Rabbit skeletal muscle PO2 during hypodynamic sepsis (original) (raw)
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AJP: Heart and Circulatory Physiology, 2004
Inherent in the inflammatory response to sepsis is abnormal microvascular perfusion. Maldistribution of capillary red blood cell (RBC) flow in rat skeletal muscle has been characterized by increased 1) stopped-flow capillaries, 2) capillary oxygen extraction, and 3) ratio of fast-flow to normal-flow capillaries. On the basis of experimental data for functional capillary density (FCD), RBC velocity, and hemoglobin O2 saturation during sepsis, a mathematical model was used to calculate tissue O2 consumption (Vo2), tissue Po2 (Pt) profiles, and O2 delivery by fast-flow capillaries, which could not be measured experimentally. The model describes coupled capillary and tissue O2 transport using realistic blood and tissue biophysics and three-dimensional arrays of heterogeneously spaced capillaries and was solved numerically using a previously validated scheme. While total blood flow was maintained, capillary flow distribution was varied from 60/30/10% (normal/fast/stopped) in control to 33/33/33% (normal/fast/stopped) in average sepsis (AS) and 25/25/50% (normal/fast/stopped) in extreme sepsis (ES). Simulations found approximately two- and fourfold increases in tissue Vo2 in AS and ES, respectively. Average (minimum) Pt decreased from 43 (40) mmHg in control to 34 (27) and 26 (15) mmHg in AS and ES, respectively, and clustering fast-flow capillaries (increased flow heterogeneity) reduced minimum Pt to 14.5 mmHg. Thus, although fast capillaries prevented tissue dysoxia, they did not prevent increased hypoxia as the degree of microvascular injury increased. The model predicts that decreased FCD, increased fast flow, and increased Vo2 in sepsis expose skeletal muscle to significant regions of hypoxia, which could affect local cellular and organ function.
The prognostic value of muscle StO2 in septic patients
Intensive Care Medicine, 2007
Objective:: To quantify sepsis-induced alterations in changes in muscle tissue oxygenation (StO 2 ) after an ischemic challenge using near-infrared spectroscopy (NIRS), and to test the hypothesis that these alterations are related to outcome. Design: Prospective study. Setting: Thirty-one-bed, university hospital Department of Intensive Care. Patients: Seventy-two patients with severe sepsis or septic shock, 18 hemodynamically stable, acutely ill patients without infection, and 18 healthy volunteers. Interventions: Three-minute occlusion of the brachial artery using a cuff inflated 50 mmHg above systolic arterial pressure. Measurements and main results: Thenar eminence StO 2 was measured continuously by NIRS before (StO 2 baseline), during, and after the 3-min occlusion. Changes in StO 2 were assessed by the slope of increase in StO 2 during the first 14 s following the ischemic period and by the difference between the maximum StO 2 and StO 2 baseline (∆). The slope was lower in septic patients than in controls and volunteers [2.3 (1.3-3.6), 4.8 (3.5-6.0), and 4.7 (3.2-6.3) %/s, p < 0.001]. ∆ was also significantly lower in septic patients than in the other groups. Slopes were lower in septic patients with than without shock [2.0 (1.2-2.9) vs 3.2 (1.8-4.5) %/s, p < 0.05]. In 52 septic patients, in whom the slope was obtained every 24 h for 48 h, slopes were higher in survivors than in non-survivors and tended to increase in survivors but not in non-survivors. Conclusions: Altered recovery in StO 2 after an ischemic challenge is frequent in septic patients and more pronounced in the presence of shock. The presence and persistence of these alterations in the first 24 h of sepsis are associated with worse outcome.
Substrate balances across skeletal muscle tissue in severe sepsis
Clinical Nutrition, 1984
Substrate metabolism of skeletal muscle was studied by the forearm technique in eight patients with severe sepsis. The data were compared to those of 13 patients after elective surgery. In the septic group forearm blood flow was increased, but muscular utilisation of oxygen was diminished. Arterial concentrations of free fatty acids and ketone bodies were low. Thus, both only played a minor role in the supply of skeletal muscle with substrates. From the decreased production of lactate and alanine and the comparable utilisation of glucose we conclude that in the septic patients energy expenditure of skeletal muscle was mainly met by oxidation of glucose. In contrast to reduced lipolysis of adipose tissue intramuscular lipolysis may still be working since muscular production of lactate and glycerol was correlated. These findings suggest a changing pattern of arterial supply of substrates and utilisation of substrates by skeletal muscle during deterioration of clinical condition in the course of sepsis.
Sepsis and the muscle tissue. A narrative review
Romanian Journal of Internal Medicine, 2021
Sepsis and septic shock are considered major factors in the development of myopathy in critically ill patients, which is correlated with increased morbidity rates and ICU length of stay. The underlying pathophysiology is complex, involving mitochondrial dysfunction, increased protein breakdown and muscle inexcitability. Sepsis induced myopathy is characterized by several electrophysiological and histopathological abnormalities of the muscle, also has clinical consequences such as flaccid weakness and failure to wean from ventilator. In order to reach definite diagnosis, clinical assessment, electrophysiological studies and muscle biopsy must be performed, which can be challenging in daily practice. Ultrasonography as a screening tool can be a promising alternative, especially in the ICU setting. Sepsis and mechanical ventilation have additive effects leading to diaphragm dysfunction thus complicating the patient’s clinical course and recovery. Here, we summarize the effects of the s...
Large changes in renal microvascular PO2during acute normovolemic hemodilution
2006
Objective To examine the effects of short-term cyclic stretch on apoptosis in alveolar type II cells (A549). To study in vitro the direct influence of alveolar type II cells on mechanical stretch. Methods A549 were treated with different doses of lipopolysaccharide (LPS), 0 ng/ml, 1 ng/ml, 10 ng/ml, 100 ng/ml, 1000 ng/ml, and then A549 were lengthened 5%, 15%, 30% using a FLEXCELL tension unit 4000, a vacuum-driven device that applies strain to cells, which were cultured in six-well plates coated with collagen-I, and 12 cycles/min for 4 hours. Apoptosis was measured using the flow cytometry method that measures annexin V and propidium iodide (PI) staining. The morphological changes of apoptotic cells were observed by transmission electron microscope. Results Apoptosis could be induced in alveolar type II cells (A549) by mechanical stretch. The percentage of annexin V + PI cells increased after being treated with cyclic stretch for 4 hours by 5%, 15%, 30% in all groups. The morphological features of apoptotic cells demonstrated by transmission electron microscope were as follows: shrinkage of the cell, chromatin condensation and aggregation under the nuclear membrane as a crescent or lump, membrane-encapsulated nuclear fragment or cell organ formed by invagination of the cell membrane, and apoptotic body formation followed by vacuolization. Conclusion Apoptosis induced by mechanical stretch and LPS is dose dependent. Mechanical stretch aggravates apoptosis especially in cells treated with LPS. Annexin V and PI double staining is a specific, sensitive, and quantitative method for analyzing apoptotic cells. It is also helpful to clarify the protective mechanism of low-volume ventilation in ARDS. PaO 2 /FiO 2 430 [421; 440] # 380 [349; 397] 165 [68; 289] # C (ml/cmH 2 O) 28 [24; 32]* 18 [16; 21]* 12 [8; 17]* R i (cmH 2 O/l/s) 4.1 [3.9; 4.5] 4.5 [4.3; 5.1] 5.1 [3.7; 7.9] # P < 0.05 control vs 24-hour peritonitis, *P < 0.05 control vs 12-hour and 24-hour peritonitis.