PubMed · 15728408
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R P Cole, M L Halperin. 2005. Evaluating acid-base disorders.. https://doi.org/10.1093/qjmed%2Fhci032
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AIM: To evaluate the role of intestinal endotoxemia in the genesis of hepatopulmonary syndrome. METHODS: A rat model of cirrhosis was prepared with the method of compound factors. At the end of the eighth week, rats with cirrhosis were treated with 300 microg LPS/100 g body weight, and 1 g/rat of glycine about four h prior to LPS. After three h of LPS treatment, blood and tissues were collected for various measurements. Kupffer cells were isolated from male Wistar rats and cultured, and divided into five groups. Supernatant was harvested at 3 h after treatment with LPS for measurement of tumor necrosis factor-alpha (TNF-alpha). RESULTS: Our results showed that in rats with cirrhosis, slowed and deepened breath with occasional pause was. PaO2, PaCO2 and standard bicarbonate (SB) in arterial blood were decreased. Arterial O2 and actual bicarbonate (AB) were markedly decreased. There was a close correlation between decreased O2 and endotoxin. Metabolic acidosis accompanying respiratory alkalosis was the primary type of acid-base imbalance. The alveolar-arterial oxygen gradient was sharply widened. Massive accumulation of giant macrophages in the alveolar spaces and its wall and widened alveolar wall architecture were observed. The number of bacterial translocations in mesenteric lymph nodes increased. The ratio of TC99M-MAA brain-over-lung radioactivity rose. Endotoxin, and TNF-alpha, endothelin-1 (ET-1), nitric oxide (NO) in plasma and ET-1, carbon monoxide (CO) in lung homogenates increased. After administration of a given dosage of LPS in rats with cirrhosis, various pathological parameters worsened. Plasma level of endotoxin was related to TNF-alpha, ET-1, NO in plasma and ET-1, NO, CO in lung homogenates. TNF-alpha level was related to ET-1 and NO in plasma and lung homogenates and CO in lung homogenate as well. The level of TNF-alpha increased after infusion of LPS into culture supernatant of Kupffer cells in vitro. However, TNF-alpha significantly decreased after pretreatment with glycine, PD98059 and SB212850. Glycine could antagonize the effect of LPS in vivo and in vitro. CONCLUSION: Intestinal endotoxemia accompanying by cirrhosis may be an important mechanism in the development of hepatopulmonary syndrome in rats. Overproduction of TNF-alpha due to endotoxin stimulation of Kupffer cells via mitogen-activated protein kinase (MAPK) signal transduction pathway may be a major mechanism mediating the pathologic alterations of hepatopulmonary syndrome.
Differential diagnosis in disordered acid-base homeostasis is usually possible by measuring the pH, pCO2, pO2 and bicarbonate concentration, and enables differentiation between respiratory alkalosis and acidosis, and metabolic alkalosis and acidosis. Compensatory counter-regulation (respiratory or renal) can make correct assessment of the primary disorder problematic. Treatment of the underlying disease, in particular the provision of adequate oxygenation in respiratory disorders is of the essence. In chronic forms of metabolic acidosis, for example in chronic renal insufficiency and elderly patients, bicarbonate substitution should be initiated in order to prevent the negative effects on various organ systems. Sodium bicarbonate formulations that can be assimilated from the small bowel are especially tolerable and suitable.
OBJECTIVE: Whole body hypoperfusion and lower torso ischaemia-reperfusion contribute to post-operative organ dysfunction in patients undergoing repair of ruptured abdominal aortic aneurysm (AAA). Serum lactate and base deficit are markers of tissue ischaemia and are used to assess the adequacy of resuscitation. This study examines the prognostic value of immediate post-operative levels of serum lactate and base deficit in ruptured AAA. METHODS: Thirty patients (24 men and 6 women of median age 74, range 51-85, years) who survived to at least 12h after ruptured AAA repair were studied retrospectively. The relationship between immediate post-operative lactate, base deficit and mortality was determined. RESULTS: Fifteen patients (50%) died, all from organ failure. An elevated lactate (>2.1 mmol/l) and base deficit (<-2 mmol/l) were present in 20 (67%) and 27 (90%) patients, respectively. Lactate (p<0.001) and base deficit (p=0.003) were significantly higher in non-survivors compared with survivors. Lactate (p=0.021) and base deficit levels (p=0.028) were independently significant for predicting mortality and a significant interaction existed between lactate and base deficit levels for predicting mortality (p=0.027). The sensitivity and specificity of lactate > or =4.0 mmol/l was 13 of 15 (87%) and 12 of 15 (80%), respectively, and base deficit < or =-7 mmol/l was 12 of 15 (80%) and 12 of 15 (80%), respectively. The likelihood ratios for a positive result with the defined cut-off values for lactate and base deficit were 4.3 and 4.0, respectively. Lactate > or =4.0 mmol/l and base deficit or =-7 mmol/l were associated with a 4% probability of death. CONCLUSION: These data demonstrate that an immediate post-operative serum lactate > or =4.0 mmol/l and base deficit < or =-7 mmol/l are good predictors of outcome after ruptured AAA repair. The prognostic value of these simple and inexpensive tests require corroboration in a larger prospective study.