The effects of selective nitric oxide synthase blocker on survival, mesenteric blood flow and multiple organ failure induced by zymosan1

2005 ◽  
Vol 124 (1) ◽  
pp. 67-73 ◽  
Author(s):  
Pinar Tanriverdi ◽  
Bulent C. Yuksel ◽  
Kemal Rasa ◽  
Gulnur Guler ◽  
Alper B. Iskit ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Multiple Organ ◽  
Mesenteric Blood Flow ◽  
Oxide Synthase

INDUCIBLE NITRIC OXIDE SYNTHASE KNOCKOUT MICE EXHIBIT RESISTANCE TO THE MULTIPLE ORGAN FAILURE INDUCED BY ZYMOSAN

Shock ◽  
2001 ◽  
Vol 16 (1) ◽  
pp. 51-58 ◽  
Author(s):  
Salvatore Cuzzocrea ◽  
Emanuela Mazzon ◽  
Laura Dugo ◽  
Alberto Barbera ◽  
Tommaso Centorrino ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Inducible Nitric Oxide Synthase ◽  
Knockout Mice ◽  
Multiple Organ ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Inhibition of nitric oxide synthase in the paraventricular nucleus prevents the hyperthermia-induced reduction of mesenteric blood flow in rats

2010 ◽  
Vol 299 (2) ◽  
pp. R596-R602 ◽  
Author(s):  
Feng Chen ◽  
Yuliang Wang ◽  
Joo Lee Cham ◽  
Emilio Badoer
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Core Temperature ◽  
Paraventricular Nucleus ◽  
Cardiovascular Responses ◽  
Body Core Temperature ◽  
Mesenteric Blood Flow ◽  
Body Core ◽  
Oxide Synthase

Increasing body core temperature reflexly decreases mesenteric blood flow (MBF), and the hypothalamic paraventricular nucleus (PVN) plays an essential role in this response. Nitric oxide (NO) is involved in temperature regulation and is concentrated within the PVN. The present study investigated whether NO in the PVN contributes to the cardiovascular responses elicited by hyperthermia. Anesthetized rats were microinjected bilaterally in the PVN (100 nl/side) with saline or NG-nitro-l-arginine methyl ester (l-NAME), a nitric oxide synthase inhibitor (100 or 200 nmol/100 nl) ( n = 5/group). Body core temperature was then elevated from 37°C to 39°C, and blood pressure (BP), heart rate (HR), MBF, and mesenteric vascular conductance (MVC) were monitored. In separate groups, l-NAME (200 nmol) ( n = 5) or saline ( n = 5) was microinjected in the PVN, but body core temperature was not elevated. In control rats, increasing body core temperature resulted in no marked change of BP but an increase in HR and significant decreases in MBF (15%) and MVC. Pretreatment with 100 nmol l-NAME did not affect the responses. In contrast, 200 nmol l-NAME prevented the normal reduction in MBF and MVC but did not significantly affect the BP and HR responses. In rats in which body core temperature was not increased, l-NAME reduced MBF by 19%. The present results suggest that endogenous NO in the PVN is important in mediating the reduction of MBF induced by hyperthermia. In the absence of hyperthermia, however, endogenous NO in the PVN may play a role in maintaining mesenteric vasodilation.

Decreased mesenteric blood flow in experimental multiple organ failure

1992 ◽  
Vol 52 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Steven Scalia ◽  
Pramod Sharma ◽  
Jorge Rodriguez ◽  
Frank Roche ◽  
Fred Luchette ◽  
...  
Keyword(s):  
Blood Flow ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Multiple Organ ◽  
Mesenteric Blood Flow

Nitric oxide synthase inhibition in healthy adults reduces regional and total cerebral macrovascular blood flow and microvascular perfusion

2021 ◽  
Author(s):  
Katrina J. Carter ◽  
Aaron T. Ward ◽  
J. Mikhail Kellawan ◽  
Marlowe W. Eldridge ◽  
Awni Al‐Subu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Healthy Adults ◽  
Microvascular Perfusion ◽  
Oxide Synthase

scholarly journals Rapid nontranscriptional activation of endothelial nitric oxide synthase mediates increased cerebral blood flow and stroke protection by corticosteroids

2003 ◽  
Vol 111 (5) ◽  
pp. 759-759
Author(s):  
Florian P. Limbourg ◽  
Zhihong Huang ◽  
Jean-Christophe Plumier ◽  
Tommaso Simoncini ◽  
Masayuki Fujioka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Angiotensin II and nitric oxide in neural control of intrarenal blood flow

2005 ◽  
Vol 289 (3) ◽  
pp. R745-R754 ◽  
Author(s):  
Niwanthi W. Rajapakse ◽  
Amanda K. Sampson ◽  
Gabriela A. Eppel ◽  
Roger G. Evans
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Nitric Oxide Synthase ◽  
Neural Control ◽  
Renin Angiotensin System ◽  
Renal Medulla ◽  
Renal Nerve ◽  
Intrarenal Blood Flow ◽  
Oxide Synthase

We investigated the roles of the renin-angiotensin system and the significance of interactions between angiotensin II and nitric oxide, in responses of regional kidney perfusion to electrical renal nerve stimulation (RNS) in pentobarbital sodium-anesthetized rabbits. Under control conditions, RNS (0.5–8 Hz) reduced total renal blood flow (RBF; −89 ± 3% at 8 Hz) and cortical perfusion (CBF; −90 ± 2% at 8 Hz) more than medullary perfusion (MBF; −55 ± 5% at 8 Hz). Angiotensin II type 1 (AT1)-receptor antagonism (candesartan) blunted RNS-induced reductions in RBF ( P = 0.03), CBF ( P = 0.007), and MBF ( P = 0.04), particularly at 4 and 8 Hz. Nitric oxide synthase inhibition with NG-nitro-l-arginine (l-NNA) enhanced RBF ( P = 0.003), CBF ( P = 0.001), and MBF ( P = 0.03) responses to RNS, particularly at frequencies of 2 Hz and less. After candesartan pretreatment, l-NNA significantly enhanced RNS-induced reductions in RBF ( P = 0.04) and CBF ( P = 0.007) but not MBF ( P = 0.66). Renal arterial infusion of angiotensin II (5 ng·kg−1·min−1) selectively enhanced responses of MBF to RNS in l-NNA-pretreated but not in vehicle-pretreated rabbits. In contrast, greater doses of angiotensin II (5–15 ng·kg−1·min−1) blunted responses of MBF to RNS in rabbits with intact nitric oxide synthase. These results suggest that endogenous angiotensin II enhances, whereas nitric oxide blunts, neurally mediated vasoconstriction in the renal cortical and medullary circulations. In the renal medulla, but not the cortex, angiotensin II also appears to be able to blunt neurally mediated vasoconstriction.

scholarly journals The Role of Neuronal Nitric Oxide Synthase in Regulation of Cerebral Blood Flow in Normocapnia and Hypercapnia in Rats

1995 ◽  
Vol 15 (5) ◽  
pp. 774-778 ◽  
Author(s):  
Qiong Wang ◽  
Dale A. Pelligrino ◽  
Verna L. Baughman ◽  
Heidi M. Koenig ◽  
Ronald F. Albrecht
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Inhibitory Action ◽  
Neuronal Nitric Oxide Synthase ◽  
Muscarinic Agonist ◽  
Doppler Flowmetry ◽  
Nos Inhibitors ◽  
Oxide Synthase

The nitric oxide synthase (NOS) inhibitors, nitro-L-arginine, its methyl ester, and N-monomethyl-L-arginine, have been shown to attenuate resting CBF and hypercapnia-induced cerebrovasodilation. Those agents nonspecifically inhibit the endothelial and neuronal NOS (eNOS and nNOS). In the present study, we used a novel nNOS inhibitor, 7-nitroindazole (7-NI) to examine the role of nNOS in CBF during normocapnia and hypercapnia in fentanyl/N2O-anesthetized rats. CBF was monitored using laser-Doppler flowmetry. Administration of 7-NI (80 mg kg−1 i.p.) reduced cortical brain NOS activity by 57%, the resting CBF by 19–27%, and the CBF response to hypercapnia by 60%. The 60% reduction was similar in magnitude to the CBF reductions observed in previous studies in which nonspecific NOS inhibitors were used. In the present study, 7-NI did not increase the MABP. Furthermore, the CBF response to oxotremorine, a blood–brain barrier permeant muscarinic agonist that induces cerebrovasodilation via endothelium-derived NO, was unaffected by 7-NI. These results confirmed that 7-NI does not influence eNOS; they also indicated that the effects of 7-NI on the resting CBF and on the CBF response to hypercapnia in this study were solely related to its inhibitory action on nNOS. The results further suggest that the NO synthesized by the action of nNOS participates in regulation of basal CBF and is the major, if not the only, category of NO contributing to the hypercapnic CBF response.

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