Coronary artery occlusion alters expression of substance P and its mRNA in spinal dorsal horn in rats

Guo, Zheng; Niu, Yan-Lan; Zhang, J.-W.; Yao, Tai-Ping

doi:10.1016/j.neuroscience.2006.12.008

Cited by 27 publications

(14 citation statements)

References 19 publications

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“…The procedure of coronary artery occlusion and sham surgery was carried out under anesthesia with sodium pentobarbital (induction with 65 mg kg − 1 , i.p., and maintained with 15 mg kg − 1 h − 1 , i.v.) as previously reported [15]. Briefly, the left anterior descending coronary artery was ligated in animals of the CAO groups.…”

Section: Acute Myocardial Infarction Modelmentioning

confidence: 99%

“…One hundred and twenty animals, 60 nondenervated and 60 denervated, were respectively divided into 20 groups (6 animals in each group). The peptides in the ischemic myocardium and dorsal root ganglia (DRG) were measured using enzyme immunoassay (EIA) as previously reported [14,15]. Expressions of SP and CGRP in the spinal dorsal horn of upper thoracic segments (T1-T5) were examined using an immunohistochemistry assay (IhcA).…”

Section: Expression Of Sp and Cgrpmentioning

confidence: 99%

“…It was reported that increase of some sensory neuropeptides, including calcitonin gene related peptide (CGRP) and substance P (SP) [1][2][3], in myocardium may suggest an association of afferent nerves and their containing neuropeptides with acute myocardial ischemia and infarction [1,[4][5][6][7][8][9][10]. Capsaicin sensitive afferent neurons are known existed in cardiovascular system [11][12][13][14][15] and related to the transmission of cardiac nociception. However, once activated by stimuli, the afferent nerves can also release the transmitters from their peripheral terminals eliciting functional consequences [16].…”

Section: Introductionmentioning

confidence: 99%

“…During myocardial ischemia, capsaicin sensitive sensory nerves may integrate and respond to anerobic metabolites [18] sending signals to the central nervous system and releasing neurotransmitters to the myocardium, including SP and CGRP [16], which are the main neuropeptides contained in afferent sensory neurons [13,19]. The participation of the neuropeptides in the pathology of acute myocardial infarction and a cardioprotective role were suggested [11,14,15,[20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

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Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats

Zhang

Guo

Wang

et al. 2012

International Journal of Cardiology

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Section: Acute Myocardial Infarction Modelmentioning

confidence: 99%

Section: Expression Of Sp and Cgrpmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats

Zhang

Guo

Wang

et al. 2012

International Journal of Cardiology

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“…We thus produced rat myocardial infarction (MI) model via permanent ligation of left anterior descending artery (LAD) [22][23][24] and our study showed that Ad-HIF-1α-Trip treatment significantly increased the expressions of angiogenesis cytokines including VEGF, FLGF and PDGF. Furthermore, a prominent improvement of angiogenesis, reduction of infarct size and improvement of cardiac function were also observed.…”

Section: Introductionmentioning

confidence: 99%

Effects of Triple-Mutated Hypoxia-Inducible Factor-1α on Angiogenesis and Cardiac Function Improvement in Rats with Myocardial Infarction

Cui

et al. 2018

Cell Physiol Biochem

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Background/Aims: The effects of hypoxia-inducible factor-1α (HIF-1α) on angiogenesis and cardiac function improvement in rats with myocardial infarction (MI) is unknown and our current study was to evaluate whether HIF-1α would be beneficial for angiogenesis and cardiac function improvement in MI rats. Methods: A mutant of adenovirus HIF-1α (Ad-HIF-1α-Trip) was constructed by three sites mutation (Pro402, Pro564 and Asn803) in HIF-1α. The rat MI model was produced by permanent ligation of left anterior descending artery and 1×10⁹ PFU adenovirus (Ad) vector particles of Ad-Null, Ad- HIF-1a-564/402, Ad- HIF-1a-Trip, 250ng vascular endothelial growth factor (VEGF) in 0.5ml saline or only 0.5 ml saline were injected intramuscularly around the infarct border zone. Real-time PCR, ELISA and western blotting were used to evaluate angiogenesis factors expression. Capillary density and necrotic areas were detected by immunohistochemistry staining and TTC staining, respectively. Cardiac function assessment was done by echocardiography before operation and on day 7, 14 and 28 after MI. Blood samples were drawn for the measurement of cardiac biomarkers, liver function and kidney function. Results: On day 7, compared to the other groups, the expressions of HIF-1α and angiogenesis factors, and the capillary density were all significantly higher in the Ad-HIF-1α-Trip group. However, on day 28, no significant between-group differences were observed. After 72 hours of MI, serum level of cardiac biomarkers and the necrotic areas were significantly lower in the Ad-HIF-1a-Trip group compared to the other groups. Echocardiography showed that on day 7, cardiac functions were significantly reduced in all groups compared to the baseline. Cardiac function in the Ad-HIF-1α-Trip group was decreased less profoundly through day 7 to day 28 compared to the other groups. Importantly, no significant differences in liver and renal function were observed. Conclusion: Mutation of Pro402, Pro564 and Asn803 are beneficial for enhancement of the efficacy of HIF-1α. Ad-HIF–1α-Trip is able to improve angiogenesis and cardiac function, which may be a promising avenue for treatment of ischemic heart disease in the future.

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Mechanisms of Cardiac Pain

Foreman

Garrett

Blair

2015

Comprehensive Physiology

190

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Angina pectoris is cardiac pain that typically is manifested as referred pain to the chest and upper left arm. Atypical pain to describe localization of the perception, generally experienced more by women, is referred to the back, neck, and/or jaw. This article summarizes the neurophysiological and pharmacological mechanisms for referred cardiac pain. Spinal cardiac afferent fibers mediate typical anginal pain via pathways from the spinal cord to the thalamus and ultimately cerebral cortex. Spinal neurotransmission involves substance P, glutamate, and transient receptor potential vanilloid-1 (TRPV1) receptors; release of neurokinins such as nuclear factor kappa b (NF-kb) in the spinal cord can modulate neurotransmission. Vagal cardiac afferent fibers likely mediate atypical anginal pain and contribute to cardiac ischemia without accompanying pain via relays through the nucleus of the solitary tract and the C1-C2 spinal segments. The psychological state of an individual can modulate cardiac nociception via pathways involving the amygdala. Descending pathways originating from nucleus raphe magnus and the pons also can modulate cardiac nociception. Sensory input from other visceral organs can mimic cardiac pain due to convergence of this input with cardiac input onto spinothalamic tract neurons. Reduction of converging nociceptive input from the gallbladder and gastrointestinal tract can diminish cardiac pain. Much work remains to be performed to discern the interactions among complex neural pathways that ultimately produce or do not produce the sensations associated with cardiac pain.

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Coronary artery occlusion alters expression of substance P and its mRNA in spinal dorsal horn in rats

Cited by 27 publications

References 19 publications

Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats

Degeneration of capsaicin sensitive sensory nerves enhances myocardial injury in acute myocardial infarction in rats

Effects of Triple-Mutated Hypoxia-Inducible Factor-1α on Angiogenesis and Cardiac Function Improvement in Rats with Myocardial Infarction

Mechanisms of Cardiac Pain

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