Academic literature on the topic 'Substance P; cerebral edema; rats'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Substance P; cerebral edema; rats.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Substance P; cerebral edema; rats"
1
Levasseur, Joseph E., John L. Patterson, Claudia I. Garcia, Michael A. Moskowitz, Sung C. Choi, and Hermes A. Kontos. "Effect of neonatal capsaicin treatment on neurogenic pulmonary edema from fluid-percussion brain injury in the adult rat." Journal of Neurosurgery 78, no. 4 (April 1993): 610–18. http://dx.doi.org/10.3171/jns.1993.78.4.0610.
Full textAbstract:
✓ The frequent occurrence of acute death from pulmonary failure in experimental head injury studies on Sprague-Dawley rats prompted an investigation into the manner in which acute neurogenic pulmonary edema develops in these animals as a result of an applied fluid pressure pulse to the cerebral hemispheres. Studies were performed in adult animals using histamine H1 and H2 blocking agents, or in adult animals treated as neonates with capsaicin to destroy unmyelinated C-fibers. Recordings were made of either the pulmonary arterial or the right ventricular pressure, and the left atrial and femoral arterial pressures before, during, and after injury to provide a record of the hemodynamic response throughout the development of neurogenic pulmonary edema. Head injury triggered the almost immediate development of pressure transients with and without neurogenic pulmonary edema. All rats, regardless of treatment, reacted with nearly identical systemic arterial pressure responses; however, the pulmonary responses followed a time course that was independent of systemic arterial pressure changes. Acute neurogenic pulmonary edema was always associated with a substantial increase in pulmonary arterial and left atrial pressures; conversely, pressure increases of similar magnitude were not always associated with edema. Histamine H1 and H2 blockers significantly reduced the pulmonary pressure surges only in rats free of neurogenic pulmonary edema. All capsaicin-treated rats showed suppressed pulmonary pressure responses, normal lung water content, elevated lung surface tension, and significantly reduced levels of immunoreactive substance P in the spinal cord and vagus nerve. While the pressures cannot clarify how edema influences the observed hemodynamics, they do not support the view that edema is the direct consequence of pulmonary hypertension. It is proposed that neurogenic pulmonary edema is a functional disturbance provoked by adverse stimuli from outside the lungs and that in the rat the primary afferent fiber is essential to the production of this entity.
2
Yang, Guo-Yuan, A. Lorris Betz, Thomas L. Chenevert, James A. Brunberg, and Julian T. Hoff. "Experimental intracerebral hemorrhage: relationship between brain edema, blood flow, and blood-brain barrier permeability in rats." Journal of Neurosurgery 81, no. 1 (July 1994): 93–102. http://dx.doi.org/10.3171/jns.1994.81.1.0093.
Full textAbstract:
✓ There have been few investigations of brain edema formation after intracerebral hemorrhage (ICH), despite the fact that mass effect and edema are important clinical complications. The present study was designed to investigate the time course for the formation and resolution of brain edema and to determine how changes in cerebral blood flow (CBF) and blood-brain barrier (BBB) permeability are temporally related to edema formation following ICH. Anesthetized adult rats received a sterile injection of 100 µl of autologous blood into the caudate nucleus. Water and ion contents were measured immediately, at 4 and 12 hours, and daily to Day 7 (10 time points, six rats at each time) after experimental ICH. The water content of the ipsilateral basal ganglia increased progressively (p < 0.002) over the first 24 hours, then remained constant until after Day 5, when the edema began to resolve. Edema was most severe in the tissue immediately surrounding the hemorrhage; however, it was also present in the ipsilateral cortex, the contralateral cortex, and the basal ganglia. Measurements of local CBF (using [14C]-iodoantipyrine) and BBB permeability (using [3H]-α-aminoisobutyric acid) were obtained in separate groups of six to eight rats at various time intervals between 1 and 48 hours after ICH. Cerebral blood flow was reduced to 50% of control at 1 hour, returned to control values by 4 hours, but then decreased to less than 50% of control between 24 and 48 hours after ICH. The BBB permeability increased significantly prior to the occurrence of significant edema in the tissue surrounding the clot. However, BBB permeability in the more distant structures remained normal despite the development of edema. These results demonstrate a time course for the formation and resolution of brain edema following ICH similar to that observed during focal ischemia. Brain edema forms in the immediate vicinity of the clot as a result of both BBB disruption and the local generation of osmotically active substances and then spreads to adjacent structures. While local ischemia, due to the mass effect of the hemorrhage, may play a role in producing cytotoxic and vasogenic edema, the release of toxic substances from the clot should also be considered. Since edema is nearly maximal by 24 hours after ICH, therapy directed at reducing edema formation must be instituted within the 1st day.
3
Stroemer, R. Paul, and Nancy J. Rothwell. "Cortical Protection by Localized Striatal Injection of IL-1ra Following Cerebral Ischemia in the Rat." Journal of Cerebral Blood Flow & Metabolism 17, no. 6 (June 1997): 597–604. http://dx.doi.org/10.1097/00004647-199706000-00001.
Full textAbstract:
Interleukin-1 (IL-1) receptor antagonist (IL-1ra) markedly reduces infarct volume induced by middle cerebral artery occlusion (MCAO) in the rat, when injected either centrally (intracerebroventricularly) or peripherally. The site or sites of action of IL-1 in stroke pathology, however, are not known. The present study investigated the site(s) of action of IL-1/IL-1ra in ischemic brain damage by studying the effects of local injection of IL-1ra into the cortex or striatum following permanent MCAO in the rat. Cortical injection of IL-1ra (5 µg) did not affect infarct volume in the cortex or striatum measured 24 h after MCAO. In contrast, striatal injection of IL-1ra ipsilateral to the infarction caused a significant and highly reproducible reduction of cortical (37%, p < 0.001) and striatal damage (27%, p < 0.001, corrected for edema) compared with vehicle-injected animals. Injection of IL-1ra (5 µg) into the striatum, contralateral to the infarction, resulted in a small (9%) but significant (p < 0.001) reduction of ipsilateral cortical damage, with no effect on ipsilateral striatal damage. Injection of a higher dose of IL-1ra (7.5 µg) in the contralateral striatum caused a further inhibition of ipsilateral cortical damage (24%, p < 0.001) and a significant reduction of ipsilateral striatal damage (16%, p < 0.001). In separate groups of rats, it was established that core temperature (measured continuously in free-moving animals with remote radiotelemetry) was not affected by striatal or cortical injection of IL-1ra. These data show that injection of IL-1ra into the striatum but not the cortex reduces infarct volume in both the striatum and the cortex, independently of effects on core temperature. These results imply that blocking striatal IL-1 contributes to IL-1ra-protective effects. We hypothesize that IL-1 may influence striatal distal cortical damage through either the release of specific substances or activation of polysynaptic pathways.
4
Song, Jiali, Rongqing Chen, Lin Yang, Ge Zhang, Weichen Li, Zhanqi Zhao, Canhua Xu, Xiuzhen Dong, and Feng Fu. "Electrical Impedance Changes at Different Phases of Cerebral Edema in Rats with Ischemic Brain Injury." BioMed Research International 2018 (June 4, 2018): 1–10. http://dx.doi.org/10.1155/2018/9765174.
Full textAbstract:
Cerebral edema contributes significantly to the morbidity and mortality associated with many common neurologic conditions. Clinically, a diagnostic tool that can be used to monitor cerebral edema in real-time and differentiate between different types of cerebral edema is urgently needed. Because there are differences in electrical impedance between normal cortical tissue and cerebral edema tissue, electrical impedance tomography (EIT) can potentially be used to detect cerebral edema. Accurate recording of the electrical impedance properties of cerebral edema tissue at different time points is important when detecting cerebral edema with EIT. In this study, a rat cerebral edema model was established; then, following the onset of ischemic brain injury, variation in the electrical impedance of cerebral edema was measured at different time points within a 24-hour period and the corresponding morphologic variation was analyzed. After the first six hours, following the onset of ischemic brain injury, the resistivity of brain tissue increased (p < 0.05); during this period, brain cell volume increased (p < 0.05) and the intercellular space decreased (p < 0.05) (behaving like cytotoxic cerebral edema). From 6 to 24 hours, the resistivity of brain tissue decreased; during this time, brain cell volume unchanged (p > 0.05) while intercellular space increased (p < 0.05) (behaving like vasogenic cerebral edema). These findings support the notion that EIT can be used to monitor the development of cerebral edema in real-time and differentiate between different types of brain edema.
5
Donkin, James J., Alan J. Nimmo, Ibolja Cernak, Peter C. Blumbergs, and Robert Vink. "Substance P is Associated with the Development of Brain Edema and Functional Deficits after Traumatic Brain Injury." Journal of Cerebral Blood Flow & Metabolism 29, no. 8 (May 13, 2009): 1388–98. http://dx.doi.org/10.1038/jcbfm.2009.63.
Full textAbstract:
Brain edema and swelling is a critical factor in the high mortality and morbidity associated with traumatic brain injury (TBI). Despite this, the mechanisms associated with its development are poorly understood and interventions have not changed in over 30 years. Although neuropeptides and neurogenic inflammation have been implicated in peripheral edema formation, their role in the development of central nervous system edema after brain trauma has not been investigated. This study examines the role of the neuropeptide, substance P (SP), in the development of edema and functional deficits after brain trauma in rats. After severe diffuse TBI in adult male rats, neuronal and perivascular SP immunoreactivity were increased markedly. Perivascular SP colocalized with exogenously administered Evans blue, supporting a role for SP in vascular permeability. Inhibition of SP action by administration of the neurokinin-1 (NIC,) antagonist, N-acetyl-l-tryptophan, at 30 mins after trauma attenuated vascular permeability and edema formation. Administration of the NIC, antagonist also improved both motor and cognitive neurologic outcomes. These findings suggest that SP release is integrally linked to the increased vascular permeability and edema formation after brain trauma, and that treatment with an NIC, receptor antagonist reduces edema and improves neurologic outcome.
6
Mansfield, Robert T., Joanne K. Schiding, Ronald L. Hamilton, and Patrick M. Kochanek. "Effects of Hypothermia on Traumatic Brain Injury in Immature Rats." Journal of Cerebral Blood Flow & Metabolism 16, no. 2 (March 1996): 244–52. http://dx.doi.org/10.1097/00004647-199603000-00009.
Full textAbstract:
Hypothermia is beneficial in adult models of traumatic brain injury (TBI), but it has not been evaluated in an immature animal model. We hypothesized that brief hypothermia applied after TBI would reduce cerebral edema and lesion volume in immature rats. Male Wistar rats (3–4 weeks of age, 90–140 g) were anesthetized, intubated, mechanically ventilated, and subjected to TBI by a weight drop onto the exposed right parietal cortex. Hypothermic rats were then cooled to a brain temperature of 32.0 ± 0.5°C for 4 h, and control rats were maintained at a brain temperature of 37.0 ± 0.5°C. Cerebral edema (wet — dry weight method) was assessed at 4 and 24 h, and lesion volume was assessed at 5 days. At 4 h, a reduction of percent brain water in the traumatized hemisphere was observed in hypothermic versus normothermic rats (81.75 ± 0.60 vs. 82.53 ± 0.67%; p < 0.05), but by 24 h posttrauma, the groups were similar (p = 0.82). Total lesion volume (47.2 ± 8.5 vs. 44.4 ± 10.0 mm3; p = 0.51) and necrotic volume (20.2 ± 6.3 vs. 20.0 ± 7.9 mm3; p = 0.95) were similar in the hypothermic and normothermic groups. We conclude that in this model, a transient (4-h) application of moderate (32°C) hypothermia reduces the cerebral edema characteristically seen in immature rats at 4 h, but this reduction is not sustained at 24 h. Attenuating or delaying the development of cerebral edema could have important therapeutic relevance after TBI. Transient hypothermia, however, did not reduce lesion volume at 5 days posttrauma.
7
Kollmar, Rainer, Thomas Frietsch, Dimitrios Georgiadis, Wolf-Rüdiger Schäbitz, Klaus F. Waschke, Wolfgang Kuschinsky, and Stefan Schwab. "Early Effects of Acid-Base Management during Hypothermia on Cerebral Infarct Volume, Edema, and Cerebral Blood Flow in Acute Focal Cerebral Ischemia in Rats." Anesthesiology 97, no. 4 (October 1, 2002): 868–74. http://dx.doi.org/10.1097/00000542-200210000-00018.
Full textAbstract:
Background Although the frequency for the use of moderate hypothermia in acute ischemic stroke is increasing, the optimal acid-base management during hypothermia remains unclear. This study investigates the effect of pH- and alpha-stat acid-base management on cerebral blood flow (CBF), infarct volume, and cerebral edema in a model of transient focal cerebral ischemia in rats. Methods Twenty Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion (MCAO) for 2 h during normothermic conditions followed by 5 h of reperfusion during hypothermia (33 degrees C). Animals were artificially ventilated with either alpha- (n = 10) or pH-stat management (n = 10). CBF was analyzed 7 h after induction of MCAO by iodo[(14)C]antipyrine autoradiography. Cerebral infarct volume and cerebral edema were measured by high-contrast silver infarct staining (SIS). Results Compared with the alpha-stat regimen, pH-stat management reduced cerebral infarct volume (98.3 +/- 33.2 mm(3) vs. 53.6 +/- 21.6 mm(3); P > or = 0.05 mean +/- SD) and cerebral edema (10.6 +/- 4.0% vs. 3.1 +/- 2.4%; P > or = 0.05). Global CBF during pH-stat management exceeded that of alpha-stat animals (69.5 +/- 12.3 ml x 100 g(-1) x min(-1) vs. 54.7 +/- 13.3 ml x 100 g(-1) x min; P > or = 0.05). The regional CBF of the ischemic hemisphere was 62.1 +/- 11.2 ml x 100 g(-1) x min(-1) in the pH-stat group versus 48.2 +/- 7.2 ml x 100 g(-1) x min(-1) in the alpha-stat group ( P> or = 0.05). Conclusions In the very early reperfusion period (5 h), pH-stat management significantly decreases cerebral infarct volume and edema as compared with alpha-stat during moderate hypothermia, probably by increasing CBF.
8
Sohn, Youngjoo, Ho Chang Kang, Kon Sik Kim, Sun-Min Park, Nak-Won Sohn, Hyuk-Sang Jung, and Sung-Hoon Kim. "Protective Effects of Natrii Sulfas on Cerebral Focal Ischemia Induced by MCAO in Rats." American Journal of Chinese Medicine 37, no. 02 (January 2009): 273–93. http://dx.doi.org/10.1142/s0192415x09006849.
Full textAbstract:
This study examined the effect of Natrii sulfas, a treatment for stroke patients suffering constipation in Oriental medicine, on the physiological indices and brain edema of rats. Brain edema was induced by a middle cerebral artery occlusion (MCAO), Natrii sulfas was administered after the MCAO. At 3, 6, 15, 24, and 48 hours after reperfusion, the physiological indices such as the fecal weight, urine volume and water content in the stools were assessed. The edema index was measured 48 hours after reperfusion. At 48 hours, the expressions of iNOS, MMP9, VEGF, GFAP, Bax, Bcl-2, c-Fos, and HSP72 positive astrocytes were observed on the brain tissues by immunohistochemistry. Natrii sulfas significantly improved the decrease in fecal weight, urine volume and water content in the stool caused by the ischemic insult (p < 0.05) and attenuated the brain edema caused by the ischemia insult (p < 0.05). Natrii sulfas significantly down-regulated iNOS and MMP9 expressions and attenuated the astrocyte swelling due to brain edema in the penumbra of the cerebral cortex of MCAO rats. Natrii sulfas reduced the excess Bax and HSP72 expressions in ischemic brain, which was statistically significant in the penumbra of the cerebral cortex but not in the caudate putamen. These results suggest Natrii sulfas has a protective effect on ischemia-induced brain edema and improves the physiological symptoms.
9
Cherpakov, R. A., and O. A. Grebenchikov. "Effect of Lithium Chloride Concentration on Its Neuroprotective Properties in Ischemic Stroke in Rats." General Reanimatology 17, no. 5 (October 23, 2021): 101–10. http://dx.doi.org/10.15360/1813-9779-2021-5-101-110.
Full textAbstract:
Currently, a number of experimental studies have demonstrated compelling evidence of neuro-, cardio-, and nephroprotective properties of medications containing lithium chloride.Aim of the study. To evaluate the effect of various concentrations of lithium chloride on ischemic stroke volume and perifocal edema in rats after cerebral ischemia.Material and methods. Male mongrel rats weighing 315±13.5 g were used in the study. The focal ischemia model according to Longa et al. was employed. The animals (n=35) were divided into 5 groups: sham-operated, control group (ischemic stroke model with NaCl 0.9% administration) and three groups who received lithium chloride in different concentrations (4.2 mg/kg, 21 mg/kg and 63 mg/kg). Lithium chloride was administered immediately after cessation of middle cerebral artery occlusion and then every 24 h until euthanasia. To assess the degree of brain damage, the animals underwent magnetic resonance imaging (MRI) on day 2, and brain sections stained with 2,3,5-triphenyltetrazolium chloride were evaluated after euthanasia on day 7. Intergroup differences were assessed using the Mann-Whitney criterion.Results. According to MRI data, lithium chloride at a dose of 4.2 mg/kg had no significant effect on ischemic stroke volume and perifocal edema versus the control group on day 2 (P=0.9). With lithium chloride at 21 mg/kg, stroke volume and perifocal edema were significantly lower than in the control group (by 25%, P=0.04 and 18%, P=0.03, respectively). Lithium chloride at a dose of 63 mg/kg was more likely to reduce stroke volume (by 45%, P=0.004) and perifocal edema (by 35%, P=0.007). When determining lesion volume on day 7, the data were comparable to those obtained on day 2. With the 21 mg/kg dose, stroke volume was 20% lower than in the control group (P=0.04). Lithium chloride, 63 mg/kg, reduced stroke volume by 40% (P=0.004).Conclusion. Lithium chloride dose affects necrotic focus formation and manifestations of perifocal cerebral edema after middle cerebral artery occlusion. The maximum reduction in the volume of ischemic stroke and perifocal edema was observed when the 63 mg/kg dose was used.
10
Borson, D. B., J. J. Brokaw, K. Sekizawa, D. M. McDonald, and J. A. Nadel. "Neutral endopeptidase and neurogenic inflammation in rats with respiratory infections." Journal of Applied Physiology 66, no. 6 (June 1, 1989): 2653–58. http://dx.doi.org/10.1152/jappl.1989.66.6.2653.
Full textAbstract:
Neuropeptides such as substance P are implicated in inflammation mediated by sensory nerves (neurogenic inflammation), but the roles in disease of these peptides and the peptidases that degrade them are not understood. It is well established that inflammation is a prominent feature of several airway diseases, including viral infections, asthma, bronchitis, and cystic fibrosis. These diseases are characterized by cough, airway edema, and abnormal secretory and bronchoconstrictor responses, all of which can be elicited by substance P. The effects of substance P and other peptides that may be involved in inflammation are decreased by endogenous neutral endopeptidase (NEP; also called enkephalinase, EC 3.4.24.11), which is a peptidase that degrades substance P and other peptides. In the present study, we report that rats with histories of infections caused by common respiratory tract pathogens (parainfluenza virus type 1, rat corona-virus, and Mycoplasma pulmonis) not only have greater susceptibility to neurogenic inflammatory responses than do pathogen-free rats but also have a lower activity of NEP in the trachea. This reduction in NEP activity may cause the increased susceptibility to neurogenic inflammation by allowing higher concentrations of substance P to reach tachykinin receptors in the trachea. Thus decreased NEP activity may exacerbate some of the pathological responses in animals with respiratory tract infections.
Dissertations / Theses on the topic "Substance P; cerebral edema; rats"
1
Hassan, Islam Khamis Ahmed Mohamed. "The role of substance P in cerebral edema associated with rat and human infarction and contusion." Thesis, 2006. http://hdl.handle.net/2440/69464.
Full textAbstract:
An important influence on the severity of both traumatic brain injury (TBI) and stroke is cerebral edema, but its mechanism is poorly understood. Recent evidence suggests that substance P (SP) plays a role in this edema and that injured SP-containing perivascular nerve fibres are involved. A study which examined tissue obtained from rat models and human post mortem infarct and contusion tissue, demonstrated that in all the examined tissue, perivascular SP-IR was present in astrocytic processes rather than in nerve fibres. This implies that perivascular astrocytic processes might be more important than perivascular nerve fibres in any effect that SP may have on the blood brain barrier in the settings of infarction and contusion.Thesis (M.Med.Sc.) -- University of Adelaide, Dept. of Pathology, 2006
Book chapters on the topic "Substance P; cerebral edema; rats"
1
Potargowicz, E., and W. Z. Traczyk. "Suppression of Noradrenaline-Induced Ovulation by Administration of Substance P into the Third Cerebral Ventricle in Pseudo-Pregnant Rats." In Substance P and Neurokinins, 321–23. New York, NY: Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4612-4672-5_108.
Full text