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-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.

scholarly journals Hepatopulmonary Syndrome. Review

2021 ◽  
Vol 6 (3) ◽  
pp. 45-52
Author(s):  
V. V. Potii ◽  
◽  
V. T. Kiriienko ◽  
E. I. Glukhova ◽  
O. S. Kunickaya ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Hypertension ◽  
Hepatopulmonary Syndrome ◽  
Gas Analysis ◽  
Arterial Oxygen ◽  
Common Symptom ◽  
Portopulmonary Hypertension ◽  
Oxygen Gradient ◽  
Arterial Blood ◽  
Intrapulmonary Shunting

Liver cirrhosis is often accompanied by complications from the pulmonary system. These include hydrothorax, portopulmonary hypertension and hepatopulmonary syndrome. Hepatic hydrothorax affects about 6-10% of patients with end-stage disease, which results in the passage of ascetic fluid into the pleural space through diaphragm defects. The common cause of the hepatopulmonary syndrome and portopulmonary hypertension is portal hypertension and portosystemic shunting, indicating that vasoactive and angiogenetic factors originating from the liver normally control the pulmonary circulation. Portopulmonary hypertension is like pulmonary arterial hypertension, which develops against the background of portal hypertension as a result of chronic liver disease or without other causes of increased pressure in the pulmonary vessels. The prevalence of portopulmonary hypertension ranges from 2% to 8.5% among patients with portal hypertension and is associated with a poor prognosis. Hepatopulmonary syndrome is characterized by intrapulmonary dilatation of microvessels, which causes intrapulmonary shunting and leads to impaired gas exchange in liver diseases, and is associated with a decrease in the quality and duration of life in patients with cirrhosis. Nitric oxide overproduction and angiogenesis seem to be the hallmarks of a complicated pathogenetic mechanism, leading to intrapulmonary shunting and ventilation-perfusion mismatch. A classification of hepatopulmonary syndrome according to the severity of hypoxemia has been suggested. Hepatopulmonary syndrome includes a triad: hepatic dysfunction and / or portal hypertension, dilatation of intrapulmonary vessels, and increased alveolar-arterial oxygen gradient. The prevalence of hepatopulmonary syndrome varies depending on the study groups from 5% to 30%. The most common symptom of the complication is shortness of breath, but in most cases, hepatopulmonary syndrome is asymptomatic. A decrease in oxygen saturation less than 96% corresponds to a decrease in PaO2<70 mm Hg and testifies to the possible development of hepatopulmonary syndrome. In the case of a positive screening, the patient should undergo arterial blood gas analysis, which helps to determine PaO2 and alveolar to arterial oxygen gradient. Conclusion. Contrast-enhanced echocardiography with agitated saline is the gold standard in the diagnosis of intrapulmonary dilatation. The only effective treatment for hepatopulmonary syndrome is liver transplantation. Complete recovery of hepatopulmonary syndrome after liver transplantation is observed within a year in most patients with cirrhosis and hepatopulmonary syndrome

scholarly journals A case of hepatopulmonary syndrome solved by mycophenolate mofetil (an inhibitor of angiogenesis and nitric oxide production)

2013 ◽  
Vol 58 (3) ◽  
pp. 630-633 ◽  
Author(s):  
Helena Moreira Silva ◽  
Guilhermina Reis ◽  
Margarida Guedes ◽  
Esmeralda Cleto ◽  
José Ramón Vizcaíno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mycophenolate Mofetil ◽  
Hepatopulmonary Syndrome ◽  
Nitric Oxide Production ◽  
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.

scholarly journals Frequency of hyperoxaemia during and after major surgery

2020 ◽  
Vol 48 (3) ◽  
pp. 213-220
Author(s):  
Dharshi Karalapillai ◽  
Laurence Weinberg ◽  
Philip J Peyton ◽  
Louise Ellard ◽  
Raymond Hu ◽  
...  
Keyword(s):  
Controlled Trial ◽  
Arterial Oxygen Tension ◽  
Blood Gases ◽  
Tertiary Hospital ◽  
Arterial Oxygen ◽  
Major Surgery ◽  
Arterial Line ◽  
Hospital Data ◽  
Arterial Blood Gas ◽  
Arterial Blood

The oxygen concentration (FiO2) and arterial oxygen tension (PaO2) delivered in patients undergoing major surgery is poorly understood. We aimed to assess current practice with regard to the delivered FiO2 and the resulting PaO2 in patients undergoing major surgery. We performed a retrospective cohort study in a tertiary hospital. Data were collected prospectively as part of a larger randomised controlled trial but were analysed retrospectively. Patients were included if receiving controlled mandatory ventilation and arterial line monitoring. Anaesthetists determined the FiO2 and the oxygenation saturation (SpO2) targets. An arterial blood gas (ABG) was obtained 15–20 minutes after induction of anaesthesia, immediately before the emergence phase of anaesthesia and 15 minutes after arrival in the post-anaesthesia care unit (PACU). We defined hyperoxaemia as a PaO2 of >150 mmHg and included a further threshold of PaO2 >200 mmHg. We studied 373 patients. The median (interquartile range (IQR)) lowest intraoperative FiO2 and SpO2 values were 0.45 (IQR 0.4–0.5) and 97% (IQR 96–98%), respectively, with a median PaO2 on the first and second ABG of 237 mmHg (IQR 171–291 mmHg) and 189 mmHg (IQR 145–239 mmHg), respectively. In the PACU, the median lowest oxygen flow rate was 6 L/min (IQR 3–6 L/min), and the PaO2 was 158 mmHg (IQR 120–192 mmHg). Hyperoxaemia occurred in 82%, 73% and 54% of participants on the first and second intraoperative and postoperative ABGs respectively. A PaO2 of >200 mmHg occurred in 64%, 41% and 21% of these blood gases, respectively. In an Australian tertiary hospital, a liberal approach to FiO2 and PaO2 was most common and resulted in a high incidence of perioperative hyperoxaemia.

502: Pressure Induces Nitric Oxide Production by Human Ureteral Cells in Vitro

2005 ◽  
Vol 173 (4S) ◽  
pp. 137-137
Author(s):  
Michael M. Ohebshalom ◽  
Stella K. Maeng ◽  
Jie Chen ◽  
Dix P. Poppas ◽  
Diane Felsen
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Production ◽  
Oxide Production
Sign in / Sign up

Export Citation Format

Share Document