[Measurement of urinary sodium and potassium excretion with the proportional sampling device (partition cup) compared with 24-hour whole urine collection].
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Adult↗
Biomedical subjects
Y Katayama
Publications and source records attributed to Y Katayama.
Bilateral lesions of the dorsolateral funiculus of the cat spinal cord: effects on basal nociceptive reflexes and nociceptive suppression produced by cholinergic activation of the pontine parabrachial region.
In cats, bilateral microinjections of the cholinergic agonist, carbachol (0.6 micrograms in 0.2 microliter), into an area surrounding the lateral half of the brachium conjunctivum (BC) produces a non-narcotic suppression of nociceptive responses, as assessed by flexion reflexes (tail-flick and calibrated pinch tests). Bilateral lesions of the dorsolateral funiculi (DLF) of the thoracic spina cord (T2) significantly reduced the magnitude of this nociceptive suppression. Nociceptive suppression following carbachol microinjections into sites along the dorsal aspect of BC was reduced by DLF lesions to a greater degree than nociceptive suppression following injections into sites within or ventral to BC. Relatively superficial DLF lesions produced reductions in nociceptive suppression which were equivalent to reductions induced by deeper lesions. DLF lesions, either superficial or deep, produced equivalent, reliable decreases in tail-flick test assessments of baseline nociceptive thresholds. The magnitude of decreases in baseline nociceptive thresholds produced by DLF lesions was not correlated with the magnitude of reduction of carbachol-induced suppression of nociceptive responses, indicating that DLF lesions suppress anti-nociception independent of baseline alterations. These data suggest that non-narcotic analgesia produced by cholinergic activation of cells along the dorsal aspect of BC may be predominantly mediated by fibers descending within the DLF. However, results of the retrograde horseradish peroxidase (HRP) tracing studies reported in the present investigation indicate that this pain suppression is probably mediated by polysynaptic pathways since this region dorsal to BC projects neither through DLF nor extra-DLF pathways. Retrograde HRP data show that areas ventral to and including BC projects to the cord via both DLF and extra-DLF pathways. Since DLF lesions were less effective in reducing analgesia attained from ventral compared to dorsal sites, spinal pathways other than DLF may mediate reflex suppression following carbachol microinjection into these more ventral sites. Possible cholinergic contributions to endogenous, non-opiate forms of analgesia are discussed.
Acetylcholine↗
Immunoreactive avian pancreatic polypeptide in the chicken retina: overall distribution.
The distribution of avian pancreatic polypeptide (APP)-like immunoreactivity (APP-IR) in the chicken retina was investigated by means of immunohistochemistry. The observation from frozen sections showed that APP-IR is localized in the stratified amacrine cells of the first sublayer. Examination of whole-mounts revealed that APP-IR fibers from a dense fiber plexus at the peripheral margin area and peripheral portion of the retina where they run circumferentially. APP-IR neurons are located in the peripheral portion. From the three-dimensional profiles, APP-IR amacrine cells could be divided into two types.
Animals↗
Muscarinic cholinergic mediation of opiate and non-opiate environmentally induced analgesias.
Previous studies have demonstrated that brief front paw shock and brief hind paw shock produce prolonged opiate and non-opiate analgesia, respectively. Additionally, opiate analgesia can be classically conditioned by using either front paw shock or hind paw shock as the unconditioned stimulus. However, beyond this point little is known regarding the neurochemistry of these phenomena. The present series of studies examined the potential involvement of nicotinic and muscarinic cholinergic systems in these 3 forms of environmentally induced analgesia. These experiments demonstrate that muscarinic cholinergic sites within the central nervous system are critically involved in the mediation of both hind paw (non-opiate) foot shock-induced analgesia ( FSIA ) and classically conditioned (opiate) analgesia since scopolamine, but not equimolar methylscopolamine, significantly attenuated analgesia. Furthermore, the primary muscarinic site(s) appears to exist at a supraspinal, rather than spinal, level since delivery of scopolamine directly to the lumbosacral cord produced, at most, only a slight decrease in analgesia. Nicotinic systems do not appear to be importantly involved in any of these forms of environmentally induced analgesias since mecamylamine had no effect on either front paw FSIA or hind paw FSIA and, at most, produced only a slight reduction in classically conditioned analgesia. These data and a review of the literature suggest that the critical cholinergic sites involved in hind paw FSIA exist within the caudal brainstem whereas cholinergic sites within more rostral brain levels probably mediate classically conditioned analgesia.
Analgesia↗
Evidence for involvement of cholinoceptive cells of the parabrachial region in environmentally induced nociceptive suppression in the cat.
We have previously observed that activation of muscarinic receptors within the pontine parabrachial region (PBR) of cats produces potent analgesia. This study demonstrated that bilateral microinjections of the muscarinic antagonist atropine (each 4.0 micrograms in 1.0 microliter) into PBR attenuated nociceptive suppression elicited by exposure of cats to novel environmental changes without affecting general responsiveness to environmental stimulation. This observation suggests that muscarinic cholinoceptive cells in PBR function physiologically to modulate nociceptive responsiveness in response to certain environmental stimuli.
Animals↗
Behavioral evidence for a cholinoceptive pontine inhibitory area: descending control of spinal motor output and sensory input.
Earlier studies have shown that microinjection of the cholinergic agonist carbamylcholine (carbachol) into the rostral pontine tegmentum of the cat elicits postural atonia. However, conflicting reports exist regarding other concomitant behavioral changes. The present study has demonstrated that a variety of functions supporting animals' responsiveness to external stimuli including postural somatomotor, sympathetic visceromotor and nociceptive somatosensory functions are differentially affected depending upon the injection sites. Sites associated with maximal effects on each of these functions are clustered in the dorsal pontine tegmentum, i.e. cholinoceptive pontine inhibitory area (CPIA). In a medial area of CPIA, which corresponds to an area caudal to the ventral tegmental nucleus of Gudden and ventromedial to the principal nucleus of locus coeruleus, postural somatomotor and sympathetic visceromotor functions were maximally suppressed. In a laterally adjacent area ventral to the principal nucleus of locus coeruleus, somatomotor function was predominantly suppressed. Nociceptive somatosensory function was primarily suppressed following microinjections into a more lateral area surrounding the lateral half of the brachium conjunctivum. Several lines of evidence suggest that each of these phenomena ultimately involves descending influences on the spinal motor output and/or sensory input. There was no correlation between maximal suppression of these spinal cord functions and signs of desynchronized sleep such as rapid eye movement. Carbachol microinjection into wide areas of CPIA also suppressed orienting behaviors. Taken together, these data suggest that CPIA is a system which primarily regulates animals' responsiveness to external stimuli, in part by influencing segmentally organized behaviors.
Animals↗
Non-opiate analgesia induced by carbachol microinjection into the pontine parabrachial region of the cat.
These studies investigated the effect of microinjection of the cholinergic agonist carbamylcholine (carbachol) into various sites of the dorsolateral pontine tegmentum of the cat. Carbachol microinjection into an area surrounding the lateral half of the brachium conjunctivum (parabrachial region, PBR) produced profound suppression of nociceptive responses. In the dorsal part of PBR, carbachol microinjection produced no generalized sensory, emotional or motor deficits, indicating that nociceptive transmission was primarily affected. Carbachol microinjection into the ventral part of PBR resulted in slight suppression of motor responses in addition to profound nociceptive suppression. Carbachol-produced analgesia (CPA) observed within PBR blocked supraspinally as well as spinally integrated responses normally elicited by either phasic or tonic noxious stimuli. Atropine sulfate, but not mecamylamine hydrochloride, significantly antagonized CPA, indicating that muscarinic receptors mediate this phenomenon. The opiate antagonist naloxone, systemically administered either prior to or after carbachol microinjection, did not reliably attenuate CPA. Microinjection of morphine into the sites from which CPA had previously been obtained did not produce significant effects on nociceptive responses. Thus, opiate mechanisms appear not to be necessary either for the activation of this system or for the production of the resultant analgesia. These findings indicate that the neural population examined in the present study is anatomically and pharmacologically distinct from previously identified opiate-mediated pain inhibitory systems. Results are discussed in light of other recent evidence indicating the existence of endogenous non-opiate pain inhibitory systems.
Animals↗
Actions of ATP on the soma of bullfrog primary afferent neurons and its modulating action on the GABA-induced response.
Adenosine 5'-triphosphate (ATP) produced a long-lasting depolarization in bullfrog spinal ganglion cells. Since the ATP-induced slow depolarization was associated with an increase in membrane resistance and a reverse in polarity (about--90 mV) which was most likely brought about by an inactivation of membrane potassium conductance. In some cells, a rapid and transient depolarization followed by the long-lasting depolarization was produced by ATP and it was markedly reduced in sodium-free solution. ATP reversibly augmented the GABA-induced depolarization which was caused by ionophoresis of GABA. These observations were confirmed using a voltage clamp method. Dose-response analysis of the action of ATP on the GABA-induced response suggests that the facilitatory action of ATP on the GABA response is effected on the GABA receptor channel complexes without changing the GABA affinity.
Adenosine Triphosphate↗
Activation of pontine cholinergic sites implicated in unconsciousness following cerebral concussion in the cat.
Low levels of cerebral concussion in the cat produce reversible behavioral suppression presumably associated with unconsciousness. This injury is also associated with increased rates of glucose utilization in regions within the dorsomedial pontine tegmentum. Microinjection of carbachol into these regions produced behavioral suppression resembling that following concussion. These data, together with previously published observations on cholinergic responses to brain injury, suggest that concussive unconsciousness may be attributable in part to activation of cholinergic pontine sites.
Animals↗
Two types of acetylcholine receptors on the soma of primary afferent neurons.
Acetylcholine (ACh) caused two types of depolarizations of the soma membrane of bullfrog primary afferent neurons (dorsal root ganglion cells); the one, a rapid transient depolarization, was nicotinic and the other, a long-lasting one, was muscarinic in nature, respectively. The rapid transient depolarization was due to a simultaneous increase in sodium and potassium conductance, whereas the slow one was caused by a decrease in membrane potassium conductance. These results indicate that the soma of bullfrog primary afferent neuron is endowed with nicotinic and muscarinic receptors.
Acetylcholine↗
The thin glomerular basement membrane in children with haematuria.
To determine the specificity and significance of widespread attenuation of the glomerular basement membrane on electron microscopy, 240 renal biopsies from 218 children were studied retrospectively. Twenty-three patients showed diffuse attenuation and three of them are cases of hereditary nephritis. The other 20 patients are characterized by persistent microscopic haematuria, absence of proteinuria, normal blood pressure and renal function, and minimal glomerular changes. In 10 of these 20 children, microscopic haematuria was also present in the family. We conclude that widespread attenuation of the glomerular basement membrane is a characteristic of benign familial and non-familial haematuria. The thin glomerular basement membrane may be responsible for the haematuria and may result from incomplete glomerular maturation.
Basement Membrane↗
Studies of four Japanese families with hereditary angioneurotic edema: simultaneous activation of plasma protease systems and exogenous triggering stimuli.
Forty-five relatives of 4 families with hereditary angioneurotic edema (HANE) were studied. Twenty-five, including 11 asymptomatic kindreds with the disposition, showed typical changes in complement system compatible with HANE. Follow-up study of HANE patients showed that, even in remission period, complement, coagulation and fibrinolytic systems can be activated. During edema attacks, moderate haemoconcentration and neutrophilia were encountered and kallikrein-kinin system was found to be also activated. Replacement therapy with C 1-inhibitor preparation for an edema attack revealed that clinical improvement paralleled the increase in blood levels of high molecular weight kininogen. Thus, HANE attack is considered to be elicited in kindreds with the hereditary disposition by activation of plasma protease systems, particularly by that of kallikrein-kinin system. On the other hand, exogenous triggers that can initiate activation of the protease systems can be classified into 2, neuro-humoral (sympathetic nerve response) and physico-chemical, categories. Hence, the edema attack of kindreds with the hereditary disposition can at least be modified by the biosynthesis of plasma factors and the individual susceptibility to the liberated catecholamines. These two different reaction processes are considered to be linked by the release of plasminogen activator and/or Hageman factor activating enzyme.
Angioedema↗
Continuous recording of intracranial pressure in the awake, drug-free cat.
A simple and quantitatively reliable technique for continuous recording of intracranial pressure in awake, drug-free cats is presented. In addition, behavioral responses to acute elevation of intracranial pressure by slow intraventricular infusion in awake cats are described.
Animals↗
Carcinoma in anorectal fistula of rectal mucosal origin.
A case report of mucinous adenocarcinoma in anorectal fistula of rectal mucosal origin, though many cases reported were thought to be of anal duct origin. The patient, a 51-year-old male, was operated for anal fistula twelve years previously. He presented to us for anal pain, anorectal stricture, and perianal induration. Abdominoperineal resection was performed for proper management. On gross no visible mucosal lesion of anal canal and rectosigmoid colon was revealed. On cross section a gelatinous tumor was found mostly outside the rectal muscle layer, and an internal opening of the lesion was detected in the rectal mucosa. Histologically, the rectal mucosa extended into the edge of the internal opening and the carcinoma appeared just adjacent to this rectal mucosa. Periodate-borohydride/saponification/PAS stain also indicated that the mucin produced by the carcinoma had the nature of rectal mucosal origin. We considered that the carcinoma of this case originated at the internal opening and developed into the antecedent fistulous track.
Adenocarcinoma, Mucinous↗
Sites and mechanisms of actions of enkephalin in the feline parasympathetic ganglion.
Intracellular recordings were made in vitro from neurones of the cat parasympathetic ciliary ganglion with a current- or voltage-clamp technique. (Met5)enkephalin and (leu5)enkephalin (10 nM to 10 microM) were applied by superfusion. Both caused a membrane hyperpolarization which persisted in a calcium-free/high-magnesium solution, and both reduced the amplitude of excitatory post-synaptic potentials (e.p.s.p.s). These actions of enkephalin were antagonized by naloxone. The enkephalin-induced hyperpolarization was associated with an increase in membrane conductance, reversed in polarity at -90 mV and was not altered by changing external sodium and chloride concentrations. This indicates that the enkephalin hyperpolarization is due mainly to activation of potassium conductance. Enkephalin decreased the mean quantal content of e.p.s.p.s recorded in low-calcium/high-magnesium solution, without changing quantal size. Furthermore, the increase in the frequency of miniature e.p.s.p.s after tetanic preganglionic stimulations was inhibited by enkephalin. Acetylcholine potentials were not altered by enkephalin. These findings suggest that enkephalin reduces transmitter release. The experiments suggest that enkephalin may inhibit ganglionic transmission by both pre- and post-synaptic actions in a mammalian parasympathetic ganglion.
Acetylcholine↗
Intracranial pressure variations associated with activation of the cholinoceptive pontine inhibitory area in the unanesthetized drug-free cat.
Intracranial pressure (ICP) was recorded continuously in chronically prepared, unanesthetized cats in order to investigate the effects on ICP of the cholinergic agonist, carbamylcholine (carbachol), injected by microsyringe needles into the dorsal pontine tegmentum. As reported previously, carbachol microinjections into the medial part of the cholinoceptive pontine inhibitory area (CPIA) located ventromedially to the locus coeruleus produced a comatose state characterized by a profound unresponsiveness to external stimuli, desynchronized electroencephalograms (EEG's), and suppression of postural somatomotor and sympathetic visceromotor functions. Four of six ICP records following carbachol microinjections into the CPIA showed small but significant increases which occurred in association with these carbachol effects. Tracings of ICP increases ranged up to 3.2 mm Hg and were similar in shape to plateau waves. The start and resolution of these carbachol-induced ICP variations were closely associated with the onset and termination of EEG desynchronization and signs of reduced cervical sympathetic tone, but not with changes in systemic arterial blood pressure or arterial pCO2. Temporal associations between ICP increases, desynchronized EEG's, and signs of reduced sympathetic tone were repeatedly confirmed during recovery periods associated both with recurrent comatose states following wakefulness produced by various intensities of external stimulation and with spontaneously occurring states resembling rapid eye movement sleep. The authors infer that carbachol-induced ICP variations may be produced by increased cerebral blood volume in response to accelerated cerebral metabolism and reduced vasoconstrictor tone of cervical sympathetic nerves. The simultaneous occurrence of continuously accelerated cerebral metabolism and reduced cervical sympathetic tone can neither be seen in physiologically normal, awake organisms nor produced by other known experimental manipulations of the central nervous system. Such a paradoxical relationship appears to be a unique consequence of activity within the CPIA. These data suggest that episodic activity within the CPIA may provide at least one endogenous neural basis for plateau waves seen during certain pathological conditions such as disturbed cerebrospinal fluid (CSF) absorption or with reduced equilibrium volume of CSF space.
Animals↗
[Experimental cerebral ischemia after bilateral common carotid artery ligation in SHRSP, SHRSR and Wistar rats: correlation between blood pressure and degree of ischemia].
Three different pressure groups of rats, stroke-prone spontaneously hypertensive rats (SHRSP, 200-270 mmHg), stroke-resistant SHR (SHRSR, 160-240 mmHg), and Wistar rats (WR, 120-160 mmHg) were used to investigate the effect of prior existing hypertension on the severity of brain damage induced by ischemia. The cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and the survival rate, cerebral blood flow, cerebral energy metabolites (ATP, lactate c-AMP) and water content were measured. Colloidal carbon perfusion was also performed. Sixteen-week-old male rats were used. The survival rate was observed until 24 hours after BLCL. Cerebral blood flow was measured in parietal cortex by hydrogen clearance method. ATP was measured by luciferin-luciferase method, and lactate by enzymatic method using LDH. c-AMP was measured by radioimmunoassay. Brain water content was measured by freeze-dry method. These measurements were done for animals surviving 6 hours of BLCL. Colloidal carbon perfusion was done according to Ames' Method. The survival rate was lower in the hypertension group. The survival of SHRSP and SHRSR were 20% compared to 71% in WR after 24 hours of BLCL. The cerebral circulation of SHRSP fell abruptly and was near to zero after one hour of BLCL. In SHRSR this fall of cerebral blood flow was prominent in the rats of higher blood pressure. On the other hand there was no apparent fall of cerebral blood flow in WR after BLCL. The cerebral energy metabolites. ATP and c-AMP showed the lowest level in SHRSP which had the negative correlation to blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine Triphosphate↗
[Thalamic relay nucleus stimulation for relief of intractable pain. Clinical results and beta-endorphin immunoreactivity in cerebrospinal fluid].
Chronic implantation of a stimulating electrode in the thalamic relay nucleus (11 cases), in the periaqueductal gray (1 case) and in the internal capsule (2 cases) was performed in fourteen cases which suffered from intractable pain. All these cases could get pain relief at least initial two months. Ventricular fluids were collected before and after stimulation with optimal combination of parameters, and measurements of beta-endorphin were performed by radio-immunoassay. Intrathecal morphine (1mg) injection was performed in eight cases. Cerebrospinal fluids were collected by lumbar tap before and 24 hours after morphine injection. beta-endorphin immunoreactivity was measured by the same method. Pain relief was judged to be excellent if the patient so claimed, and if he discontinued analgesics. Pain relief was thought to be good when it was not completely controllable by stimulation but was sufficiently improved that the patient could do without analgesics. It was thought to be fair when patient could not discontinue analgesics, and poor when patient could not get pain relief. We usually attempt to prevent the stimulation-tolerance by administration of the monoamine precursors , i.e., 1-dopa and 1-tryptophan, on the basis of the experimental observation reported previously. In somatogenic pain patients, the thalamic relay nucleus stimulation was performed in 7 cases (excellent; 3, good; 1, fair; 3) and the periaqueductal gray stimulation in one case (good).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗