OBJECTIVE: To evaluate the effects of nitroglycerin (glyceryl trinitrate) on intestinal microcirculation during endotoxaemic shock. DESIGN: Controlled experimental study. SETTING: Research laboratory. SUBJECTS: 20 anaesthetised, mechanically ventilated sheep. INTERVENTIONS: Septic shock was induced by endotoxin infusion. After 60 minutes without resuscitation, sheep received fluid resuscitation and were randomised to control or nitroglycerin groups. Nitroglycerin was infused at a rate of 0.2 µg/kg/min for 90 minutes. MAIN OUTCOME MEASURE: Improved villi microcirculation. RESULTS: Endotoxin lowered arterial blood pressure, cardiac output and intestinal blood flow, which were improved by fluid resuscitation. Mean (SD) ileal intramucosal-arterial PCO2 gradient increased during shock and remained elevated after resuscitation in control and nitroglycerin groups (8 [8], 15 [9] and 17 [9], and 6 [6], 13 [11] and 14 [9]mmHg, respectively; P < 0.05, baseline v shock and resuscitation for both groups). Villi microvascular flow index was reduced during shock and remained lower than baseline after the resuscitation in both groups (3.0 [0.0], 2.5 [0.2] and 2.7 [0.2], and 3.0 [0.0], 2.3 [0.3] and 2.6 [0.3], respectively; P < 0.05, baseline v shock and resuscitation for both groups). The red blood cell velocity behaved similarly (859 [443], 553 [236] and 670 [276], and 886 [440], 447 [124] and 606 [235] µm/s, respectively; P < 0.05, baseline v shock and resuscitation for both groups). CONCLUSIONS: In endotoxaemic sheep, low doses of nitroglycerin failed to improve the subtle but persistent villi hypoperfusion that remains present after fluid resuscitation.
OBJECTIVE: To evaluate the effects of nitroglycerin (glyceryl trinitrate) on intestinal microcirculation during endotoxaemic shock. DESIGN: Controlled experimental study. SETTING: Research laboratory. SUBJECTS: 20 anaesthetised, mechanically ventilated sheep. INTERVENTIONS:Septic shock was induced by endotoxin infusion. After 60 minutes without resuscitation, sheep received fluid resuscitation and were randomised to control or nitroglycerin groups. Nitroglycerin was infused at a rate of 0.2 µg/kg/min for 90 minutes. MAIN OUTCOME MEASURE: Improved villi microcirculation. RESULTS: Endotoxin lowered arterial blood pressure, cardiac output and intestinal blood flow, which were improved by fluid resuscitation. Mean (SD) ileal intramucosal-arterial PCO2 gradient increased during shock and remained elevated after resuscitation in control and nitroglycerin groups (8 [8], 15 [9] and 17 [9], and 6 [6], 13 [11] and 14 [9]mmHg, respectively; P < 0.05, baseline v shock and resuscitation for both groups). Villi microvascular flow index was reduced during shock and remained lower than baseline after the resuscitation in both groups (3.0 [0.0], 2.5 [0.2] and 2.7 [0.2], and 3.0 [0.0], 2.3 [0.3] and 2.6 [0.3], respectively; P < 0.05, baseline v shock and resuscitation for both groups). The red blood cell velocity behaved similarly (859 [443], 553 [236] and 670 [276], and 886 [440], 447 [124] and 606 [235] µm/s, respectively; P < 0.05, baseline v shock and resuscitation for both groups). CONCLUSIONS: In endotoxaemic sheep, low doses of nitroglycerin failed to improve the subtle but persistent villi hypoperfusion that remains present after fluid resuscitation.