Nitric Oxide Controls Microcirculatory Blood Flow by Multiple Mechanisms

2015 ◽  
pp. 51-62 ◽  
Author(s):  
U. Pohl ◽  
C. de Wit ◽  
Ph. von Bismarck ◽  
Ch. Weiss
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Microcirculatory Blood Flow

1618: Real-Time Monitoring of Nitric Oxide and Blood Flow During Ischemia-Reperfusion in the Rat Testis

2006 ◽  
Vol 175 (4S) ◽  
pp. 521-521
Author(s):  
Motoaki Saito ◽  
Tomoharu Kono ◽  
Yukako Kinoshita ◽  
Itaru Satoh ◽  
Keisuke Satoh
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Real Time ◽  
Ischemia Reperfusion ◽  
Real Time Monitoring ◽  
Rat Testis

Role of Nitric Oxide on Papillary Blood Flow and Pressure Natriuresis

Hypertension ◽  
1995 ◽  
Vol 25 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Francisco J. Fenoy ◽  
Paloma Ferrer ◽  
Luis Carbonell ◽  
Miguel García-Salom
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pressure Natriuresis

Interactions Between Nitric Oxide and Angiotensin II on Renal Cortical and Papillary Blood Flow

Hypertension ◽  
1997 ◽  
Vol 30 (5) ◽  
pp. 1175-1182 ◽  
Author(s):  
María Isabel Madrid ◽  
Miguel García-Salom ◽  
Jerónimo Tornel ◽  
Marc de Gasparo ◽  
Francisco J. Fenoy
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Angiotensin Ii

scholarly journals The use of pulse pressure variation for predicting impairment of microcirculatory blood flow

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Christoph R. Behem ◽  
Michael F. Graessler ◽  
Till Friedheim ◽  
Rahel Kluttig ◽  
Hans O. Pinnschmidt ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Reperfusion Injury ◽  
Pulse Pressure ◽  
Pulse Pressure Variation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Pressure Variation ◽  
Volume Loading ◽  
Microcirculatory Blood Flow

AbstractDynamic parameters of preload have been widely recommended to guide fluid therapy based on the principle of fluid responsiveness and with regard to cardiac output. An equally important aspect is however to also avoid volume-overload. This accounts particularly when capillary leakage is present and volume-overload will promote impairment of microcirculatory blood flow. The aim of this study was to evaluate, whether an impairment of intestinal microcirculation caused by volume-load potentially can be predicted using pulse pressure variation in an experimental model of ischemia/reperfusion injury. The study was designed as a prospective explorative large animal pilot study. The study was performed in 8 anesthetized domestic pigs (German landrace). Ischemia/reperfusion was induced during aortic surgery. 6 h after ischemia/reperfusion-injury measurements were performed during 4 consecutive volume-loading-steps, each consisting of 6 ml kg−1 bodyweight−1. Mean microcirculatory blood flow (mean Flux) of the ileum was measured using direct laser-speckle-contrast-imaging. Receiver operating characteristic analysis was performed to determine the ability of pulse pressure variation to predict a decrease in microcirculation. A reduction of ≥ 10% mean Flux was considered a relevant decrease. After ischemia–reperfusion, volume-loading-steps led to a significant increase of cardiac output as well as mean arterial pressure, while pulse pressure variation and mean Flux were significantly reduced (Pairwise comparison ischemia/reperfusion-injury vs. volume loading step no. 4): cardiac output (l min−1) 1.68 (1.02–2.35) versus 2.84 (2.15–3.53), p = 0.002, mean arterial pressure (mmHg) 29.89 (21.65–38.12) versus 52.34 (43.55–61.14), p < 0.001, pulse pressure variation (%) 24.84 (17.45–32.22) versus 9.59 (1.68–17.49), p = 0.004, mean Flux (p.u.) 414.95 (295.18–534.72) versus 327.21 (206.95–447.48), p = 0.006. Receiver operating characteristic analysis revealed an area under the curve of 0.88 (CI 95% 0.73–1.00; p value < 0.001) for pulse pressure variation for predicting a decrease of microcirculatory blood flow. The results of our study show that pulse pressure variation does have the potential to predict decreases of intestinal microcirculatory blood flow due to volume-load after ischemia/reperfusion-injury. This should encourage further translational research and might help to prevent microcirculatory impairment due to excessive fluid resuscitation and to guide fluid therapy in the future.

Nitric oxide release in rat skeletal muscle capillary

1996 ◽  
Vol 270 (5) ◽  
pp. H1696-H1703 ◽  
Author(s):  
D. Mitchell ◽  
K. Tyml
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Leukocyte Adhesion ◽  
Microvascular Blood Flow ◽  
Capillary Length ◽  
Nitric Oxide Release ◽  
Longus Muscle ◽  
Potent Vasodilator ◽  
Capillary Bed ◽  
Synthase Inhibitor

Nitric oxide (NO) has been shown to be a potent vasodilator released from endothelial cells (EC) in large blood vessels, but NO release has not been examined in the capillary bed. Because the capillary bed represents the largest source of EC, it may be the largest source of vascular NO. In the present study, we used intravital microscopy to examine the effect of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on the microvasculature of the rat extensor digitorum longus muscle. L-NAME (30 mM) applied locally to a capillary (300 micron(s) from the feeding arteriole) reduced red blood cell (RBC) velocity [VRBC; control VRBC = 238 +/- 58 (SE) micron/s; delta VRBC = -76 +/- 8%] and RBC flux (4.4 +/- 0.7 to 2.8 +/- 0.7 RBC/s) significantly in the capillary, but did not change feeding arteriole diameter (Dcon = 6.3 +/- 0.7 micron, delta D = 5 +/- 7%) or draining venule diameter (Dcon = 10.1 +/- 0.6 micron, delta D = 4 +/- 2%). Because of the VRBC change, the flux reduction was equivalent to an increased local hemoconcentration from 1.8 to 5 RBCs per 100 micron capillary length. L-NAME also caused an increase in the number of adhering leukocytes in the venule from 0.29 to 1.43 cells/100 micron. L-NAME (30 mM) applied either to arterioles or to venules did not change capillary VRBC. Bradykinin (BK) locally applied to the capillary caused significant increases in VRBC (delta VRBC = 111 +/- 23%) and in arteriolar diameter (delta D = 40 +/- 5%). This BK response was blocked by capillary pretreatment with 30 mM L-NAME (delta VRBC = -4 +/- 27%; delta D = 5 +/- 9% after BK). We concluded that NO may be released from capillary EC both basally and in response to the vasodilator BK. We hypothesize that 1) low basal levels of NO affect capillary blood flow by modulating local hemoconcentration and leukocyte adhesion, and 2) higher levels of NO (stimulated by BK) may cause a remote vasodilation to increase microvascular blood flow.

scholarly journals Examination of Potential Mechanisms in the Enhancement of Cerebral Blood Flow by Hypoglycemia and Pharmacological Doses of Deoxyglucose

1997 ◽  
Vol 17 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Naoaki Horinaka ◽  
Nicole Artz ◽  
Jane Jehle ◽  
Shinichi Takahashi ◽  
Charles Kennedy ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Plasma Lactate ◽  
Insulin Hypoglycemia ◽  
Glucose Levels ◽  
Arterial Blood ◽  
Arterial Plasma

Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [14C]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 m M, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3– concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p. injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 m M) or pharmacological doses of deoxyglucose.

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