L-arginine augments nitric oxide production and mesenteric blood flow in ovine endotoxemia

1996 ◽  
Vol 271 (4) ◽  
pp. H1296-H1301
Author(s):  
K. G. Allman ◽  
A. P. Stoddart ◽  
M. M. Kennedy ◽  
J. D. Young
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Nitric Oxide Production ◽  
Mesenteric Blood Flow ◽  
Oxide Production ◽  
Arterial Blood ◽  
Nitrate Concentrations

We studied the effects of administrating the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), or the nitric oxide precursor, L-arginine, on hemodynamic variables and serum nitrate concentrations in an anesthetized ovine model of endotoxemia to assess the effects on regional visceral blood flow and to determine whether L-arginine availability limits nitric oxide production. Animals received Escherichia coli endotoxin (2 micrograms/kg) followed 2 h later by L-NAME (25 mg/kg), L-arginine (0.575 g/kg), or saline administered over 1 h followed by an infusion of the same dose over 8 h (n = 6 per group). Renal and mesenteric blood flow were measured by placement of electromagnetic flow probes, and serum nitrate concentrations were determined using vanadium III chloride or nitrate reductase reduction to nitric oxide or nitrite, respectively. The results showed L-NAME significantly increased systemic vascular resistance (P < 0.01), decreased serum nitrate concentrations (P < 0.05), and caused a transient reduction in mesenteric blood flow (P < 0.05). L-Arginine caused a reduction in systemic vascular resistance (P < 0.01), increased mesenteric blood flow (P < 0.001) and conductance (P < 0.05). There were no significant changes in renal arterial blood flow in either group. We conclude that the availability of L-arginine limits nitric oxide production in endotoxemia and, furthermore, that L-arginine administration in this model causes significant mesenteric vasodilatation. L-NAME administration had only limited effect on visceral blood flow despite a marked increase in systemic vascular resistance and a reduction in nitric oxide production.

Effects of striatal nitric oxide production on regional cerebral blood flow and seizure development in rats exposed to extreme hyperoxia

2015 ◽  
Vol 119 (11) ◽  
pp. 1282-1288 ◽  
Author(s):  
Heath G. Gasier ◽  
Ivan T. Demchenko ◽  
Barry W. Allen ◽  
Claude A. Piantadosi
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Brain Structures ◽  
Nitric Oxide Production ◽  
Regional Cerebral Blood ◽  
Oxide Production ◽  
Arterial Blood ◽  
The Brain

The endogenous vasodilator and signaling molecule nitric oxide has been implicated in cerebral hyperemia, sympathoexcitation, and seizures induced by hyperbaric oxygen (HBO2) at or above 3 atmospheres absolute (ATA). It is unknown whether these events in the onset of central nervous system oxygen toxicity originate within specific brain structures and whether blood flow is diverted to the brain from peripheral organs with high basal flow, such as the kidney. To explore these questions, total and regional cerebral blood flow (CBF) were measured in brain structures of the central autonomic network in anesthetized rats in HBO2at 6 ATA. Electroencephalogram (EEG) recordings, cardiovascular hemodynamics, and renal blood flow (RBF) were also monitored. As expected, mean arterial blood pressure and total and regional CBF increased preceding EEG spikes while RBF was unaltered. Of the brain structures examined, the earliest rise in CBF occurred in the striatum, suggesting increased neuronal activation. Continuous unilateral or bilateral striatal infusion of the nitric oxide synthase inhibitor Nω-nitro-l-arginine methyl ester attenuated CBF responses in that structure, but global EEG discharges persisted and did not differ from controls. Our novel findings indicate that: 1) cerebral hyperemia in extreme HBO2in rats does not occur at the expense of renal perfusion, highlighting the remarkable autoregulatory capability of the kidney, and 2) in spite of a sentinel increase in striatal blood flow, additional brain structure(s) likely govern the pathogenesis of HBO2-induced seizures because EEG discharge latency was unchanged by local blockade of striatal nitric oxide production and concomitant hyperemia.

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

scholarly journals The Role of Garlic in Hepatopulmonary Syndrome: A Randomized Controlled Trial

2010 ◽  
Vol 24 (3) ◽  
pp. 183-188 ◽  
Author(s):  
Binay K De ◽  
Deep Dutta ◽  
Subrata K Pal ◽  
Subhabrata Gangopadhyay ◽  
Sumanta Das Baksi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Placebo Group ◽  
Controlled Trial ◽  
Hepatopulmonary Syndrome ◽  
Arterial Oxygen ◽  
Nitric Oxide Production ◽  
Arterial Blood Gas ◽  
Oxygen Gradient ◽  
Oxide Production ◽  
Arterial Blood

BACKGROUND: Increased nitric oxide production in cirrhosis has been commonly implicated in the genesis of hepatopulmonary syndrome (HPS). Initial studies suggested that garlic, a constituent of the daily diet, may have a role in the treatment of HPS by altering nitric oxide production.OBJECTIVE: To evaluate the effects of oral garlic supplementation on arterial blood gas parameters, and overall morbidity and mortality in patients with HPS.METHODS: Twenty-one and 20 HPS patients were randomly assigned to receive either oral garlic supplementation or placebo, respectively, and were evaluated monthly over a period of nine to 18 months.RESULTS: After nine months, garlic supplementation was associated with a 24.66% increase in baseline arterial oxygen levels (83.05 mmHg versus 66.62 mmHg; P<0.001), compared with only a 7.37% increase (68.75 mmHg versus 64.05 mmHg; P=0.02) among subjects in the placebo group. There was also a 28.35% decrease in alveolar-arterial oxygen gradient (21.35 mmHg versus 29.77 mmHg; P<0.001) among patients with HPS who received garlic, in contrast with only a 10.73% decrease (29.11 mmHg versus 32.61 mmHg; P=0.12) among those in the placebo group. After nine months, the arterial oxygen level was significantly higher (83.05 mmHg versus 68.75 mmHg; P<0.001) and the alveolar-arterial oxygen gradient was significantly lower (21.35 mmHg versus 29.11 mmHg; P<0.001) among patients receiving garlic compared with those receiving placebo. Reversal of HPS was observed in 14 of 21 patients (66.67%) on garlic supplementation (intent-to-treat analysis) and in one of 20 patients (5%) on placebo. Two of 21 patients undergoing garlic supplementation died during follow-up in contrast to seven of 20 patients who were on placebo.CONCLUSIONS: Garlic supplementation may be beneficial in patients with HPS for the reversal of intrapulmonary shunts as well as reducing hypoxemia and mortality.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Effects of Intraabdominanlly Insufflated Carbon Dioxide and Elevated Intraabdominal Pressure on Splanchnic Circulation 

1998 ◽  
Vol 89 (2) ◽  
pp. 475-482 ◽  
Author(s):  
Manfred Blobner ◽  
Ralph Bogdanski ◽  
Eberhard Kochs ◽  
Julia Henke ◽  
Alexander Findeis ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Splanchnic Circulation ◽  
Arterial Blood Flow ◽  
Intraabdominal Pressure ◽  
Arterial Blood ◽  
Baseline Values ◽  
Air Insufflation

Background Intraabdominally insufflated carbon dioxide (CO2) during laparoscopy may have a specific effect on splanchnic circulation that may be unrelated to the effects of increased intraabdominal pressure alone. Therefore, the influences of insufflation with CO2 versus air on splanchnic circulation were compared. Methods Pigs were chronically instrumented for continuous recording of mesenteric artery, portal venous, inferior vena cava, and pulmonary arterial blood flow and portal venous pressure. After induction of anesthesia, CO2 or air was insufflated in 14 and 10 pigs, respectively. With the pigs in the supine position, intraabdominal pressure was increased in steps of 4 mmHg up to 24 mmHg by graded gas insufflation. Results During air insufflation, mesenteric artery vascular resistance was unchanged, whereas mesenteric arterial blood flow decreased with increasing intraabdominal pressure. Shortly after CO2 insufflation to an intraabdominal pressure of 4 mmHg, mean arterial pressure, mesenteric arterial blood flow, and mesenteric arterial vascular resistance were increased by 21%, 12% and 9%, respectively. Subsequently, with the onset of CO2 resorption in the third minute, mean arterial pressure declined to baseline values and mesenteric arterial vascular resistance declined to 85% of baseline values, whereas mesenteric arterial blood flow continued to increase to a maximum of 24% higher than baseline values. At steady-state conditions during CO2 insufflation, mesenteric arterial blood flow was increased up to an intraabdominal pressure 16 mmHg but decreased at higher intraabdominal pressures. Conclusions In contrast to air insufflation, intraabdominal insufflation of CO2 resulted in a moderate splanchnic hyperemia at an intraabdominal pressure &lt; or = 12 mmHg. At higher intraabdominal pressure values, pressure-induced changes became more important than the type of gas used.

Pulmonary blood flow, pressure and resistance following tetraethylammonium and aminophylline

1961 ◽  
Vol 200 (2) ◽  
pp. 287-291 ◽  
Author(s):  
M. Harasawa ◽  
S. Rodbard
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Arterial Blood Flow ◽  
Tetraethylammonium Chloride ◽  
Blood Flows ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Flow Pressure

The effects of tetraethylammonium chloride (TEAC) and aminophylline on the pulmonary vascular resistance were studied in thoracotomized dogs. Pulmonary arterial blood flow and pressure, and systemic blood pressure were measured simultaneously. Both drugs showed marked hypotensive effects on the systemic vessels. In every instance pulmonary arterial pressures and blood flows were reduced by TEAC given via the pulmonary artery and increased by aminophylline. However, the calculated pulmonary vascular resistance remained essentially unchanged in all experiments. These data challenge the concept that the pulmonary vessels respond to these drugs by active vasodilatation

scholarly journals 930-103 Endogenous Nitric Oxide Production Contributes to Increases in Coronary Blood Flow During Exercise

1995 ◽  
Vol 25 (2) ◽  
pp. 115A
Author(s):  
Yutaka Ishibashi ◽  
Dirk J. Duncker ◽  
Christopher Klassen ◽  
Erik Hexeberg ◽  
Todd Pavek ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Endogenous Nitric Oxide
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