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      Microvascular Blood Flow Is Altered in Patients with Sepsis

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          Abstract

          Microvascular blood flow alterations are frequent in animal models of sepsis and may impair tissue oxygenation. We hypothesized that alterations of the microcirculation are present in patients with sepsis. We used an orthogonal polarization spectral imaging technique to investigate the sublingual microcirculation in 10 healthy volunteers, 16 patients before cardiac surgery, 10 acutely ill patients without sepsis (intensive care unit control subjects), and 50 patients with severe sepsis. The effects of topical application of acetylcholine (10(-2) M) were tested in 11 patients with sepsis. In each subject, five to seven sublingual areas were recorded and analyzed semiquantitatively. Data were analyzed with nonparametric tests and are presented as medians (25th-75th percentiles). No significant difference in microvascular blood flow was observed between healthy volunteers and patients before cardiac surgery or intensive care unit control subjects. The density of all vessels was significantly reduced in patients with severe sepsis (4.5 [4.2-5.2] versus 5.4 [5.4-6.3]/mm in volunteers, p < 0.01). The proportion of perfused small (< 20 microm) vessels was reduced in patients with sepsis (48 [33-61] versus 90 [89-92]% in volunteers, p < 0.001). These alterations were more severe in nonsurvivors. The topical application of acetylcholine totally reversed these alterations. In conclusion, microvascular blood flow alterations are frequent in patients with sepsis and are more severe in patients with a worse outcome.

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          Most cited references30

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          The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine.

          Despite its very potent vasodilating action in vivo, acetylcholine (ACh) does not always produce relaxation of isolated preparations of blood vessels in vitro. For example, in the helical strip of the rabbit descending thoracic aorta, the only reported response to ACh has been graded contractions, occurring at concentrations above 0.1 muM and mediated by muscarinic receptors. Recently, we observed that in a ring preparation from the rabbit thoracic aorta, ACh produced marked relaxation at concentrations lower than those required to produce contraction (confirming an earlier report by Jelliffe). In investigating this apparent discrepancy, we discovered that the loss of relaxation of ACh in the case of the strip was the result of unintentional rubbing of its intimal surface against foreign surfaces during its preparation. If care was taken to avoid rubbing of the intimal surface during preparation, the tissue, whether ring, transverse strip or helical strip, always exhibited relaxation to ACh, and the possibility was considered that rubbing of the intimal surface had removed endothelial cells. We demonstrate here that relaxation of isolated preparations of rabbit thoracic aorta and other blood vessels by ACh requires the presence of endothelial cells, and that ACh, acting on muscarinic receptors of these cells, stimulates release of a substance(s) that causes relaxation of the vascular smooth muscle. We propose that this may be one of the principal mechanisms for ACh-induced vasodilation in vivo. Preliminary reports on some aspects of the work have been reported elsewhere.
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            Mitochondrial membrane potential and apoptosis peripheral blood monocytes in severe human sepsis.

            Reduced mitochondrial membrane potential (Delta(Psi)m), which is considered as an initial and irreversible step towards apoptosis, as well as cell death regulating proteins, such as Fas, Hsp70, or Bcl-2, may play an important role in sepsis. We studied the relationship between sepsis severity and peripheral blood monocyte Delta(Psi)m, cell death (necrosis and apoptosis), soluble Fas ligand, Hsp70, and Bcl-2 expression over time in 18 patients with sepsis, and compared these data with those of a group of 17 healthy control subjects. All measurements were performed within 3 d of the onset of severe sepsis (T1), then 7 to 10 d later (T2), and finally at hospital discharge (T3). Delta(Psi)m was expressed as the percent monocytes with altered Delta(Psi)m (%Delta(Psi)m). Patients with sepsis had greater %Delta(Psi)m at T1 and T2 but not at T3 (14.6 +/- 2.6% and 15.9 +/- 2%, respectively, versus control 6.6 +/- 0.2%, p < 0.01). Septic patients exhibited greater cell death in their monocytes and had greater Hsp70 expression only at T1. Bcl-2 levels were similar in septic and control subjects. Comparing survivors with non-survivors of sepsis, nonsurvivors had a greater %Delta(Psi)m at T1 (26.4 +/- 5.3% versus 10.1 +/- 2.7%, p < 0.01) and a significant decrease in Bcl-2 expression, whereas no difference was found in Hsp70 levels. These results indicate that mitochondrial dysfunction and subsequent cell death occur in severe sepsis and suggest that %Delta(Psi)m is a marker of severity in human sepsis. mitochondria; apoptosis; sepsis; heat-shock protein 70; proto-oncogene protein c-Bcl-2
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              Decreased capillary density in vivo in bowel mucosa of rats with normotensive sepsis.

              Translocation of bacteria and endotoxin leading to sepsis occurs in animals subjected to burns or intestinal ischemia. This may be mediated in part by bowel mucosal microcirculatory dysfunction. However, the direct effect of sepsis on the mucosal microcirculation is unknown. The objective of this study was to develop a technique for intravital microscopy of the mucosa of the small bowel in an animal model of normotensive sepsis. We tested the hypothesis that normotensive sepsis induced by cecal ligation and perforation leads to a decrease in perfused capillaries in the small bowel mucosa at 24 hr. Twelve male Sprague-Dawley rats were hemodynamically monitored and randomly assigned to cecal ligation and perforation (CLP) or control laparotomy (sham). Twenty-four hours after initial surgery each animal was reanesthetized and the mucosal surface of the distal small bowel prepared for intravital microscopy. Laser doppler measurements of bowel wall blood flow were made immediately and repeated after a 30-min stabilization period. Intravital microscopy of the mucosal microcirculation of six villi per animal was performed and the images recorded on videotape (2 min/villus). The areas surrounded by perfused capillaries (intercapillary area) were then measured using video analysis software. Laser doppler flowmetry revealed a decrease in bowel wall blood flow during the stabilization period in the shams that did not occur in the CLP rats. The intercapillary areas were significantly greater in the CLP rats compared to sham rats (1329 +/- 316 microns2 vs 979 +/- 217 microns2, P = 0.044). The intercapillary areas were also more highly variable in the CLP group (median coefficient of variation 102 vs 83% in the sham group, P = 0.025). Intravital microscopy may be used to examine microcirculatory function of the small bowel mucosa. Sepsis induced by CLP leads to a decrease in the number of perfused capillaries in the small bowel mucosa.
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                Author and article information

                Journal
                American Journal of Respiratory and Critical Care Medicine
                Am J Respir Crit Care Med
                American Thoracic Society
                1073-449X
                1535-4970
                July 2002
                July 2002
                : 166
                : 1
                : 98-104
                Article
                10.1164/rccm.200109-016OC
                12091178
                6a472013-2259-4cb0-92e5-74e546fdd562
                © 2002
                History

                Molecular medicine,Neurosciences
                Molecular medicine, Neurosciences

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