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Biomedical subjects

L M Patterson

Publications and source records attributed to L M Patterson.

18 recordsLinked to original sources
PubMed2005

Melanin concentrating hormone innervation of caudal brainstem areas involved in gastrointestinal functions and energy balance.

Neural signaling by melanin-concentrating hormone and its receptor (SLC-1) has been implicated in the control of energy balance, but due to the wide distribution of melanin-concentrating hormone-containing fibers throughout the neuraxis, its critical sites of action for a particular effect have not been identified. The present study aimed to anatomically and functionally characterize melanin-concentrating hormone innervation of the rat caudal brainstem, as this brain area plays an important role in the neural control of ingestive behavior and autonomic outflow. Using retrograde tracing we demonstrate that a significant proportion (5-15%) of primarily perifornical and far-lateral hypothalamic melanin-concentrating hormone neurons projects to the dorsal vagal complex. In the caudal brainstem, melanin-concentrating hormone-ir axon profiles are distributed densely in most areas including the nucleus of the solitary tract, dorsal motor nucleus of the vagus, and sympathetic premotor areas in the ventral medulla. Close anatomical appositions can be demonstrated between melanin-concentrating hormone-ir axon profiles and tyrosine hydroxylase, GABA, GLP-1, NOS-expressing, and nucleus of the solitary tract neurons activated by gastric nutrient infusion. In medulla slice preparations, bath application of melanin-concentrating hormone inhibited in a concentration-dependent manner the amplitude of excitatory postsynaptic currents evoked by solitary tract stimulation via a pre-synaptic mechanism. Fourth ventricular administration of melanin-concentrating hormone (10 microg) in freely moving rats decreased core body temperature but did not change locomotor activity and food and water intake. We conclude that the rich hypothalamo-medullary melanin-concentrating hormone projections in the rat are mainly inhibitory to nucleus of the solitary tract neurons, but are not involved in the control of food intake. Projections to ventral medullary sites may play a role in the inhibitory effect of melanin-concentrating hormone on energy expenditure.

Animals↗
PubMed2001

Food-related gastrointestinal signals activate caudal brainstem neurons expressing both NMDA and AMPA receptors.

Vagal mechano- and chemosensors in the gastrointestinal tract and the portal-hepatic axis signaling the arrival of nutrients are major determinants of the satiation process. Although glutamate and its various receptor subtypes have been shown to transmit gustatory and cardiovascular sensory information at the level of the solitary nucleus (nucleus tractus solitarius; NTS), their involvement in the transmission of gastrointestinal satiety signals is not clear. Gastrointestinal sensors were stimulated by gastric balloon distension or by intraduodenal infusion of either linoleic acid or glucose in chronically catheterized, non-anesthetized rats, leading to activation of second order neurons in the NTS as detected by c-Fos immunohistochemistry. Subsequent (double)-immunohistochemistry for either NMDA or AMPA glutamate receptors was used to determine the percentage of activated neurons expressing a particular receptor subtype. Gastric distension and duodenal nutrient stimuli produced slightly, but significantly different patterns of c-Fos induction in the dorsal vagal complex. Expression of NMDA receptors, as detected by a NR2ab subunit-specific antibody, was abundant throughout the dorsal medulla. The percentage of neurons in the NTS activated by gastric distension (63.9+/-2.9%), linoleic acid (62.8+/-1.4%), and glucose (64.1+/-1.4%), expressing NMDA receptor was similar. Expression of AMPA receptors, as detected by a GLUR2/3 subunit-specific antibody, was equally abundant throughout the dorsal medulla. Again, the percentage of activated neurons expressing GLUR2/3 was similar for the gastric distension (59.8-65.6%) and duodenal linoleic acid (60.6-67.0%) stimuli, and for the various subnuclei of the NTS. Finally, GLUR1-specific immunoreactivity was much less abundant, with only a small percentage of distension-activated (4.4+/-0.4%) and linoleic acid-activated (5.1+/-0.4%) neurons expressing this receptor subunit. The results suggest a widespread, general involvement of both NMDA and AMPA receptors in primary afferent signal transmission at the level of the NTS, with no differential recruitment of the examined receptor subtypes by the different gastrointestinal sensory stimuli. This may indicate a high degree of convergence among sensory signals, or alternatively, the presence of other transmission systems such as peptides referring sensory specificity to second order neurons.

Animals↗
PubMed2001

Vagal-enteric interface: vagal activation-induced expression of c-Fos and p-CREB in neurons of the upper gastrointestinal tract and pancreas.

Many gastrointestinal and pancreatic functions are under strong modulatory control by the brain via the vagus nerve. To start identifying location and neurochemical phenotype of the enteric neurons receiving functional vagal efferent input, we activated vagal preganglionic neurons either by electrical or chemical stimulation and examined the expression of phosphorylated CREB (c-AMP response element binding protein) and the immediate early gene c-Fos. There was no spontaneous expression of both markers in the pancreas and considerable spontaneous expression of p-CREB but not Fos in the upper GI-tract. Unilateral electrical vagal stimulation-induced p-CREB was found in 40% of neurons in the head of the pancreas. Fos expression was found in 70-90% of neurons in the esophagus and stomach, in 20-30% of myenteric plexus neurons and 5-15% in submucosal neurons of the proximal duodenum. Double-labeling experiments showed that a majority of pancreatic neurons and about 25-35% of neurons in the stomach and duodenum contain NADPH-diaphorase and that many of these receive functional vagal input. Other neurons that can be vagally activated contain gastrin-releasing peptide or calretinin. Chemical stimulation of the dorsal surface of the caudal brainstem with the stable TRH analog RX77368 resulted in selective activation of vagal efferents with expression of Fos in a small number of gastric myenteric plexus neurons. The results demonstrate the suitability of this method to investigate magnitude and local distribution of vagal input to the enteric nervous system as well as specificity of its neurochemically coded pathways. They represent the first step in the identification of function-specific units of parasympathetic vagal outflow.

Activating Transcription Factor 1↗
PubMed2001

Immunohistochemical identification of cholecystokinin A receptors on interstitial cells of Cajal, smooth muscle, and enteric neurons in rat pylorus.

One of the physiological functions of circulating cholecystokinin (CCK) is in the control of the pyloric sphincter and the subsequent delivery of nutrients to the small intestine. In order to identify the site(s) of action of CCK in the gastropyloric region, we performed immunohistochemistry using an antibody directed to the C-terminal region of the cholecystokinin A receptor (CCKAR). In the rat, cells that display strong CCKAR immunoreactivity and fit the morphological description of interstitial cells of Cajal (ICC) were found in the distal sphincter muscle and in the circular muscle of the proximal duodenum. Double labeling showed that these cells coexpressed vimentin, but that not all vimentin-positive cells expressed CCKAR. Confirmation that the CCKAR-expressing cells were ICC also came from kit double-labeling experiments in mice. In addition to ICC, circular smooth muscle cells at the tip of the comma-shaped sphincter muscle, but not elsewhere, also exhibited strong, membrane-bound CCKAR immunoreactivity. With higher antibody concentrations, the entire circular muscle displayed moderate CCKAR immunoreactivity, suggesting that circular smooth muscle cells express low levels of CCKAR. Select neurons in the myenteric ganglia near the sphincter muscle proper, the distal antrum, and proximal duodenum, as well as a few single neurons in the submucosa, also expressed strong CCKAR immunoreactivity. Finally, CCKAR-immunoreactive ICC and neurons were not specifically related to vagal afferent intramuscular and intraganglionic endings, and vagal afferents themselves did not exhibit any CCKAR immunoreactivity. These results suggest a role for ICC and enteric neurons in the mediation of CCK effects on pyloric sphincter pressure in addition to direct effects of the hormone on circular smooth muscle.

Afferent Pathways↗
PubMed2000

Additive satiety-delaying effects of capsaicin-induced visceral deafferentation and NMDA receptor blockade suggest separate pathways.

Both ablation of visceral afferents and blockade of NMDA receptor-mediated glutamatergic transmission by MK-801 result in overconsumption of sucrose solution and other food, apparently by interrupting visceral signals and thus delaying satiation. If these two manipulations act on the same pathway, namely, the propagation of vagal afferent signals to NTS neurons, their effects would be expected to be non-additive. To test this hypothesis, two groups of rats - one with prior systemic capsaicin (n=11) and one with vehicle treatment (n=10) - were trained to drink 15% sucrose solution after 15 h food deprivation every 3-4 days, and then injected with MK-801 (100 microg/kg, i.p.) or saline. Both capsaicin and MK-801 produced the expected significant (P<.001) increase in 30 and 60 min sucrose intake if compared to their respective controls. Administration of MK-801 to capsaicin-treated rats further increased 60 min sucrose intake significantly (P<.001) in a fully additive fashion. These results suggest that the two treatments do not impinge on the same neural pathway to delay satiation. MK-801 may interfere with signals from capsaicin-resistant vagal afferents, or alternatively may act on other areas in the brain or periphery.

Animals↗
PubMed1999

Postmortem retrieval of total joint replacement components.

Improved understanding of the clinical outcomes of orthopedic implants requires the study of implants at the end of their service life. Previous studies focused on the retrieval of so-called failed implants during surgical revision. Interest is now moving to the study of successful implants, which are those still in place at the patient's death. A procedure was developed for recruitment of implant patients and their families and for safe and effective device and tissue retrieval after death. More than 50 retrievals were performed to support various research efforts.

Arthroplasty, Replacement↗
PubMed1999

Effect of brain stem NMDA-receptor blockade by MK-801 on behavioral and fos responses to vagal satiety signals.

To test the possible role of N-methyl-D-aspartate (NMDA) glutamate receptors in the transmission of gastrointestinal satiety signals at the level of the nucleus of the solitary tract (NTS), we assessed the effect of fourth ventricular infusion of the noncompetitive NMDA receptor antagonist MK-801 on short-term sucrose intake and on gastric distension-induced Fos expression in the dorsal vagal complex of unanesthetized rats. MK-801, although not affecting initial rate of intake, significantly increased sucrose intake during the later phase of the meal (10-30 min, 8.9 +/- 1.0 vs. 2.9 +/- 0.8 ml, P < 0.01). In the medial subnucleus of the NTS, the area postrema, and the dorsal motor nucleus, MK-801 did not reduce gastric distension-induced Fos expression and itself did not significantly induce Fos expression. In the dorsomedial, commissural, and gelatinosus subnuclei, MK-801 in itself produced significant Fos expression and significantly reduced (-75%, P < 0.05) the ability of gastric distension to induce Fos expression, assuming an additive model with two separate populations of neurons activated by distension and the blocker. Although these results are consistent with NMDA receptor-mediated glutamatergic transmission of vagal satiety signals in general, they lend limited support for such a role in the transmission of specific gastric distension signals.

Animals↗
PubMed1998

Metal release in patients who have had a primary total hip arthroplasty. A prospective, controlled, longitudinal study.

UNLABELLED: There is an increasing recognition that, in the long term, total joint replacement may be associated with adverse local and remote tissue responses that are mediated by the degradation products of prosthetic materials. Particular interest has centered on the metal-degradation products of total joint replacements because of the known toxicities of the metal elements that make up the alloys used in the implants. We measured the concentrations of titanium, aluminum, cobalt, and chromium in the serum and the concentration of chromium in the urine of seventy-five patients during a three-year prospective, longitudinal study. Twenty patients had had a so-called hybrid total hip replacement (insertion of a modular cobalt-alloy femoral stem and head with cement and a titanium acetabular cup without cement), fifteen had had insertion of an extensively porous-coated cobalt-alloy stem with a cobalt-alloy head and a titanium-alloy socket without cement, and twenty had had insertion of a proximally porous-coated titanium-alloy stem with a cobalt-alloy head and a titanium socket without cement. The remaining twenty patients did not have an implant and served as controls. The results of our study showed that, thirty-six months postoperatively, patients who have a well functioning prosthesis with components containing titanium have as much as a threefold increase in the concentration of titanium in the serum and those who have a well functioning prosthesis with cobalt-alloy components have as much as a fivefold and an eightfold increase in the concentrations of chromium in the serum and urine, respectively. The predominant source of the disseminated chromium-degradation products is probably the modular head-neck junction and may be a function of the geometry of the coupling. Passive dissolution of extensively porous-coated cobalt-alloy stems was not found to be a dominant mode of metal release. CLINICAL RELEVANCE: Increased concentrations of circulating metal-degradation products derived from orthopaedic implants may have deleterious biological effects over the long term that warrant investigation. This is a particularly timely concern because of recent clinical trends, including the reintroduction of metal-on-metal bearing surfaces and the increasing popularity of extensively porous-coated devices with large surface areas of exposed metal. Accurate monitoring of the concentrations of metal in the serum and urine after total hip replacement also can provide insights into the mechanisms of metal release. Our findings suggest that fretting corrosion at the head-neck coupling is an important source of metal release that can lead to increased concentrations of chromium in the serum. Determinations of the concentrations of metal in the serum and urine may be useful in the diagnosis of patients who are symptomatic after a total joint replacement as increased levels are indicative of at least one mode of mechanical dysfunction (for example, fretting corrosion) of the device.

Adult↗
PubMed1997

Capsaicin-resistant vagal afferent fibers in the rat gastrointestinal tract: anatomical identification and functional integrity.

The presence and distribution of vagal fibers and terminals throughout esophagus and gastrointestinal tract that could be anterogradely labeled by nodose ganglion tracer injections was quantitatively assessed in capsaicin- and vehicle-pretreated adult rats, in order to identify the capsaicin-resistant population. Up to 90% of the intraganglionic laminar endings (IGLEs), in the myenteric plexus of the esophagus, and 70-90% in the stomach, as well as 57% of the intramuscular endings or arrays (IMAs) in the fundic stomach survived the capsaicin treatment, while in the upper small intestine only few and in the lower small intestine, the cecum and colon, virtually no IGLEs survived capsaicin treatment. Intramucosal terminals were not assessed. Furthermore, gastric balloon distension-induced c-Fos expression in the dorsal vagal complex was not significantly decreased in capsaicin-treated rats. It is concluded that among primary vagal afferents there is a capsaicin-resistant population that primarily innervates the esophagus and upper gastrointestinal tract, and a capsaicin-sensitive population that innervates mainly the lower tract. At least vagal gastric tension-sensitive afferents also seems to be functionally intact in that they may be capable of synaptically activating second-order neurons in the brainstem.

Animals↗
PubMed1997

Distribution and structure of vagal afferent intraganglionic laminar endings (IGLEs) in the rat gastrointestinal tract.

Intraganglionic laminar endings (IGLEs) are special terminal structures of vagal afferent fibers and have been demonstrated in the myenteric plexus of esophagus and stomach. In order to quantitatively map their presence and distribution over the entire gastrointestinal tract, including the small and large intestines, vagal afferents were anterogradely labeled in vivo by microinjections of the fluorescent carbocyanine dye DiI into the left or right nodose ganglion of adult male rats. In the most successfully labeled cases the highest density of IGLEs was found in the stomach, with about half to one-third of the myenteric ganglia receiving at least one IGLE. The proportion of myenteric ganglia innervated by IGLEs decreased in the small intestine; however, because of its large surface area this gut segment was estimated to contain the highest total number of IGLEs. Both the cecum and colon also contained significant numbers of IGLEs. In the stomach, this vagal afferent innervation by IGLEs was more or less lateralized, with less than 20% of labeled IGLEs found on the contralateral side with respect to the injection. The left/ventral vagus contributed a larger proportion of IGLEs to the proximal duodenum, while the right/dorsal vagus contributed a larger proportion of IGLEs to the distal duodenum and jejunum. Laser scanning confocal microscopy on select specimens revealed further structural details. The parent axon typically formed two or more branches that flanked the ganglia laterally, and in turn produced numerous highly arborizing laminar terminal branches that covered one or both flat sides of the ganglion in a dome-like fashion. The similar distribution patterns and structural details suggest a uniform function for the IGLEs throughout the gastrointestinal tract, but there is as yet no clear proof for any of the hypothesized roles as specialized mechanosensors or local effector terminals.

Animals↗
PubMed1997

Limited excitatory local effector function of gastric vagal afferent intraganglionic terminals in rats.

Intraganglionic laminar endings (IGLEs) are complex terminal structures of vagal afferent origin, distributed throughout the myenteric plexus of the esophagus and gastrointestinal tract and without a known function. They may serve local effector function by means of peripheral axon reflexes, analogously to dorsal root afferents. To test this possibility, vagal afferent fibers were antidromically activated by suprathreshold electrical stimulation of the cervical vagus nerve in anesthetized rats that underwent prior supranodose vagotomy, and responses of myenteric neurons were monitored with Fos immunocytochemistry. Stimulation of vagal afferents produced Fos expression in a slightly, but significantly, higher proportion of myenteric plexus neurons of the gastric corpus (1.02 +/- 0.21%, P < 0.05) and esophagus (1.59 +/- 0.46%, P < 0.05) than in control animals with sham-stimulation (corpus, 0.12 +/- 0.05%; esophagus, 0.18 +/- 0.18%). Stimulation of vagal efferents produced widespread Fos induction in myenteric neurons. Given the many enteric neurons in close anatomic contact with IGLEs and the low proportion of Fos activated neurons after selective afferent stimulation, the results do not support a widespread excitatory local effector function of IGLEs. However, inhibitory effects and/or weak excitatory synaptic inputs that do not engage Fos expression cannot be ruled out.

Analysis of Variance↗
PubMed1996

Innervation of rat abdominal paraganglia by calretinin-like immunoreactive nerve fibers.

The extended hepatic pedicle of the rat containing the vagal hepatic branch and associated paraganglia was dissected as whole mount, processed for calretinin immunocytochemistry, and analyzed by laser-scanning confocal microscopy. About half of the 8-12 paraganglia of the region were innervated to a various degree by calretinin-immunoreactive (CAL-IR) nerve fibers that formed basket-like varicose terminals around small clusters of glomus tissue. Neither the numerous capillaries, nor the occasional non-CAL-IR neuron accompanying some paraganglia, were recipients of CAL-IR terminals. In animals with prior left cervical vagotomy the number of CAL-IR fibers was decreased but not abolished. Since about 30% of neurons in the nodose ganglia, a few neurons within the vagal hepatic branch/hepatic hilus area, and numerous neurons in the gastric myenteric plexus were CAL-IR, these neurons represent other potential sources of CAL-IR innervation of the paraganglia.

Animals↗
PubMed1996

Anatomical relationship between vagal afferent fibers and CCK-immunoreactive entero-endocrine cells in the rat small intestinal mucosa.

There is evidence for a pathway involving small intestinal CCK-producing entero-endocrine cells and visceral afferent nerve fibers in signaling the effect of luminal nutrients on gastrointestinal and food intake regulation. In order to investigate the type of anatomical apposition that exists between CCK cells and vagal afferents, CCK immunocytochemistry was performed on tissue from rats whose vagal afferent fibers to the abdomen had previously been labeled in vivo by injecting the fluorescent carbocyanine dye DiI into the nodose ganglia. CCK immunoreactive (CCK-IR) cells were more abundant than vagal afferent fibers, but both were present throughout the small intestine as well as in crypts and villi. Few CCK-IR cells were in close (< 5 microns) anatomical contact with vagal afferent axons, and the latter did not produce suspicious terminal specializations near CCK-IR cells. Most labeled vagal afferent axons, which distributed strictly within the crypt and villous lamina propria, were at distances of tens to hundreds of microns to the nearest CCK-IR cell. These findings strongly support the idea that CCK released from entero-endocrine cells acts on vagal sensory fibers in a paracrine fashion, but do not rule out the presence of a few very close, neurocrine-like contacts or a humoral mode of action. Possible implications of such an arrangement on CCK-mediated satiety are discussed.

Afferent Pathways↗
PubMed1993

Adaptation six months after multiple trauma: a pilot study.

This pilot study investigated the functional and psychosocial adaptation of 18 survivors of multiple trauma who were in the home setting 6 months after discharge from a tertiary trauma center. Seventeen subjects reported complete functional independence and one reported the need for assistance with self-care activities as measured by the Modified Barthel Index. All subjects reported problems with psychosocial adaptation as measured by the Psychosocial Adjustment to Illness Scale (PAIS). Subjects with high PAIS scores (worst adaptation) reported problems in all domains of the PAIS, whereas those with low PAIS scores (best adaptation) reported most problems in health care orientation. Mann-Whitney U tests were significant for gender, household composition and employment status when compared with low PAIS scores (p < 0.05). An analysis of variance confirmed employment status was the best predictive factor for low PAIS scores.

Abbreviated Injury Scale↗
PubMedDate not supplied

Diabetes insipidus versus syndrome of inappropriate antidiuretic hormone.

Diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone (SIADH) are two endocrine disorders presenting a challenge to the critical care nurse. The challenge lies in the recognition and assessment of the effects on the patient's fluid balance and in the planning of interventions to prevent complications.

Diabetes Insipidus↗
PubMedDate not supplied

Implementation of a pain management program in a community hospital.

Literature reports and staff concerns about management of patients' pain prompted nurses in a 337-bed suburban community hospital to implement a pain management education program. The Task Force tackled physician collaboration, securing resources, revising documentation tools, and designing an educational workshop. Their efforts resulted in the purchase of audiovisual materials for staff and patient use, addition of information about patient-controlled analgesia (PCA) devices to the hospital closed-circuit patient education TV channel, distribution of the Agency for Health Care Policy and Research (AHCPR) guidelines to hospital staff, revision of documentation tools, and the implementation of a 4-hour pain management education workshop for all professional nurses. Quality monitoring after the workshop reflected an improvement in nursing documentation of pain management.

Analgesia, Patient-Controlled↗