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Titolo:
The influence of tumour necrosis factor-alpha on the cardiovascular systemof anaesthetized rats
Autore:
Tabrizchi, R;
Indirizzi:
Mem Univ Newfoundland, Fac Med, Hlth Sci Ctr, Div Basic Med Sci, St Johns,NF A1B 3V6, Canada Mem Univ Newfoundland St Johns NF Canada A1B 3V6 Johns,NF A1B 3V6, Canada
Titolo Testata:
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
fascicolo: 3, volume: 363, anno: 2001,
pagine: 307 - 321
SICI:
0028-1298(200103)363:3<307:TIOTNF>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
CIRCULATORY FILLING PRESSURE; ARGININE METHYL-ESTER; NITRIC-OXIDE; ANESTHETIZED RATS; RECEPTOR AGONIST; CONSCIOUS RATS; CARDIAC-OUTPUT; VENOUS RETURN; HEART-FAILURE; SEPTIC SHOCK;
Keywords:
arterial resistance; cardiac output; blood pressure; mean circulatory filling pressure; nitric oxide synthase; resistance to venous return; tumour necrosis factor-alpha;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Tabrizchi, R Mem Univ Newfoundland, Fac Med, Hlth Sci Ctr, Div Basic Med Sci, St Johns,NF A1B 3V6, Canada Mem Univ Newfoundland St Johns NF Canada A1B 3V6 3V6, Canada
Citazione:
R. Tabrizchi, "The influence of tumour necrosis factor-alpha on the cardiovascular systemof anaesthetized rats", N-S ARCH PH, 363(3), 2001, pp. 307-321

Abstract

The effects of two vasoactive agents (adenosine AZA agonist, CGS 21680, and adrenoceptor agonist, noradrenaline) were examined on cardiac output (CO), heart rate (HR), blood pressure (BP), mean circulatory filling pressure (P-mcf), resistance to venous return, arterial resistance, dP/dt, plasma levels of NO2-/NO3-, and inducible nitric oxide synthase (iNOS) activity in lungs ex vivo, following treatment with tumour necrosis factor-a (TNF-alpha; 30 mug/kg) in anaesthetized rats. Treatment with TNF-alpha produced significant reduction in CO (41+/-2%), dP/dt (26+/-3%), BP (26+/-2%) and P-mcf (27/-4%; n=6; mean+/-SEM), but increased arterial resistance. There were no significant changes in the plasma levels of NO2-/NO(3)(-)levels over time following treatment with TNF-alpha, but there was a significant increase (approximately twofold) in the activity of the iNOS in the lungs of animals treated with TNF-alpha. Administration of CGS 21680 (1.0 mug/kg per min) significantly increased CO (44+/-6%), HR (12+/-2%), P-mcf (24+/-4%) and dP/dt (24+/-5%) in TNF-alpha -treated rats. CGS 21680 also significantly reduced arterial resistance (33+/-2%) without altering resistance to venous return inTNF-alpha -treated rats. While noradrenaline (1.0 mug/kg per min) infusiondid not significantly increase CO, it did significantly increase HR (12+/-1%), BP (55+/-9%), P-mcf (47+/-5%), dP/dt (65+/-7%), resistance to venous return (64+/-20%), and arterial resistance (41+/-16%) in TNF-alpha -treated animals. The reduction in BP due to administration of TNF-alpha is the result of significant reduction in CO. Consequently, the decline in CO can be attributed to a combination of a negative inotropic effect as well as a reduction in P-mcf. It is evident that infusion with CGS 21680 could reverse the negative impact of TNF-alpha on CO by increasing dP/dt, P-mcf and HR as well as a reduction in arterial resistance. The fact that noradrenaline did not significantly increase CO in TNF-alpha -treated rats can be attributed to increased arterial resistance as well increase in resistance to venous return.

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Documento generato il 28/11/20 alle ore 12:39:42