PubMed · 2750564
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K Grumboch, Y Abrams. Epidural anesthesia.. https://pubmed.ncbi.nlm.nih.gov/2750564/
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OBJECTIVE: To investigate whether sympathetic blockade by means of thoracic epidural anaesthesia (TEA) increases intestinal perfusion during normotensive endotoxaemia. DESIGN: A prospective, randomised and controlled animal study. SETTING: Animal laboratory in a university hospital. SUBJECTS: Sprague-Dawley male rats. INTERVENTIONS: The rats were anaesthetised with urethane and ketamine, mechanically ventilated and haemodynamically monitored. Lidocaine or saline were infused continuously via thoracic epidural catheters followed by a continuous intravenous infusion of Escherichia coli lipopolysaccharide (1.5 mg/kg per h). Densities of perfused and non-perfused capillaries (i.e., with and without erythrocyte perfusion, respectively) as well as erythrocyte velocity in both the mucosa and the muscularis of the terminal ileum were determined using intravital microscopy. MEASUREMENTS AND RESULTS: Measurements were performed at baseline, after 30 min of epidural infusion as well as after 60 and 120 min of lipopolysaccharide infusion. In animals receiving TEA, mean arterial pressure and heart rate were significantly reduced throughout the experiment. In the muscularis the endotoxaemia-induced increase in non-perfused capillaries was absent with epidural lidocaine (0 [0/0] versus 39 [36/137] cm(-1), median [25(th)/75(th) percentile]), whereas in the mucosa perfused capillary density declined to a greater extent than in controls (-47 [-53/-23]%) versus -19 [-34/+10]%, p<0.05). Erythrocyte velocity decreased with endotoxaemia and was not influenced by epidural lidocaine. CONCLUSIONS: Microvascular perfusion data during endotoxaemia show a redistribution of blood flow towards the mucosa. TEA seems to impede this redistribution resulting in improved muscularis and worsened mucosal microvascular perfusion.
BACKGROUND: The effects of thoracic epidural anaesthesia (TEA) on gastric mucosal microvascular haemoglobin oxygenation (microHbO(2)) are unclear. At the splanchnic level, reduction of sympathetic tone may promote vasodilation and increase microHbO(2). However, these splanchnic effects are counteracted by systemic effects of TEA (e.g., decreased cardiac output (CO) and mean arterial pressure (MAP)), thus making the net effect on microHbO(2) difficult to predict. In this respect, effects of TEA on microHbO(2) may differ between physiological and compromised circulatory conditions, and additionally may depend on adequate fluid resuscitation. Furthermore, TEA may alter the relationship between regional microHbO(2) and systemic oxygen-transport (DO(2)). METHODS: Chronically instrumented dogs (flow probes for CO measurement) were anaesthetized, their lungs ventilated and randomly received TEA with lidocaine (n=6) or epidural saline (controls, n=6). Animals were studied under physiological and compromised circulatory conditions (PEEP 10 cm H(2)O), both with and without fluid resuscitation. We measured gastric mucosal microHbO(2) by reflectance spectrophotometry, systemic DO(2), and systemic haemodynamics (CO, MAP). RESULTS: Under physiological conditions, TEA preserved microHbO(2) (47 (3)% and 49 (5)%, mean (sem)) despite significantly decreasing DO(2) (11.3 (0.8) to 10.0 (0.7) ml kg(-1) min(-1)) and MAP (66 (2) to 59 (3) mm Hg). However, during compromised circulatory conditions, TEA aggravated the reduction in microHbO(2) (to 32 (1)%), DO(2) (to 6.7 (0.8) ml kg(-1) min(-1)) and MAP (to 52 (4) mm Hg), compared with controls. During TEA, fluid resuscitation completely restored these variables. TEA preserved the correlation between microHbO(2) and DO(2), compared with controls. CONCLUSIONS: TEA maintains microHbO(2) under physiological conditions, but aggravates the reduction of microHbO(2) induced by cardiocirculatory depression, thereby preserving the relationship between gastric mucosal and systemic oxygenation.