Coronary and Systemic Hemodynamic Effects of Tetramethylpyrazine in the Dog

Dai, Xue-Zheng; Bache, Robert J.

doi:10.1097/00005344-198509000-00005

Cited by 51 publications

(22 citation statements)

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“…This result is consistent with an earlier study in which this plant inhibited the contractions induced by a receptor agonist and by membrane depolarization (Wu et al, 1989). It has been reported that tetramethylpyrazine (TMP), a component of Ligusticum wallichi, directly affects Ca 2+ -influx through the cellular membrane and Ca 2+ -release from the sarcoplasmic reticulum, which results in a decrease in [Ca 2+ ] i in the vascular system (Dai and Bache, 1985;Pang et al, 1996). These results suggest that Ligusticum wallichi has a potent vasorelaxation effect and this effect may afford protection to the cardiovascular system.…”

Section: Discussionsupporting

confidence: 93%

Ligusticum wallichi-induced vasorelaxation mediated by mitogen-activated protein kinase in rat aortic smooth muscle

Kim

et al. 2004

Journal of Ethnopharmacology

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Section: Discussionsupporting

confidence: 93%

Ligusticum wallichi-induced vasorelaxation mediated by mitogen-activated protein kinase in rat aortic smooth muscle

Kim

et al. 2004

Journal of Ethnopharmacology

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“…This drug has been widely used in China for treatment of angina pectoris and cerebral ischaemic syndromes (Lu et al 1978;Lui Chuong 1978). In addition, pharmacological studies also indicate that TMP (1) reduces arterial resistance and increases coronary (Dai and Bache 1985) and cerebral blood flow in dogs (Feng et al 1988), (2) has inhibitory effects on platelet function in vivo and in vitro (Lui Chuong 1978), and (3) improves the microcirculation (Dai and Bache 1985) and reduces capillary permeability (Tuttle et al 1989). We have demonstrated that the vasodilatation caused by TMP is due to the intracellular accumulation of cyclic AMP (via inhibition on phosphodiesterase IV) and the blockade of the release of calcium from internal stores (Wu et al 1989).…”

Section: Introductionmentioning

confidence: 99%

Tetramethylpyrazine prevents inducible NO synthase expression and improves survival in rodent models of endotoxic shock

Liao

Chen

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

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This study is to investigate the possible mechanism of beneficial effects of tetramethylpyrazine (TMP) on endotoxic shock which we showed in our preliminary study (Liao et al. 1998; Proc Natl Sci Counc Repub China B 22:46-54). Here, we have confirmed the beneficial effects of TMP on the hypotension, vascular hyporeactivity to noradrenaline (NA), release of tumour necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) in a rat model of circulatory shock induced by bacterial endotoxin (E. coli lipopolysaccharide, LPS). In addition, we further examined the expression of inducible NO synthase in the lung and in the aorta from these rats and evaluated the effect of TMP on the 36-h survival rate in a murine model of endotoxaemia. Male Wistar-Kyoto rats were anaesthetised and instrumented for the measurement of mean arterial pressure (MAP) and heart rate (HR). Injection of LPS (10 mg kg(-1), i.v.) resulted in an acute fall followed by a substantial fall in MAP within 4 h and an increase in HR. In contrast, animals pretreated with TMP (10 mg kg(-1), i.p.; at 30 min prior to LPS) maintained a significantly higher MAP but the tachycardia was further enhanced at 1-2 h when compared to rats given only LPS (LPS rats). The pressor effect of NA (1 microg kg(-1), i.v.) was also significantly reduced after the treatment of rats with LPS. Similarly, the thoracic aorta obtained from rats at 4 h after LPS showed a significant reduction in the contractile responses elicited by NA (1 microM). Pretreatment of LPS rats with TMP partially, but significantly, prevented this LPS-induced hyporeactivity to NA in vivo and ex vivo. The injection of LPS resulted in a bell-shaped change in plasma TNF-alpha level which reached a maximum at 1 h, whereas the effect of LPS on the plasma level of nitrate (an indicator of NO formation) was increased in a time-dependent manner. This increment of both TNF-alpha and nitrate levels was significantly reduced in LPS rats pretreated with TMP. Endotoxaemia for 4 h caused a significantly increased protein expression of iNOS in the lung and the aorta. In LPS rats pretreated with TMP, iNOS protein expression in lung and aorta homogenates was attenuated by 75+/-3% and 57+/-6%, respectively. In addition, the lack of evidence of pressor effect of TMP on rats with endotoxaemia for 4 h suggested that TMP inhibits the induction of iNOS rather than directly inhibiting NOS activity. Treatment of conscious ICR mice with a high dose of endotoxin (60 mg kg(-1), i.p.) resulted in a survival rate of only 15% at 36 h (n=20). However, therapeutic application of TMP (10 mg kg(-1), i.p.; at 0, 6, 15 and 24 h after LPS) increased the 36 h survival rate to 55% (n=20). Thus, TMP inhibits the expression of iNOS and mitigates the delayed circulatory failure caused by endotoxic shock in the rat. In addition, TMP also improves survival in a murine model of severe endotoxaemia.

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“…Intravenous administration of 2-15 mg/kg tetramethylpyrazine was reported to increase the coronary blood flow from 37 to 74 mL/min but decrease the mean coronary vascular resistance from 1770 to 700 dyn·s·cm −3 in a dose-related manner in anesthetized dogs. 10) Moreover, pretreatment of tetramethylpyrazine (80 mg/ kg, i.v.) suppressed the endothelin-1-induced coronary vasoconstriction in anesthetized dogs.…”

Section: Discussionmentioning

confidence: 99%

Assessment of the Anti-anginal Effect of Tetramethylpyrazine Using Vasopressin-Induced Angina Model Rats

Cao

Nakamura

Wada

et al. 2016

Biological & Pharmaceutical Bulletin

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Intravenous tetramethylpyrazine has been widely used in China as a complementary and/or alternative medicine to treat patients with ischemic heart disease. We assessed the anti-anginal effect of tetramethylpyrazine (10 mg/kg, intravenously (i.v.), n 6) in comparison with that of its vehicle, saline (1 mL/kg, i.v., n 6), using vasopressin-induced angina model rats. First, Donryu rats were anesthetized with pentobarbital sodium (60 mg/kg, intraperitoneally (i.p.)), and the surface lead I electrocardiogram was continuously monitored. Administration of vasopressin (0.5 IU/kg, i.v.) to the rats depressed the S-wave level of the electrocardiogram, indicating the onset of subendocardial ischemia. However, pretreatment with tetramethylpyrazine suppressed the vasopressin-induced depression of the S-wave level, which was not observed following pretreatment with its vehicle alone (saline), suggesting that tetramethylpyrazine ameliorated the vasopressininduced subendocardial ischemia in vivo. These results may provide experimental evidence for the empirically known clinical efficacy of tetramethylpyrazine against ischemic heart disease, and could provide clues to better understanding its in vivo mechanism of action.

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Coronary and Systemic Hemodynamic Effects of Tetramethylpyrazine in the Dog

Cited by 51 publications

References 0 publications

Ligusticum wallichi-induced vasorelaxation mediated by mitogen-activated protein kinase in rat aortic smooth muscle

Ligusticum wallichi-induced vasorelaxation mediated by mitogen-activated protein kinase in rat aortic smooth muscle

Tetramethylpyrazine prevents inducible NO synthase expression and improves survival in rodent models of endotoxic shock

Assessment of the Anti-anginal Effect of Tetramethylpyrazine Using Vasopressin-Induced Angina Model Rats

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