Right ventricular overload causes the decrease in cardiac output after nitric oxide synthesis inhibition in endotoxemia

Critical Care Medicine

Volumn 26, Issue 4, 1998, Pages 738-747

  Cohen, Rubin I ^a,b,c   Shapir, Yehuda ^a,b   Chen, Ling ^a,b   Scharf, Steven M ^a,b  

^a SCHNEIDER CHILDREN'S HOSPITAL   (United States)

^b ALBERT EINSTEIN COLLEGE OF MEDICINE   (United States)

^c LONG ISLAND JEWISH MEDICAL CENTER   (United States)

Author keywords

Cardiac output; Endotoxin; L NAME; Left ventricle; Nitric oxide inhibition; Pulmonary hypertension; Right ventricle; Sepsis; Septic shock; Tonometry

Indexed keywords

ENDOTOXIN; N(G) NITROARGININE METHYL ESTER; NITRIC OXIDE; SODIUM CHLORIDE;

ANIMAL EXPERIMENT; ANIMAL MODEL; AORTA OCCLUSION; ARTICLE; CONTROLLED STUDY; ENDOTOXEMIA; FEMALE; HEART OUTPUT; HEART RIGHT VENTRICLE FAILURE; HEART RIGHT VENTRICLE OVERLOAD; HEART RIGHT VENTRICLE VOLUME; LUNG ARTERY PRESSURE; MEAN ARTERIAL PRESSURE; NONHUMAN; PRIORITY JOURNAL; PULMONARY ARTERY OCCLUSION; PULMONARY HYPERTENSION; STOMACH MUCOSA; STOMACH PH; SWINE; THORACIC AORTA;

ANIMALS; CARDIAC OUTPUT; ENDOTOXEMIA; ENZYME INHIBITORS; FEMALE; GASTRIC MUCOSA; HEART VENTRICLES; HEMODYNAMIC PROCESSES; NG-NITROARGININE METHYL ESTER; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; SWINE;

EID: 0031944732     PISSN: 00903493     EISSN: None     Source Type: Journal    
DOI: 10.1097/00003246-199804000-00026     Document Type: Article

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