Microinjection of substance P and ACh into rat intermediolateral nucleus elicits cardiovascular responses

1990 ◽  
Vol 259 (2) ◽  
pp. R357-R361
Author(s):  
F. R. Calaresu ◽  
D. J. McKitrick ◽  
E. J. Weernink
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Substance P ◽  
Wistar Rats ◽  
Artificial Ventilation ◽  
Cardiovascular Responses ◽  
Male Wistar Rats ◽  
Excitatory Responses ◽  
The Right ◽  
Intermediolateral Nucleus

The effects of substance P (SP) or acetylcholine (ACh) microinjected into the intermediolateral nucleus of the spinal cord (IMLn) on arterial pressure (AP) and heart rate (HR) were investigated in 22 male Wistar rats under urethan and artificial ventilation. L-Glutamate (Glu) was microinjected into the IMLn between C7 and T4 to locate cardiovascular sites. Micropipettes containing Glu were stereotaxically positioned in 82 histologically verified sites in the IMLn between C7 and T4 on both the right and left sides. Microinjection of 4-10 nl of 0.18 M Glu in 30 of 39 explored sites at the T2 level elicited significant increases in HR (+24.2 +/- 3.1 beats/min). These changes were accompanied by significant increases in mean AP (+11.4 +/- 1.2 mmHg) at the T2 level (32/47 sites). Microinjection of 4-10 nl of SP (3 X 10(-7) to 3 X 10(-4) M) or ACh (0.005-0.5 M) in the right IMLn at the T2 level elicited increases in HR but did not affect AP. The duration of the responses to SP or ACh was significantly longer than the duration of the responses to Glu. The responses to ACh could be blocked by prior microinjection of 5 X 10(-2) M atropine. No responses were ever obtained in the left IMLn by microinjection of Glu, SP, or ACh. These results support the hypothesis that Glu, ACh, and SP mediate sympathoexcitation in the IMLn of the rat and that these excitatory responses have different temporal patterns.

Changes in the substance P-containing innervation of the lumbosacral spinal cord in male Wistar rats as a consequence of ageing

2005 ◽  
Vol 1036 (1-2) ◽  
pp. 139-144 ◽  
Author(s):  
Richard N. Ranson ◽  
David J. Priestley ◽  
Robert M. Santer ◽  
Alan H.D. Watson
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Wistar Rats ◽  
Lumbosacral Spinal Cord ◽  
Male Wistar Rats

Distribution of substance P in the spinal cord of patients with syringomyelia

1996 ◽  
Vol 84 (6) ◽  
pp. 992-998 ◽  
Author(s):  
Thomas H. Milhorat ◽  
Harrison T. M. Mu ◽  
Carole C. LaMotte ◽  
Ade T. Milhorat
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Dorsal Horn ◽  
Ventral Horn ◽  
Immunohistochemical Method ◽  
Positive Staining ◽  
Content Type ◽  
Normal Individuals ◽  
Neurologically Normal ◽  
Intermediolateral Nucleus

✓ The distribution of substance P, a putative neurotransmitter and pain-related peptide, was studied using the peroxidase—antiperoxidase immunohistochemical method in the spinal cords obtained from autopsy of 10 patients with syringomyelia and 10 age- and sex-matched, neurologically normal individuals. Substance P immunoreactivity was present in axons and in terminal-like processes in close apposition to neurons in the first, second, and third laminae of the dorsal horn. Smaller amounts of peroxidase-positive staining were found in the fifth lamina of the dorsal horn, the intermediolateral nucleus, the intermediomedial nucleus, and the ventral horn. In nine of 10 patients with syringomyelia, there was a substantial increase in substance P immunoreactivity in the first, second, third, and fifth laminae below the level of the lesion. A marked reduction or absence of staining was present in segments of the spinal cord occupied by the syrinx. Central cavities produced bilateral abnormalities, whereas eccentric cavities produced changes that were ipsilateral to the lesion. No alterations in staining were found in the spinal cord of an asymptomatic patient with a small central syrinx. The authors conclude that syringomyelia can be associated with abnormalities in spinal cord levels of substance P, which may affect the modulation and perception of pain.

scholarly journals Exercise Reduces Morphine-Induced Hyperalgesia and Antinociceptive Tolerance

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Xingrui Gong ◽  
Rongmei Fan ◽  
Qinghong Zhu ◽  
Xihong Ye ◽  
Yongmei Chen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
P38 Mapk ◽  
Wistar Rats ◽  
Chronic Morphine ◽  
Tolerance Development ◽  
P38 Inhibitor ◽  
Morphine Administration ◽  
Exercise Preconditioning ◽  
Before And After ◽  
Male Wistar Rats

Chronic morphine intake for treating various pain is frequently concomitant with morphine-induced hyperalgesia and tolerance. The mechanisms can be explained by the activation of p38-MAPK proteins in microglia in the spinal cord horn. Exercise has been shown to prevent the development of microglia overactivation. Thus, we designed to test whether exercise prevents the morphine-induced hyperalgesia and tolerance as well as suppression of p38 phosphorylation. A p38 inhibitor SB203580, exercise, and exercise preconditioning were used for treating morphine-induced hyperalgesia and tolerance development in the present study. The behavior tests for hyperalgesia and tolerance were performed in male Wistar rats before and after morphine administration. Western blotting and immunostaining for examining phosphorylated-p38 expression were performed after the behavior tests. Our results showed that SB203580 and exercise, but not exercise preconditioning, prevented the occurrence of morphine-induced hyperalgesia and tolerance. Meanwhile, exercise decreased morphine-induced phosphorylated-p38 overexpression. In summary, exercise prevented the development of morphine-induced hyperalgesia and tolerance. The mechanism may be related to inhibition of p38 phosphorylation.

Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla

1991 ◽  
Vol 260 (1) ◽  
pp. H267-H275 ◽  
Author(s):  
M. K. Bazil ◽  
F. J. Gordon
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Nmda Receptors ◽  
Excitatory Amino Acid ◽  
Cardiovascular Responses ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Pressor Responses

These studies investigated the role of spinal N-methyl-D-aspartic acid (NMDA) receptors in the mediation of cardiovascular responses evoked by L-glutamate (L-Glu) stimulation of the rostral ventrolateral medulla (RVM). Microinjections of L-Glu into the RVM of urethan-anesthetized rats increased mean arterial pressure (MAP) and heart rate. Intrathecal administration of the NMDA receptor antagonists D-(-)-2-amino-7-phosphonoheptanoic acid (D-AP-7) or 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP) reduced MAP and heart rate. Blockade of NMDA receptors by D-AP-7 or CPP in the caudal thoracic spinal cord markedly reduced RVM pressor responses with little effect on evoked tachycardia. Administration of D-AP-7 to the rostral thoracic spinal cord had no effect on RVM pressor or tachycardic responses. Intrathecal D-AP-7 and CPP abolished the cardiovascular effects of intrathecal NMDA without reducing those produced by intrathecal kainic acid or the quisqualate agonist DL-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). These results indicate that 1) tonic activation of spinal NMDA receptors participates in the maintenance of sympathetic outflow to the heart and blood vessels, 2) pressor responses evoked from the RVM require synaptic activation of spinal NMDA receptors, and 3) an excitatory amino acid may be the neurotransmitter of pressor pathways descending from the RVM to the spinal cord.

Compensation to exsanguination hypotension in healthy conscious dogs

1963 ◽  
Vol 205 (5) ◽  
pp. 1000-1004 ◽  
Author(s):  
Robert F. Rushmer ◽  
Nolan Watson ◽  
Donald Harding ◽  
Donald Baker
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Human Subjects ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Series Of Experiments ◽  
The Mean ◽  
The Right

In some earlier studies on exsanguination hypotension in conscious dogs, reduction in systemic arterial pressure to shock levels was accompanied by a transient tachycardia during the removal of blood, but the heart rate returned to level, at or near control values during extended periods with the mean arterial pressure between 40 and 60 mm Hg. This observation stimulated a series of experiments on five healthy conscious dogs in which transient hypotension was induced by withdrawing blood from the region of the right atrium to determine which mechanisms were dominant in the compensatory reaction. A surprising degree of variability in response was encountered, such that tachycardia was the main response on some occasions, increased peripheral resistance on others, and in still others, several mechanisms appeared to play a role. Similar variability in the response to exsanguination have been reported in human subjects. These observations suggest that the baroceptor reflexes are not simple servo controls and their role in everyday cardiovascular responses should be re-examined.

scholarly journals Effects of ionizing radiation on bone neoformation: histometric study in Wistar rats tibiae

2011 ◽  
Vol 26 (6) ◽  
pp. 475-480 ◽  
Author(s):  
Susette Cavicchioli Lucatto ◽  
Arnaldo Guilherme ◽  
Luciano Lauria Dib ◽  
Helena Regina Comodo Segreto ◽  
Maria Tereza de Seixas Alves ◽  
...  
Keyword(s):  
Radiation Dose ◽  
Ionizing Radiation ◽  
Radiation Effects ◽  
Wistar Rats ◽  
Bone Cells ◽  
Secondary Radiation ◽  
Male Wistar Rats ◽  
Histological Processing ◽  
The Right ◽  
Single Dosage

PURPOSE: Comparing the ionizing radiation effects on bone neoformation of rats tibiae previously submitted to radiotherapy with a single dosage of 30Gy with the contralateral tibiae that have received secondary radiation. METHODS: In thirty male Wistar rats, 30 days before surgical procedure when round defects would be created on the bone, the right tibia was irradiated with 30Gy and the left tibia received a calculated secondary radiation dose of 7Gy. Sacrifices were performed after 4, 7, 14, 21, 56 and 84 postoperative days and both tibiae were removed for histological processing. RESULTS: The left tibiae that received the dose of 7Gy has shown more bone neoformation from 14th postoperative days, giving evidences of less damage to cellular population responsible by bone neoformation. On the other hand, the dose of 30Gyon right tibiae did not exhibit significant differences among the periods, suggesting damage of long-lasting or even permanent duration. CONCLUSION: Tibiae submitted to radiation dose of 30Gy have shown more damage to bone cells than tibiae that received secondary radiation dose of 7Gy, especially observed on 14th, 56th and 84th postoperative days.

scholarly journals Assessment transcallosal Diaschisis in a model of focal cerebral ischemia in rats

2016 ◽  
pp. 87-93 ◽  
Author(s):  
Cesar Augusto Arango Dávila ◽  
Beatriz E Munoz ◽  
Daniel Manrique Castaño ◽  
Laura Potes ◽  
John Umbarila
Keyword(s):  
Wistar Rats ◽  
Right Hemisphere ◽  
Neuronal Damage ◽  
Focal Cerebral Ischemia ◽  
Metabolic Stress ◽  
Ischemic Injury ◽  
Neuronal Nuclei ◽  
Male Wistar Rats ◽  
Focal Injury ◽  
The Right

Objective: To evaluate transcallosal changes after a local ischemic injury in rats by using the monoclonal marker anti-NeuN (Mouse anti-neuronal nuclei). Methods: Twenty eight adult, male, Wistar rats were subjected to focal injury in the right hemisphere. The technique used was the experimental model of focal ischemic injury through intraluminal suture of the middle cerebral artery. Analyses were made for the five groups: and after the lesion (control), at 24 hours, 96 hours, 10 days and 20 days. Exofocal neuronal damage was inferred from neuronal immunoreactivity changes to NeuN. Results: In the cortex contralateral to the lesion, immunoreactivity was diminished. This was most notable in the supragranular layers 24 hours post ischemia. After 96 hours, there was a generalized diminishment of the inmmunoreactivity in supra and infragranular layers. At 10 and 20 days, the tissue recovered some NeuN immunoreactivity, but there were set changes in the VI layer. Conclusion: The immunoreactive changes to NeuN support the process of interhemispheric diaschisis. Changes in immunoreactivity could indicate metabolic stress secondary to the disruption in connectivity to the site of lesion.

Endogenous bradykinin in the thoracic spinal cord contributes to the exercise pressor reflex

1996 ◽  
Vol 81 (3) ◽  
pp. 1288-1294 ◽  
Author(s):  
C. L. Stebbins ◽  
S. Bonigut
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Intrathecal Injection ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Thoracic Spinal Cord ◽  
Exercise Pressor Reflex ◽  
Thoracic Spinal ◽  
Pressor Reflex ◽  
Hoe 140

This investigation tested the hypothesis that bradykinin causes excitatory effects in the thoracic spinal cord that augment the exercise pressor reflex. Thus we performed 30 s of electrically stimulated static contraction of the hindlimb in the anesthetized cat (alpha-chloralose) to provoke reflex-induced increases in mean arterial pressure, maximal rate of rise of left ventricular pressure (dP/dt), and heart rate (i.e., the exercise pressor reflex). These three responses were compared before and 15 min after intrathecal injection of 2 micrograms (n = 3), 10 micrograms (n = 6), or 50 micrograms (n = 3) of the selective bradykinin B2- receptor antagonist HOE-140 into the thoracic spinal cord or 10 micrograms of this antagonist into the lumbar (n = 3) spinal cord. In three of the six cats in which 10 micrograms of HOE-140 were injected into the thoracic spinal cord, an additional contraction was performed 60-90 min after treatment. The 2-microgram dose of HOE-140 had no effect on the exercise pressor reflex. Injection of 10 micrograms of this antagonist into the thoracic spinal cord reduced the contraction-evoked pressor, maximal dP/dt, and heart rate responses by 49 +/-7, 58 +/- 4, and 64 +/- 13%, respectively (P < 0.05). Fifty micrograms of HOE-140 failed to attenuate these responses further. In the three cats in which an additional contraction was performed 60-90 min after treatment with 10 micrograms of the antagonist, blood pressure and dP/dt responses had returned, in part, toward initial values. Neither intravenous (n = 3) nor intrathecal injection of 10 micrograms of HOE-140 into the lumbar spinal cord had any effect on the contraction-induced cardiovascular responses. Thoracic injection of 50-200 ng of bradykinin provoked a pressor response of 26 +/- 5 mmHg that was abolished by a similar injection of 10 micrograms of HOE-140. These data suggest that endogenous bradykinin contributes to the exercise pressor reflex by an excitatory action in the thoracic spinal cord.

Spinal cord regulation of sympathetic activity in intact and spinal rats

1994 ◽  
Vol 266 (4) ◽  
pp. H1485-H1493 ◽  
Author(s):  
Y. Hong ◽  
D. F. Cechetto ◽  
L. C. Weaver
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Excitatory Amino Acid ◽  
Intrathecal Injection ◽  
Cardiovascular Responses ◽  
Homocysteic Acid ◽  
Arterial Blood ◽  
Cord Injury

Excitatory amino acid (EAA) and cholinergic neurotransmission in the spinal cord of urethan-anesthetized rats was investigated to assess mechanisms regulating sympathetic activity after spinal cord injury. Blockade of EAA transmission by intrathecal injection of kynurenic acid decreased arterial blood pressure by 24 +/- 4 mmHg, heart rate by 15 +/- 10 beats/min, and renal sympathetic nerve activity (RSNA) by 85 +/- 4% in intact rats. In rats with cervical spinal transections, this blockade decreased RSNA by 51 +/- 5% and had no effect on arterial pressure and heart rate. Muscarinic blockade by intrathecal atropine decreased RSNA by 12 +/- 3 and 32 +/- 6% in intact and spinal rats, respectively, and caused no cardiovascular responses in either group. Combined blockade of EAA and muscarinic receptors in spinal rats decreased RSNA by 77 +/- 1%. Intrathecal injections of the EAA agonist D,L-homocysteic acid in spinal rats caused initial increases (335 +/- 28%) in RSNA lasting approximately 3 min and later sustained increases (157 +/- 19%) lasting 36 +/- 8 min. Only the early excitation increased arterial pressure by 17 +/- 3 mmHg, and then pressure returned to baseline values. The EAA agonist kainic acid increased RSNA by 402 +/- 90% in spinal rats, an effect lasting 70 +/- 5 min, and increased arterial pressure by only 8 +/- 2 mmHg for 12 +/- 5 min. These findings suggest that tonic activity of spinal neurons with EAA and cholinergic receptors maintains tonic RSNA after spinal cord transection. However, this activity does not play a major role in maintaining arterial pressure, even if it is increased substantially by EAA receptor stimulation.

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