Effects of methylene blue on oxygen availability and regional blood flow during endotoxic shock

Rats were exposed to hypobaric hypoxia (0.5 atm) for up to 3 wk. Hypoxic rats failed to gain weight but maintained normal brain water and ion content. Blood hematocrit was increased by 48% to a level of 71% after 3 wk of hypoxia compared with littermate controls. Brain blood flow was increased by an average of 38% in rats exposed to 15 min of 10% normobaric oxygen and by 23% after 3 h but was not different from normobaric normoxic rats after 3 wk of hypoxia. Sucrose space, as a measure of brain plasma volume, was not changed under any hypoxic conditions. The mean brain microvessel density was increased by 76% in the frontopolar cerebral cortex, 46% in the frontal motor cortex, 54% in the frontal sensory cortex, 65% in the parietal motor cortex, 68% in the parietal sensory cortex, 68% in the hippocampal CA1 region, 57% in the hippocampal CA3 region, 26% in the striatum, and 56% in the cerebellum. The results indicate that hypoxia elicits three main responses that affect brain oxygen availability. The acute effect of hypoxia is an increase in regional blood flow, which returns to control levels on continued hypoxic exposure. Longer-term effects of continued moderate hypoxic exposure are erythropoiesis and a decrease in intercapillary distance as a result of angiogenesis. The rise in hematocrit and the increase in microvessel density together increase oxygen availability to the brain to within normal limits, although this does not imply that tissue PO2 is restored to normal.

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THE EFFECT OF IBUPROFEN AND NALOXONE ON REGIONAL BLOOD FLOW DURING ENDOTOXIC SHOCK

Anesthesiology ◽

10.1097/00000542-198609001-00095 ◽

1986 ◽

Vol 65 (Supplement 3A) ◽

pp. A96

Author(s):

M. Nishijima ◽

M. Breslow ◽

C. Miller ◽

R. J. Traystman

Keyword(s):

Blood Flow ◽

Regional Blood Flow ◽

Endotoxic Shock

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Effects of Nitric Oxide Synthase Inhibition on Regional Blood Flow in a Porcine Model of Endotoxic Shock

The Journal of Trauma: Injury, Infection, and Critical Care ◽

10.1097/00005373-199508000-00025 ◽

1995 ◽

Vol 39 (2) ◽

pp. 338-343 ◽

Cited By ~ 24

Author(s):

Patrick J. Offner ◽

Frank M. Robertson ◽

Basil A. Pruitt

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Nitric Oxide Synthase ◽

Porcine Model ◽

Regional Blood Flow ◽

Endotoxic Shock ◽

Oxide Synthase

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Diaspirin cross-linked hemoglobin improves oxygen extraction capabilities in endotoxic shock

Journal of Applied Physiology ◽

10.1152/jappl.2000.89.4.1437 ◽

2000 ◽

Vol 89 (4) ◽

pp. 1437-1444 ◽

Cited By ~ 8

Author(s):

Jacques Creteur ◽

Haibo Zhang ◽

Daniel De Backer ◽

Qinghua Sun ◽

Jean-Louis Vincent

Keyword(s):

Blood Flow ◽

Cardiac Index ◽

Cardiac Tamponade ◽

Regional Blood Flow ◽

Endotoxic Shock ◽

Oxygen Extraction ◽

Whole Body ◽

Control Group ◽

Tissue Oxygen ◽

Critical Oxygen

We studied the effects of diaspirin cross-linked hemoglobin (DCLHb), a cell-free hemoglobin derived from human erythrocytes, on blood flow distribution and tissue oxygen extraction capabilities in endotoxic shock. Eighteen pentobarbital sodium-anesthetized, mechanically ventilated dogs received 2 mg/kg of E. coli endotoxin, followed by saline resuscitation to restore cardiac filling pressures to baseline levels. The animals were randomly divided into three groups: six served as control, six received DCLHb at a dose of 500 mg/kg ( group 1) and six DCLHb at a dose of 1,000 mg/kg ( group 2). Cardiac tamponade was then induced by saline injection in the pericardial sac to progressively reduce cardiac index and thereby allow study of tissue oxygen extraction capabilities. DCLHb had a dose-dependent vasopressor effect but did not significantly alter cardiac index or regional blood flow. During cardiac tamponade, critical oxygen delivery was 12.8 ± 0.7 ml · kg−1 · min−1 in the control group, but 8.6 ± 0.9 and 8.2 ± 0.7 ml · kg−1 · min−1 in groups 1 and 2, respectively (both P < 0.05 vs. control group). The critical oxygen extraction ratio was 39.1 ± 3.1% in the control group but 58.7 ± 12.8% and 60.2 ± 9.0% in groups 1and 2, respectively. We conclude that DCLHb can improve whole body oxygen extraction capabilities during endotoxic shock in dogs.

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Effect of naloxone and ibuprofen on organ blood flow during endotoxic shock in pig

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.1.h177 ◽

1988 ◽

Vol 255 (1) ◽

pp. H177-H184 ◽

Cited By ~ 1

Author(s):

M. K. Nishijima ◽

M. J. Breslow ◽

C. F. Miller ◽

R. J. Traystman

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Arterial Blood Pressure ◽

Mean Arterial Blood Pressure ◽

Regional Blood Flow ◽

Endotoxic Shock ◽

Organ Blood Flow ◽

Group Iii ◽

Arterial Blood ◽

Group I

The effects of an opiate antagonist naloxone and a cyclooxygenase inhibitor ibuprofen on organ blood flow during endotoxic shock were evaluated in a fluid-resuscitated porcine endotoxic shock model. Radiolabeled microspheres were used to measure regional blood flow. Escherichia coli endotoxin (0.1 mg/kg), infused intravenously over 40 min, reduced mean arterial blood pressure to 50 mmHg and systemic vascular resistance to 57% of control without affecting cardiac output. Endotoxin reduced blood flow to cerebrum (to 49% of control), kidney (to 25% of control), spleen, and skeletal muscle, while blood flow to left ventricle, stomach, and small and large intestines were unaffected. Sixty minutes after endotoxin administration, animals were randomized to one of three groups. Group I animals were controls and received no drug, group II animals received ibuprofen (12.5 mg/kg iv), and group III animals received naloxone (2 mg/kg iv) 60 min after endotoxin. Ibuprofen increased mean arterial blood pressure to 80 mmHg and increased blood flow to both cerebrum (to 92% of control) and kidney (to 47% of control). Plasma levels of thromboxane B2 and 6-ketoprostaglandin F1 alpha were increased 8- and 16-fold, respectively, after endotoxin, and both were decreased by ibuprofen. Naloxone increased mean arterial blood pressure to 62 mmHg but had no effect on regional blood flow or plasma cyclooxygenase metabolite levels. These data suggest that cyclooxygenase metabolites may contribute to decreased mean arterial blood pressure and reduced organ blood flow during endotoxic shock in the pig.

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