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Results for “peripheral response”

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PubMed1994

Postnatal development of nitric oxide synthase type 1 expression in the lumbar spinal cord of the rat: a comparison with the induction of c-fos in response to peripheral application of mustard oil.

The distribution of the neuronal isoform of the enzyme nitric oxide synthase (type 1) has been investigated in the lumbar spinal cords of neonatal rats (2-20 days old). Large multipolar neurones were present from day 2 around the central canal, in a band across the neck of the dorsal horn and at the thoracic level in the intermediolateral cell column, whereas staining was absent from laminae II. By 20 days the laminae II staining was similar to that found in the adult. NOS expression in lamina II paralleled the development of c-fos expression in this lamina in response to peripheral application of mustard oil.

Administration, Topical↗

PubMed1990

The effect of alpha-adrenergic blockade on responses of peripheral blood cells to acute insulin-induced hypoglycaemia in humans.

Acute hypoglycaemia provokes rapid changes in peripheral blood cell counts. To examine possible adrenergic mechanisms modulating these changes, counts of peripheral blood cells including lymphocytes, granulocytes and erythrocytes were measured in response to acute hypoglycaemia in a group of six normal subjects in control conditions (study 1), and during alpha-adrenergic blockade with phentolamine (study 2). In study 1 hypoglycaemia provoked a biphasic leucocyte response, with an early rise in lymphocyte count and a later rise in granulocyte count. The erythrocyte count increased modestly following hypoglycaemia. During alpha-adrenergic blockage, the rise in total leucocyte count was diminished, with the rise in the lymphocyte count being greatly obtunded. These findings suggest that the increments of peripheral lymphocyte and erythrocyte counts in response to acute insulin-induced hypoglycaemia are mediated via alpha-adrenoreceptors.

Adult↗

PubMed1983

Altered properties and laminar distribution of neuronal responses to peripheral stimulation in the SmI cortex of the arthritic rat.

The properties of the neuronal responses to different types of mechanical peripheral stimulation were studied during electrode penetrations in the first somatosensory cortex of anaesthetized rats with polyarthritis. Very few neurons were driven by light cutaneous stimulation (such as brushing) or by intense mechanical stimulation. Most of the neurons were driven by joint movement and/or moderate pressure on the skin. These neurons could be found in all cortical layers, the majority being located in layer V. These results contrast sharply with the properties and laminar distribution of the different functional categories of cortical neurons, as observed in normal animals.

Animals↗

PubMed1989

[Response of peripheral blood lymphocytes to antigenically nonspecific mitogens in systemic erythematosus].

In 24 patients with systemic lupus erythematosus the proliferating response of lymphocytes of the peripheral blood stream to mitogens PHA, ConA and PWM was examined. The spontaneous incorporation of 3H-thymidine was increased in two patients. The mean response to PHA and PWM was reduced, while the response to ConA was within the normal range. In the active stage of the disease the lymphocyte response was in general lower in the stage of low activity. There was no correlation between the number of CD4 and CD8 lymphocytes nor the CD4/CD8 index and the lymphocyte response to mitogens. In systemic lupus erythematosus the response to PWM was lower than in rheumatoid arthritis, while in rheumatoid arthritis the response to PHA and ConA was lower than in systemic lupus erythematosus.

Concanavalin A↗

PubMed2006

Interleukin-1 beta contributes to the upregulation of kappa opioid receptor mrna in dorsal root ganglia in response to peripheral inflammation.

During local painful inflammation, axonal transport of opioid receptors from dorsal root ganglia toward the periphery is increased, associated with a higher receptor density and enhanced efficacy of opioid analgesics at the injured site. To examine whether this increase is related to transcription, mRNA of the kappa opioid receptor in lumbar dorsal root ganglia was quantified by real time light cycler polymerase chain reaction. In dorsal root ganglia of naive rats, kappa opioid receptor mRNA expression was three-fold higher than previously shown for delta opioid receptor and two times lower than mu opioid receptor mRNA, respectively. After induction of unilateral paw inflammation by Freund's complete adjuvant, kappa opioid receptor mRNA was significantly upregulated with a peak at 12 h in ipsilateral dorsal root ganglia. This effect could be mimicked by intraplantar injection of the proinflammatory cytokine interleukin-1 beta. Kappa opioid receptor mRNA upregulation lasted longer in interleukin-1 beta-treated rats compared with Freund's complete adjuvant-treated rats. Furthermore, a significant increase in kappa opioid receptor positive neurons was detected by immunohistochemistry 24 h after local injection of Freund's complete adjuvant or interleukin-1 beta. In Freund's complete adjuvant-induced inflammation, kappa opioid receptor upregulation was blocked by treatment with interleukin-1 receptor antagonist without changing the leukocyte infiltration in the paw. In conclusion, kappa opioid receptor mRNA and protein in dorsal root ganglia are upregulated in response to peripheral inflammation. This effect can be mimicked by a single local injection of interleukin-1 beta, and Freund's complete adjuvant-induced upregulation in kappa opioid receptor mRNA and protein can be prevented by treatment with interleukin-1 receptor antagonist. These data suggest that the peripheral production of the proinflammatory cytokine interleukin-1 beta is a specific inducer of kappa opioid receptor expression in the dorsal root ganglia.

Animals↗

PubMed2006

Lamotrigine and phenytoin, but not amiodarone, impair peripheral chemoreceptor responses to hypoxia.

Amiodarone, lamotrigine, and phenytoin, common antiarrhythmic and antiepileptic drugs, inhibit a persistent sodium current in neurons (I(NaP)). Previous results from our laboratory suggested that I(NaP) is critical for functionality of peripheral chemoreceptors. In this study, we determined the effects of therapeutic levels of amiodarone, lamotrigine, and phenytoin on peripheral chemoreceptor and ventilatory responses to hypoxia. Action potentials (APs) of single chemoreceptor afferents were recorded using suction electrodes advanced into the petrosal ganglion of an in vitro rat peripheral chemoreceptor complex. AP frequency (at Po(2) approximately 150 Torr and Po(2) approximately 90 Torr), conduction time, duration, and amplitude were measured before and during perfusion with therapeutic dosages of the drug or vehicle. Hypoxia-induced catecholamine secretion within the carotid body was measured using amperometry. With the use of whole body plethysmography, respiration was measured in unanesthesized rats while breathing room air, 12% O(2), and 5% CO(2), before and after intraperitoneal administration of amiodarone, lamotrigine, phenytoin, or vehicle. Lamotrigine (10 microM) and phenytoin (5 microM), but not amiodarone (5 microM), decreased chemoreceptor AP frequency without affecting other AP parameters or magnitude of catecholamine secretion. Similarly, lamotrigine (5 mg/kg) and phenytoin (10 mg/kg) blunted the hypoxic but not the hypercapnic ventilatory response. In contrast, amiodarone (2.5 mg/kg) did not alter the ventilatory response to hypoxia or hypercapnia. We conclude that lamotrigine and phenytoin at therapeutic levels impair peripheral chemoreceptor function and ventilatory response to acute hypoxia. These are consistent with I(NaP) serving an important function in AP generation and may be clinically important in the care of patients using these drugs.

Action Potentials↗

PubMed2005

Central and peripheral psychophysiological responses to trauma-related cues in subclinical posttraumatic stress disorder: a pilot study.

This study examined verbal-subjective, peripheral and central physiological responses of motor vehicle accident (MVA) survivors with subclinical posttraumatic stress disorder (PTSD), without PTSD symptoms as well as healthy controls. Seven persons of each group were exposed to positive, neutral, accident-related and negative, non-accident-related slides. The verbal-subjective ratings of the slides did not differ between the groups. In contrast to the verbal ratings of the trauma-related materials, the behavioral and physiological responses showed a remarkable dissociation from these reports. The startle responses were enhanced to accident-related slides only in the PTSD group and MVA survivors with PTSD had a significantly lower response to the neutral slides than MVA survivors without PTSD. P200 was lower to positive, neutral and negative slides in the PTSD group compared to both other groups. The late positive complex showed no group-related effects. The data suggest that traumatized persons with PTSD show exaggerated emotional responses to trauma-related stimuli and reduced cognitive responses to several types of stimuli that may interfere with the extinction of the emotional trauma memory.

Accidents, Traffic↗

PubMed1981

Voluntary responses to peripheral stimulation in Parkinson's disease. An electrophysiological study.

Voluntary motor responses of 15 patients with Parkinson's disease and 5 normal subjects in the same age group were examined electromyographically. The reaction time (RT) (period of latency) and the successive reaction (SR) time (between two quick repetitive voluntary movements) of the facial, eye and masseter muscles following electrical stimulation from the periphery (thenar muscles) were measured. In the patients the RT and SR time following peripheral stimulation were obviously delayed. These results suggest that cortical motor areas are involved in Parkinson's disease so that, following peripheral stimulation, cortical activity is inhibited for a relatively long time. This occurs most often following two brisk repetitive voluntary muscle movements (SR).

Aged↗

PubMed1991

Thrombolytic treatment in acute myocardial infarction: neutrophil activation, peripheral leucocyte responses, and myocardial injury.

OBJECTIVE: To examine early leucocyte responses and neutrophil activation in acute myocardial infarction treated by streptokinase and to relate the findings to coronary recanalisation and indices of myocardial damage in order to provide further information about the role of neutrophils in the evolution of injury. DESIGN: Group analysis of paired blood samples, obtained before streptokinase treatment and one hour after it, and of three indirect measures of myocardial injury: left ventricular ejection fraction, QRS score, and peak creatine kinase. SETTING: The coronary care unit of a district general hospital. PATIENTS: 39 patients with acute myocardial infarction who underwent paired blood sampling (before streptokinase and one hour after streptokinase) and cardiac catheterisation 5 (3-8) days later. END POINTS: Changes in peripheral white cell and neutrophil counts and plasma elastase one hour after streptokinase infusion. Comparison of these variables in patients with and without patency of the infarct related coronary artery. Correlations between these variables and indirect measures of myocardial injury. RESULTS: Neutrophil activation, as reflected by plasma elastase, increased sharply one hour after streptokinase. Total white cell and neutrophil counts also increased. Changes tended to be more pronounced in patients with patency of the infarct related artery, though the trend was not statistically significant. Neutrophil activation before streptokinase was unrelated to indirect indices of myocardial injury but only one hour after streptokinase a weak negative correlation with left ventricular ejection fraction had developed. Peripheral neutrophil responses showed a similar relation to ejection fraction and also correlated with peak creatine kinase and QRS score. CONCLUSIONS: Thrombolytic treatment in acute myocardial infarction is associated with an abrupt reactive neutrophil response which provides an early measure of injury. It is also associated with neutrophil activation, probably in response to coronary recanalisation and myocardial reperfusion. Activated neutrophils are recognised as mediators of reperfusion injury in experimental infarction and the data in the present study provide preliminary evidence of a similar pathogenic role in the clinical setting.

Aged↗

PubMed1985

Peripheral circulatory responses to 96 hours of eucapnic hypoxia in conscious sheep.

Conscious sheep acclimatizing to hypoxia (PaO2 40 mm Hg, PaCO2 24 mm Hg) respond with increases in cardiac output (Qco) and cerebral blood flow lasting for 24 and 48 h, respectively. Coronary flow increases in a sustained fashion, while there are progressive decreases in renal, splenic and pancreatic flows. In the present study, 5 adult ewes were exposed to similar levels of normobaric hypoxia (PaO2 40 mm Hg) but the PaCO2 was maintained at eucapnic levels (32 mm Hg). VE increased (+210%) while VO2 decreased by 35%. Ventilatory sensitivity to CO2 was unchanged. Qco (thermodilution) was elevated for 96 h (+20%) as stroke volume was maintained at normoxic levels and heart rate increased (+36%). Pulmonary artery pressure increased (+35%) along with plasma catecholamine levels (+116-196%). There were sustained elevations of cerebral flow (radiolabelled microspheres) from 79.1 (+/- 9.2 SEM) to 121.6 ml X min-1 X 100 g-1 (+/- 10.8), coronary flow from 183 (+/- 22.1) to 373 ml X min-1 X 100 g-1 (+/- 46.3), diaphragm flow (+400%) and intercostal muscle flow (+186%) with no apparent redistribution of Qco. Therefore, the cardiac and peripheral circulatory response patterns are altered significantly in eucapnic hypoxia. The rate of O2 delivery to brain and several abdominal viscera is higher.

Animals↗

PubMed1984

Peripheral circulatory response to feeding in newborn low-birth-weight infants.

The effect of feeding on calf blood flow (CBF) was investigated in 27 preterm and 10 term small-for-gestational-age (SGA) neonates using the venous occlusion plethysmographic method pre- and postprandially. Blood pressure and heart rate were simultaneously monitored. Feeding consisted of commercially prepared formula with average amounts of 20 ml/kg for preterm and 30 ml/kg for term SGA infants. As a group, the preterm neonates showed no significant CBF changes 1/2 h postprandially from the control value of 8.4 +/- 2.6 ml/min/100 ml (mean +/- SD). Although the difference was not statistically significant, 10 of the 27 preterm infants showed a mean CBF decrease of 9% and 17 showed no change to a slight increase immediately postprandially. These changes were followed by a 35% mean increment in CBF of all preterm infants at 2-2 1/2 h postprandially. CBF decreased in term SGA infants by 40% at 1/2 h postprandially from a control flow of 8.6 +/- 2.9 ml/min/100 ml (p less than 0.01). CBF returned to the control level 1-1 1/2 h postprandially and superseded the control value by 16% at 2-2 1/2 h. Peripheral vascular resistance varied inversely with CBF. Blood pressure and heart rate showed no significant changes. These observations indicated that unlike term infants, most preterm infants manifest no significant immediate peripheral vascular response to feeding before the onset of a hyperdynamic circulatory state. This difference was related to gestational age rather than to birth weight as term SGA infants responded like term appropriate-for-gestational-age infants. The possible mechanisms involved in these CBF changes with feeding are discussed.

Blood Circulation↗

PubMed1995

Gliadin-specific T cell responses in peripheral blood of healthy individuals involve T cells restricted by the coeliac disease associated DQ2 heterodimer.

Coeliac disease (CD) is probably caused by an abnormal immune response towards wheat gliadin in the small intestine. We found that gliadin-specific T cells from the small intestinal mucosa of HLA-DQ2 positive CD patients were almost exclusively restricted by the disease-associated DQ2 molecule. In the peripheral blood of CD patients, a large proportion of gliadin-specific T cells were found to be restricted by DQ molecules, including DQ2, but many were instead restricted by DR or DP molecules of the patient. We have now investigated gliadin-specific T cell responses in peripheral blood from healthy individuals. Four of 20 persons tested had strong in vitro responses and were used as donors for gliadin-specific T cell clones. We found gliadin-specific T cells restricted by the CD-associated DQ2 molecule in peripheral blood for two of these four individuals. It is the presence of such T cells also in the small intestinal mucosa which seems typical of CD.

Antibodies, Monoclonal↗

PubMed1999

Depressed proliferative responses by peripheral blood mononuclear cells from early arthritis patients to mycobacterial heat shock protein 60.

OBJECTIVES: T-cell responses to mycobacterial heat shock protein 60 (M.hsp60) have been implicated in the pathogenesis of adjuvant arthritis, but whether they play a role in rheumatoid arthritis (RA) is undefined. We therefore examined T-cell responses to M.hsp60 and to other recall antigens in a cohort of patients with early RA and in healthy controls. METHODS: In vitro peripheral blood mononuclear cells' (PBMC) proliferative responses to antigen were measured by [3H]thymidine incorporation, and results correlated with clinical and laboratory features of disease. RESULTS: Whereas responses to the recall antigens tetanus toxin and purified protein derivative (PPD) were equivalent in the two groups, responses to both M.hsp60 and the Escherichia coli hsp60 were lower in the RA patients. These results could not be explained by either the higher prevalence of HLA-DR4 in the RA group, or the disease severity of the patients. CONCLUSION: In the light of results from the adjuvant arthritis model which suggest that arthritis may be ameliorated by the actions of an hsp60-reactive T-cell population, the lack of response to M.hsp60 in RA could contribute to disease persistence.

Adult↗

PubMed1986

Further evidence that insulin metabolism is a major determinant of peripheral insulin response to oral glucose in subjects with mild glucose intolerance.

In mild glucose intolerance plasma concentration of C-peptide seems to give an estimate of pancreatic B cell secretion more reliable than plasma insulin itself. In the present study we measured the plasma levels of insulin and C-peptide after oral glucose load in 100 mildly glucose intolerant subjects, focusing our attention on high and low insulin responders. According to an insulin incremental area after oral glucose higher or lower than the mean +/- SD of the mean, 16 subjects were classified as "high insulin responders", and 17 as "low insulin responders". The two groups were similar for sex, age and bw. Mean insulin incremental area was almost 9-fold greater in high insulin responders than in low insulin responders (0.88 +/- 0.03 vs 0.10 +/- 0.01 pmol/ml min, p less than 0.001). Also mean C-peptide incremental area was significantly greater in high insulin responders than in low insulin responders, but the differences between the two groups were smaller. Indeed, mean C-peptide area was approximately 2.5-fold greater in high insulin responders than in low insulin responders (1.58 +/- 0.12 vs 0.66 +/- 0.07 pmol/ml min, p less than 0.001). These results give further support to the concept that in mild glucose intolerance insulin metabolism is a major determinant of peripheral insulin response to oral glucose load.

Adult↗

PubMed2001

Peripheral flow response to transient arterial forearm occlusion does not reflect myocardial perfusion reserve.

BACKGROUND: Ultrasonographic evaluation of systemic arterial function is widely available, and a close relation of endothelial function in the coronary and brachial arteries has been documented. It is unknown, however, whether a similar correlation exists for their 2 microcirculatory territories and thus whether assessment of the systemic microcirculation can be used similarly as a surrogate marker of myocardial perfusion. METHODS AND RESULTS: Twenty-three patients with documented coronary artery disease (CAD; 66+/-9 years old, 18 men), 16 patients with syndrome X (SX; 56+/-5 years old, 13 women), and 45 healthy control subjects (C; 34+/-9 years old, 22 men) were studied. Myocardial perfusion was measured at rest and after dipyridamole (0.56 mg. kg(-1). min(-1) over 4 minutes) by PET, and brachial artery blood flow was measured at rest and after transient forearm ischemia by standard Doppler ultrasound techniques. Dipyridamole increased myocardial perfusion in all groups (mL. g(-1). min(-1): CAD, 0.89+/-0.27 versus 1.62+/-0.67, P:<0.001; SX, 0.82+/-0.16 versus 1.67+/-0.49, P:<0.001; and C, 0.82+/-0.15 versus 2.32+/-0.64, P:<0.001). Postocclusion forearm flow increased similarly in all groups (CAD, 52+/-18 versus 174+/-77 mL/min, P:<0.001; SX, 49+/-29 versus 202+/-82 mL/min, P:<0.001; and C, 61+/-34 versus 229+/-108 mL/min, P:<0.001). No significant correlations were found between peripheral and myocardial microcirculatory beds for either resting flow, hyperemic flow, or flow reserve in any of the groups (r(2)<0.1, P:=NS). CONCLUSIONS: The peripheral perfusion responses to transient forearm ischemia do not correlate with dipyridamole-induced myocardial hyperemia. The lack of correlation indicates different mechanisms of microvascular activation or regulation and confirms that extrapolations between findings in the 2 vascular beds are not suitable.

Adult↗

PubMed2006

Sympathoexcitatory response to peripheral chemoreflex activation is enhanced in juvenile rats exposed to chronic intermittent hypoxia.

In the present study, we tested the hypothesis that chronic intermittent hypoxia (CIH) produces changes in the autonomic and respiratory responses to acute peripheral chemoreflex activation. To attain this goal, 3-week-old rats were exposed to 10 days of CIH (6% O(2) for 40 s at 9 min intervals; 8 h day(-1)). They were then used to obtain a working heart-brainstem preparation and, using this unanaesthetized experimental preparation, the chemoreflex was activated with potassium cyanide (0.05%, injected via the perfusion system), and the thoracic sympathetic nerve activity (tSNA), heart rate and phrenic nerve discharge (PND) were recorded. Rats subjected to CIH (n = 12), when compared with control animals (n = 12), presented the following significant changes in response to chemoreflex activation: (a) an increase in tSNA (78 +/- 4 versus 48 +/- 3%); (b) a long-lasting increase in the frequency of the PND at 20 (0.52 +/- 0.03 versus 0.36 +/- 0.03 Hz) and 30 s (0.40 +/- 0.02 versus 0.31 +/- 0.02 Hz) after the stimulus; and (c) a greater bradycardic response (-218 +/- 20 versus -163 +/- 16 beats min(-1)). These results indicate that the autonomic and respiratory responses to chemoreflex activation in juvenile rats previously submitted to CIH are greatly increased.

Animals↗

PubMed1989

Effects of tizanidine, eperisone and afloqualone on feline dorsal horn neuronal responses to peripheral cutaneous noxious and innocuous stimuli.

The effects of eperisone and afloqualone have been compared with those of tizanidine on excitatory responses of spinal dorsal horn neurones, evoked by noxious and innocuous peripheral stimuli. Tizanidine, administered intravenously or iontophoretically, resulted in a profound, long-lasting and selective depression of the responses to noxious stimuli. In contrast, intravenous injection of eperisone produced either a rapidly reversible depression of responses to both noxious and innocuous stimuli or had no effect on these responses. Iontophoretic administration of eperisone also reduced neuronal responses to both forms of peripheral stimuli and that induced by quisqualate. This depressant action of eperisone was rapidly reversible but was often accompanied by a reduction of the amplitude of the action potentials. Afloqualone had no depressant action on any evoked response when administered iontophoretically. However, intravenous injection of this agent resulted in weak depressant effects on responses to noxious, innocuous or both types of stimuli, of a few of the neurones tested. This effect of afloqualone was not dose-dependent and was mimicked by control injections of the vehicle in which it was suspended. It is suggested that the muscle relaxants, eperisone and afloqualone, in contrast to tizanidine, do not possess any direct spinal antinociceptive activity.

Air↗

PubMedDate not supplied

Central and peripheral neural responses in acromegaly.

OBJECTIVE: To assess the function of the central and peripheral nervous systems in patients with untreated acromegaly. METHODS: We recorded the somatosensory evoked potentials (SSEPs) and brain stem auditory evoked potentials (BAEPs) in 10 patients with untreated acromegaly of brief duration and in 20 age- and sex-matched healthy control subjects to evaluate the function of the central nervous system and at least the median and tibial components of the peripheral nerves. Electrophysiologic studies were done at the time of diagnosis and before the initiation of any treatment for acromegaly. We also studied the distal motor latency, nerve conduction velocity, compound muscle action potentials, and F response in the peroneal nerve; the sensory nerve conduction velocity and sensory potential amplitude were measured in the sural nerve. RESULTS: The mean duration of acromegaly (expressed as time elapsed since patients first recognized signs or symptoms) was 2.4 years. The N(9) and N(13) latencies in median SSEPs and the N(22) latency in tibial SSEPs were significantly prolonged in patients with acromegaly in comparison with the control group; however, central nervous system components of SSEPs and all components of BAEPs were normal. We also noted abnormalities in peroneal motor and sural sensory nerves. No correlation was found between the neurophysiologic data and the basal growth hormone level, the fasting blood glucose level, or the duration of disease. CONCLUSION: Our results suggest that peripheral, but not central, nervous system involvement exists in patients with untreated acromegaly of short duration.

Journal Article↗