of the nerve was removed and replaced by a graft of laminin, its neurite outgrowth-promoting peptide, a control peptide, collagen, or by resuturing of the removed piece of the nerve. Electrophysiological measurements of muscle strength 4 months after the sciatic nerve transection showed that a laminin graft was as effective as neurorrhaphy in supporting functional recovery of an injured peripheral nerve. A laminin graft also significantly reduced autotomy in the operated animals. Immunocytochemistry confirmed that both a laminin graft and resuturing supported growth of the 200-kDa neurofilament-positive axons into the distal stump of the nerve within 20 days of operation. A graft with a neurite outgrowth-promoting peptide of the B2 chain of laminin supported similar axon growth, whereas another peptide graft also derived from laminin or a collagen graft did not support axon growth. All grafts allowed Schwann cell growth into the distal stumps of the nerves, but neurites accompanied them only in the regeneration-supporting grafts and in the resutured nerves. The Schwann cells of the regenerating nerves expressed high levels of the neurite outgrowth-promoting domain of the B2 chain of laminin, whereas the Schwann cells of the degenerating nerves failed to express this domain in the distal stumps of the degenerating nerves. These results provide the first in vivo evidence for the functional role of laminin in peripheral nerve regeneration. As the neurite outgrowth-promoting domain of the B2 chain of laminin is as efficient as laminin or resuturing in supporting a short-term recovery of an injured sciatic nerve, this area may be a regeneration-promoting domain of this glycoprotein. More importantly, as grafting significantly reduces post-traumatic pain behavior in the operated animals, the laminin graft surgery may provide a useful method for clinical restoration of the injured peripheral nerves.

Animals↗

PubMed1993

Inhibition of intestinal motility and reversal of postlaparotomy ileus by selective alpha 2-adrenergic drugs in the rat.

BACKGROUND: The effects of selective alpha-agonist medetomidine and alpha 2-antagonist atipamezole on gastrointestinal motility were studied. METHODS: The passage of intragastrically administered Evans blue in the small bowel of unanesthetized rats was followed, and the stomachs were weighted after killing the rats. RESULTS: Subcutaneous medetomidine, 0.01-0.1 mg/kg, was found to delay small intestinal transit but not gastric emptying, with a maximal effect seen at 0.03 mg/kg. Atipamezole fully reversed the effect of 0.1 mg/kg of medetomidine with a dose of 2.5 mg/kg. Atipamezole alone did not affect small intestinal transit. Subcutaneous morphine, 6 mg/kg, delayed gastric emptying and small intestinal transit, whereas intraperitoneal morphine only delayed gastric emptying. Subcutaneous atipamezole, 0.06 mg/kg, was partially able to reverse the delayed intestinal transit but did not inhibit morphine-induced gastric retention. Subcutaneous atipamezole, 0.06 mg/kg, reversed laparotomy-induced ileus completely. CONCLUSIONS: Atipamezole may provide a useful treatment for postlaparotomy ileus.

Adrenergic alpha-Agonists↗

PubMed1992

Polyamines enhance recovery after sciatic nerve trauma in the rat.

Spermine, a polyamine, is known to enhance motor functional recovery after a sciatic nerve lesion in the rat. The effect of spermine on the sensory axonal elongation after a sciatic crush was studied with the pinch-test from the sural nerve in the rat. The effect of spermidine, another polyamine, on the motor functional recovery after a trauma was studied by using the toe-spreading ability as an indicator of motor recovery after a sciatic crush in the rat. Spermine enhanced the rate of regeneration of the sensory axons by 16%. Spermidine enhanced the rate of the motor recovery by 30%. These results suggest that not only spermine but also spermidine enhance regeneration of peripheral somatic nerves.

Animals↗

PubMed1992

Enhancement of morphine-induced analgesia and attenuation of morphine-induced side-effects by cocaine in rats.

Effect of cocaine on morphine-induced analgesia and the accompanying respiratory depression, bradycardia and hypolocomotion/sedation was studied in rats. Cardiovascular and respiratory effects were studied under pentobarbitone-induced anaesthesia. Cocaine enhanced morphine-induced analgesia in the formalin test, hot plate test and heat-induced tail withdrawal test in intact rats. However, in spinal rats a similar combination of cocaine with morphine did not produce increased latencies in the tail withdrawal test. Of the three analgesic tests used, the formalin test was the most sensitive to the enhancement, as well as to the effects of morphine or cocaine alone. Morphine at the dose of 6 mg/kg produced complete analgesia in the formalin test, significant hypolocomotion/sedation, significant bradycardia and significant decrease in the respiratory rate. At an equianalgesic dose (complete analgesia in the formalin test) of morphine (3 mg/kg)-cocaine (5 mg/kg)-combination no significant changes in heart rate, respiratory rate or locomotion(/alertness) were observed. Changes in skin blood flow determined by the laser Doppler flow method were not significant in any of the experimental conditions. The results indicate that cocaine enhances morphine-induced analgesia, mainly due to supraspinal mechanisms. In contrast, the morphine-induced bradypnoea, bradycardia and hypolocomotion/sedation are attenuated by cocaine.

Analgesia↗

PubMed1992

Effects of atipamezole, an alpha 2-adrenoceptor antagonist, on the anesthesia induced by barbiturates and medetomidine.

We studied the effects of atipamezole, an alpha 2-adrenoceptor antagonist, on hypnosis induced by medetomidine, an alpha 2-adrenoceptor agonist (1 mg/kg IP), and pentobarbital (40 mg/kg IP) by testing the righting reflex in the rat. The duration of antinociception was assessed with repeated pinch tests. Medetomidine-induced hypnosis and antinociception were inhibited by atipamezole at doses greater than 0.1 mg/kg. Atipamezole restored the righting reflex at a dose ratio that was 1:10 or more to that of medetomidine used to induce hypnosis. Subcutaneous atipamezole (1.5 mg/kg) increased the duration of hypnosis induced by pentobarbital (40 mg/kg) and pentobarbital + medetomidine (0.3 mg/kg). Hypnosis induced by methohexital (60 mg/kg IP) was also prolonged by atipamezole. The capacity of atipamezole to reverse the effects of medetomidine is also reduced in the presence of barbiturates. Thus, atipamezole should be used only at low doses to reverse a combination anesthesia induced by barbiturates and medetomidine.

Adrenergic alpha-Antagonists↗

PubMed1991

Effects of atipamezole, a novel alpha 2-adrenoceptor antagonist, in open-field, plus-maze, two compartment exploratory, and forced swimming tests in the rat.

The behavioral effects of atipamezole (0.5-4.5 mg/kg), a new and highly selective alpha 2-adrenoceptor antagonist, were studied in four behavioral models: open-field, elevated plus-maze, two compartment exploratory test and forced swimming test. Atipamezole (1.5 and 4.5 mg/kg) produced a dose-dependent suppression of locomotor activity in the open field test. In the two compartment exploratory test, the same doses of atipamezole decreased locomotor activity in a 5 min test but not in a 10 min test. The numbers of transitions between the compartments were not significantly affected by atipamezole. Doses of 0.5-4.5 mg/kg did not significantly change the time spent in the open arms or the total number of arm entries in the plus-maze, and doses of 1.5 and 4.5 mg/kg decreased defecation marginally. Vocalization during the forced swimming test was increased by atipamezole (1.5 mg/kg) but the duration of immobility was not increased over the dose range (0.5-1.5 mg/kg) of atipamezole used. Our results suggest that, in the rat, atipamezole decreases motor activity in the early phase of the exploration of new surroundings. In the doses used, atipamezole may suppress defecation and increase vocalization in rats.

Adrenergic alpha-Antagonists↗

PubMed1991

Effects of different sensory and behavioral manipulations on autotomy caused by a sciatic lesion in rats.

We studied the effects of different sensory and behavioral manipulations on autotomy (self-mutilation). Lidocaine and bupivacaine pretreatments of the transected nerves delayed the onset of autotomy. Short prelesional stimulation (crush) of the transected nerve did not enhance autotomy significantly. Daily handling decreased autotomy behavior strongly and a visual cue placed on the denervated skin increased autotomy slightly. The delayed onset of the autotomy behavior after locally administered anesthetics suggests that the lesion-induced afferent barrage modified self-mutilation. The decreased self-mutilation after daily handling could be a consequence of handling stress. The increase of autotomy after the visual cue might have resulted from the attention-induced increase of the activity in ascending nociceptive tracts.

Afferent Pathways↗

PubMed1991

The effects of medetomidine, an alpha-2-adrenoceptor agonist, and cocaine on the tooth pulp-evoked jaw-opening reflex in cat.

In the pentobarbitone-anesthetized cat, the threshold of the tooth pulp-elicited jaw-opening reflex was elevated in a dose-dependent way (30-100 micrograms/kg, IP) following the administration of medetomidine, an alpha-2-adrenoceptor agonist. This elevation was significantly reduced by atipamezole (1 mg/kg, IP), an alpha-2-adrenoceptor antagonist. The inhibitory interaction between two successive dental stimuli applied to the same tooth (in-field inhibition) was suppressed by a lower dose of medetomidine (30 micrograms/kg) than the threshold elevation to single electrical pulses (55 micrograms/kg). Only the highest dose of medetomidine used (100 micrograms/kg) significantly influenced the temporally facilitated (in-field facilitation) response. In comparison, cocaine, a nonspecific monoaminergic agent, did not produce a significant threshold elevation of the tooth pulp-elicited jaw-opening reflex (1-25 mg/kg, IP). It is concluded that medetomidine, through an action on alpha-2-adrenoceptors, can suppress a predominantly nociceptive trigeminal reflex in anesthetized cats. The threshold evoked by single electric pulses, in-field inhibition, and in-field facilitation display differential sensitivities to medetomidine effects.

Adrenergic alpha-Agonists↗

PubMed1991

Involvement of supraspinal and spinal segmental alpha-2-adrenergic mechanisms in the medetomidine-induced antinociception.

The effect of systemically administered medetomidine, a selective alpha-2-adrenoceptor agonist, was studied by electrophysiological recordings of the peripherally evoked responses of three different types of sensory neuronal populations in the rat: medial thalamic neurons exclusively responding to mechanical cutaneous stimuli at noxious intensities, spinothalamic tract neurons of the spinal cord responding exclusively or differentially to mechanical cutaneous stimuli at noxious intensities, and low-threshold mechanoreceptive spinal dorsal horn neurons with ascending projections. The neuronal effects were compared with the behavioral data obtained in mechanically and thermally induced nociceptive tail reflex tests in intact and spinal rats. A reversal of the antinociceptive effects was attempted by systemically (1.5 mg/kg, i.p.) or intrathecally (25 micrograms) administered atipamezole, a selective alpha-2-adrenoceptor antagonist. Systemically administered medetomidine produced an atipamezole-reversible, dose-dependent suppressive effect on the evoked responses of nociceptive medial thalamic and spinothalamic tract neurons. A lower dose of medetomidine was needed to suppress significantly (half-maximally) evoked responses of the nociceptive medial thalamic neurons (100 micrograms/kg) than those of the nociceptive spinothalamic tract neurons (300 micrograms/kg). The decrease of evoked responses of the nociceptive spinothalamic tract neurons was accompanied by a decrease in spontaneous activity. The responses of the low-threshold mechanoreceptive projection neurons of the spinal cord were not influenced by medetomidine (30-300 micrograms/kg). The reflex studies with a (anesthetic) medetomidine dose of 300 micrograms/kg indicated that in intact and otherwise drug-free rats, medetomidine produced a significant prolongation of the nociceptive reflex response latency to a tail-pinch and heat; these antinociceptive effects of systemic medetomidine were reversed by systemically and intrathecally applied atipamezole. In spinal rats systemically applied medetomidine (300 micrograms/kg) also produced a significant prolongation of the tail-flick latency, which was reversed by systemically applied atipamezole. The results suggest that a high anesthetic dose of systemically applied medetomidine (300 micrograms/kg) can suppress nociceptive sensory neuronal and reflex responses due to spinal segmental mechanisms through an action on alpha-2-adrenoceptors. This spinal effect is selective to responses of nociceptive neurons, and at least partly postsynaptic as indicated by the concomitant decrease in spontaneous activity. At a lower, subanesthetic (but sedative) dose (100 micrograms/kg) the antinociceptive effect of systemically applied medetomidine can be explained by supraspinal alpha-2-adrenergic mechanisms.

Adrenergic alpha-Agonists↗

PubMed1991

Effect of systemic medetomidine, an alpha 2 adrenoceptor agonist, on experimental pain in humans.

The effect of systemic (intravenous) medetomidine, an alpha-2 adrenoceptor agonist, on pain thresholds was studied in healthy human subjects (n = 6). Medetomidine produced a dose-dependent (cumulative doses: 25 and 50 micrograms) sedative effect evaluated by visual analog scale. Also, a dose-dependent decrease of blood pressure but not of heart rate was seen after administration of medetomidine. Pain threshold to electric stimulation of the tooth pulp and cutaneous heat pain threshold were uninfluenced by medetomidine. An index of cutaneous thermal sensitivity to innocuous stimuli, the width of the thermoneutral zone, also was uninfluenced by medetomidine. Medetomidine produced a significant attenuation of the affective-motivational component (unpleasantness) of tourniquet-induced ischemic pain, whereas the sensory-discriminative component (pain magnitude estimate) of the ischemic pain was not attenuated. The results suggest that systemic medetomidine alone at subanesthetic but sedative and hypotensive doses does not significantly influence the intensity and thresholds of experimental pain, whereas the affective-motivational component of pain can be attenuated.

Adrenergic alpha-Agonists↗

PubMed1991

An attempted reversal of cocaine-induced analgesia by dexamethasone.

Analgesia produced by systemic cocaine (20 mg/kg intraperitoneally) was not attenuated by dexamethasone (0.25-2.5 mg/kg) in the formalin or tail pinch test in rats. The result suggests that the activation of the corticotropin releasing factor-adrenocorticotropin/beta-endorphin axis does not explain cocaine-induced analgesia.

Analgesics↗

PubMed1990

The effect of medetomidine, an alpha 2-adrenoceptor agonist, in various pain tests.

Medetomidine, a new alpha 2-adrenoceptor agonist produced dose-dependent (30-100 micrograms/kg i.p.) analgesia in the formalin test in rats, and this effect was reversed by atipamezole (1 mg/kg), a new alpha 2-adrenoceptor antagonist. However, medetomidine at the dose of 100 micrograms/kg did not influence tail flick latencies or latencies of the biting response to mechanical pinch stimuli. Moreover, medetomidine produced sedation and a decrease in locomotor activity. In comparison, the non-sedative monoaminergic agent, cocaine (25 mg/kg), produced highly significant analgesic effects in the formalin and mechanical pain tests. The cocaine effect in the formalin test was not reversed by atipamezole (1 mg/kg). It is concluded that the analgesic effect of medetomidine in the formalin test is due to supraspinal mechanisms related to sedation and is mediated by alpha 2-adrenoceptors. The alpha 2-adrenoceptors are not involved in cocaine-induced anagesia.

Adrenergic alpha-Agonists↗

PubMed1989

Effect of chronic sciatic nerve section on saphenous nerve input to midline bulboreticular formation in the rat.

The sciatic nerve was transected unilaterally 7-10 weeks before electrophysiological single unit recordings were made from somatically activated neurons in the midline bulboreticular formation of the rat. Their responses to high-intensity electrical stimulation of the saphenous nerve area were significantly stronger on the lesioned side. In control rats no such side difference was found. The result indicates that sciatic nerve transection unmasks polysynaptic somatic input to the midline bulboreticular formation.

Animals↗

PubMed1989

alpha-Difluoromethylornithine (DFMO) disturbed the sensorimotor functional recovery from a sciatic lesion.

The effects of inhibition of polyamine synthesis on the motor and sensory functional neural recovery after a sciatic crush lesion was studied by measuring sensory and motor function of a crushed sciatic nerve after daily exposure to alpha-difluoromethylornithine (DFMO). DFMO increased the time needed for functional motor recovery by 13% in the toe-spread test when the lesion was about 20 mm proximal to the target muscle. DFMO reduced the rate of sensory axonal elongation by 24% in the pinch-test.

Animals↗

PubMed1988

Putative stimulants for functional recovery after neural trauma: only spermine was effective.

The motor functional recovery after sciatic nerve crush was measured in rats treated with daily injections of (a) thyrotropin-releasing hormone (2.0 mg/kg, (b) alpha-melanocyte-stimulating hormone (0.07 mg/kg/48 h), or (c) testosterone propionate (4.4 mg/kg). The recovery of the motor function of the sciatic nerve was indicated by using the return of the toe-spreading response. None of the treatments differed significantly from saline controls in the time needed for recovery. The same procedure (without injections) was carried out with castrated and noncastrated male rats in order to test the effect of the lack of testosterone on recovery time after sciatic crush. The groups did not differ significantly as to their recovery times. The same method was used to study the effect of spermine (10.0 mg/kg/day) on the recovery of motor function. Spermine seemed to reduce the time needed for recovery from a mean value of 15.7 to 11.0 days (P less than 0.01). We also studied the effect of daily injections of spermine (13.0 mg/kg) on the sensory division of the peripheral nerve using the foot-flick test. The time needed for recovery after crush in the sciatic notch was reduced from 13.7 to 7.7 days (P less than 0.005). These results do not support the hypothesis that alpha-melantocyte-stimulating hormone, thyrotropin-releasing hormone, or testosterone enhance functional recovery of severed motor axons. Our results confirm a previous observation that spermine reduces the time needed for recovery after trauma in peripheral motor neurons. The result of the foot-flick test suggests that spermine enhances both motor and sensory recovery.

Animals↗

PubMedDate not supplied

Particulate phosphorus and sediment in surface runoff and drainflow from clayey soils.

Recent work has shown that a significant portion of the total loss of phosphorus (P) from agricultural soils may occur via subsurface drainflow. The aim of this study was to compare the concentrations of different P forms in surface and subsurface runoff, and to assess the potential algal availability of particulate phosphorus (PP) in runoff waters. The material consisted of 91 water-sample pairs (surface runoff vs. subsurface drainage waters) from two artificially drained clayey soils (a Typic Cryaquept and an Aeric Cryaquept) and was analyzed for total suspended solids (TSS), total phosphorus (TP), dissolved molybdate-reactive phosphorus (DRP), and anion exchange resin-extractable phosphorus (AER-P). On the basis of these determinations, we calculated the concentrations of PP, desorbable particulate phosphorus (PPi), and particulate unavailable (nondesorbable) phosphorus (PUP). Some water samples and the soils were also analyzed for 137Cs activity and particle-size distribution. The major P fraction in the waters studied was PP and, on average, only 7% of it was desorbable by AER. However, a mean of 47% of potentially bioavailable P (AER-P) consisted of PPi. The suspended soil material carried by drainflow contained as much PPi (47-79 mg kg-1) as did the surface runoff sediment (45-82 mg kg-1). The runoff sediments were enriched in clay-sized particles and 137Cs by a factor of about two relative to the surface soils. Our results show that desorbable PP derived from topsoil may be as important a contributor to potentially algal-available P as DRP in both surface and subsurface runoff from clayey soils.

Agriculture↗