Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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We evaluated the hepatic arterial buffer response (HABR) to portal vein (PV) occlusion during 2 h of reduced superior mesenteric arterial blood flow (median 2 mL min(-1) kg(-1), range of 1-3 mL min(-1) kg(-1)) and 1 h of reperfusion in seven pigs and in seven controls. In animals with reduced mesenteric blood flow, celiac trunk blood flow (Qtr) increased during mesenteric hypoperfusion from 4 +/- 1 mL min(-1) kg(-1) (mean +/- SD) to 16 +/- 3 mL min(-1) kg(-1) (P = 0.028), and hepatic arterial blood flow (Qha) increased from 2 +/- 1 to 10 +/- 4 mL min(-1) kg(-1) (P= 0.018). The extra-hepatic fraction of Qtr (Qtr-Qha) also increased (P = 0.028). ⋯ Despite increased cardiac output, all flows from the celiac trunk decreased during reperfusion (P = 0.028) and the HABR partially recovered. We conclude that reduced mesenteric perfusion impairs the HABR, which recovers only partially after reperfusion. The distribution of the increased celiac trunk flow secondary to PV occlusion ranges from increased HABR and decreased non-hepatic blood flow (a steal) to decreased hepatic arterial blood flow and increased non-hepatic blood flow (an inverse steal).
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Interrelation of plasma nitrotyrosine (NT) concentrations in patients of septic shock and their prognosis was examined. Blood samples were obtained from 12 patients during the first episode of septic shock at hospitalization, and their plasma NT concentrations were measured. ⋯ Plasma NT concentrations (means +/- SE) of the non-survivors and survivors were 0.68 +/- 0.13 nmol/mL (n = 7), and 0.21 +/- 0.05 nmol/mL (n = 5), respectively, the former being significantly higher than the latter. The present results suggest that plasma concentration of NT relates to prognosis in human septic shock, although further studies with a larger patient population are necessary for confirmation of the suggestion.
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Comparative Study
Pathophysiologic and clinical correlates of hypophosphatemia and the relationship with sepsis and outcome in postoperative patients after hepatectomy.
Hypophosphatemia in critically ill and postoperative (p.o.) patients is a multifactorial event, and is also related to severity of illness. This study was conducted to assess pathophysiologic correlates of hypophosphatemia and the simultaneous relationship with clinical events after hepatectomy. A total of 333 measurements were obtained in 59 patients: these were performed preoperatively and at p.o. days 1, 3, and 7 in all patients, and subsequently, until recovery or death, only in those with complications. ⋯ Plasma phosphate at p.o. day 1 was related inversely to APACHE II score (r2 = 0.4, P < 0.001), and levels lower than 1.5 mg/dL were associated with an almost 4-fold increase in the rate of complications compared with cases with higher phosphate (P < 0.001). The best single variable bridging early evidence of hypophosphatemia to subsequent development of complications was plasma cholesterol, which fell significantly from p.o. day 3 onward in patients with complications compared with those recovering normally (P < 0.01), and in nonsurvivors compared with survivors (P < 0.01). Hypophosphatemia may anticipate clinical evidence of complications by reflecting an early stronger acute-phase response, with shift of phosphate from intra- to extravascular space, or true phosphorus deficiency, which may favor development of complications by impairing high-energy substrate availability for host defense and other cell functions.
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Frequent hypokalemia was noted immediately after trauma, and it was hypothesized that hypokalemia occurred more frequently in the more severely injured. A retrospective trauma registry and chart review was done on 546 trauma patients looking at admission potassium, a variety of lab tests related to potassium, specific injuries, hospital/ICU lengths of stay, and general patient demographics. Admission hypokalemia (K < 3.6 meq/l) was more frequent in those with closed head injuries (41.1% vs. 27.5%, P < .001) and in those who suffered spinal cord injuries (54.5% vs. 33.6%, P < .05). ⋯ Hypokalemic patients more likely needed a ventilator, (26.6% vs. 16.5%, P < .01) but did not have significantly more ventilator days (P > .05). Subsequently, hypokalemic patients had longer ICU lengths of stay (LOS) (2.6 vs. 1.5 days, P < .005) and longer hospital LOS (8.5 vs. 5.6 days, P < .001). When stratified into categories of "severe": (K < 3.1 meq/l), "moderate": (K = 3.1-3.3 meq/l), and "mild": (K = 3.4-3.5 meq/l) hypokalemia, those with severe hypokalemia had significantly lower GCS (10.0 vs. 13.1, p < .05), higher serum glucose levels (167 vs. 137 mg/dl, P < .05), lower creatinine levels (.77 vs. .95 mg/dl, P < .05), and longer hospital lengths of stay (13.1 days vs. 7.6 days, P < .05 results).
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Comparative Study
A 4-amino analogue of tetrahydrobiopterin attenuates endotoxin-induced hemodynamic alterations and organ injury in rats.
Most recently we have shown that 4-aminotetrahydrobiopterin (4-ABH4), an analogue of tetrahydrobiopterin (cofactor of NO synthase), even administered 2 h after endotoxin challenge, improves survival rate in rats. The following experiment was performed to examine the effects of 4-ABH4 with respect to endotoxin-induced hemodynamic alterations and organ failure. At 2 h after endotoxic challenge (10 mg kg(-1) body weight) animals received 4-ABH4 at a dose of 1, 10, or 100 mg kg(-1) body weight. ⋯ Moreover, endotoxin-induced lung edema and intestinal necrosis were significantly reduced by 4-ABH4. Our study provides information that tetrahydrobiopterin analogue, 4-ABH4, improves LPS induced hemodynamic conditions and organ injury. This may, at least in part, account for the previously observed protection of rats by 4-ABH4 against endotoxin-induced mortality in the same endotoxic shock model.