Biomedical subjects

Nanae Hangai-Hoger

Publications and source records attributed to Nanae Hangai-Hoger.

5 recordsLinked to original sources

PubMed2006

Microvascular effects following treatment with polyethylene glycol-albumin in lipopolysaccharide-induced endotoxemia.

OBJECTIVE: To determine whether resuscitation with polyethylene glycol conjugated bovine serum albumin (2.5% weight/volume) infused at 16 mL/kg/hr (PEG-BSA-16) or at 24 mL/kg/hr (PEG-BSA-24) for 1 hr improves microcirculatory conditions in endotoxemia compared with dextran 70 (6% weight/volume) infused at 24 mL/kg/hr (Dex). DESIGN: Prospective study. SETTING: University research laboratory. SUBJECTS: Male Golden Syrian hamsters. INTERVENTIONS: Hamsters implemented with a skinfold window chamber were given an intravenous injection of lipopolysaccharide and resuscitated within 10 mins with Dex, PEG-BSA-16, or PEG-BSA-24. MEASUREMENTS AND MAIN RESULTS: Hamsters were observed during 24 hrs after lipopolysaccharide injection. Systemic variables measured included mean arterial pressure, heart rate, and systemic arterial blood gas. Microvascular function was characterized by measuring vessel diameter; red blood cell velocity; functional capillary density (FCD); P(O2) in arterioles, venules, and tissue; and perivascular nitric oxide concentration 6 hrs after lipopolysaccharide injection. At 6 hrs, animals with no treatment had the lowest FCD (6.7 +/- 5.7% of baseline). PEG-BSA provided significantly improved microvascular conditions as shown by restoration of FCD. Recovery of FCD was related to improved microvascular flow and perivascular and tissue P(O2), normalization of shear rate, and decreased perivascular nitric oxide concentration. These effects were related to improved fluid retention using PEG-BSA-24 as evidenced by the significantly lower hematocrit at 24 hrs after resuscitation. Nitric oxide at 6 hrs after induction of sepsis achieved perivascular millimolar concentrations, which were reduced to normal values by PEG-BSA-24 treatment. At 6 hrs there were significant differences in FCD, tissue P(O2), and perivascular nitric oxide concentration following PEG-BSA treatment by comparison with Dex treatment, although there were no differences in systemic variables between Dex and PEG-BSA groups. CONCLUSIONS: PEG-BSA produces improved microcirculatory conditions in the treatment of endotoxemia when compared with dextran 70.

Animals↗

PubMed2006

The vascular wall as a regulator of tissue oxygenation.

PURPOSE OF REVIEW: The development of the phosphorescence quenching oxygen measurement technique has allowed for a simultaneous measurement of intra and perivascular partial pressure oxygen along arteriolar vessels in vivo. Mapping the microvascular distribution and oxygen gradients across the vascular walls using this high-resolution technique reveals the existence of large radial gradients between the vasculature and the tissue, with concomitant longitudinal oxygen loss. Mass balance analysis along vessel segments indicates that the vascular wall has a high rate of oxygen consumption. This review presents the current status of in-vivo studies on the partitioning of oxygen between blood, the vascular wall and the surrounding tissue, thereby positioning an oxygen sink between blood and tissue regulating oxygen release. RECENT FINDINGS: Induced vasoactivity (vasoconstriction and vasodilation) has been shown to modulate oxygen consumption of the vascular wall and directly affect the portion of oxygen available to the tissue. Inhibition of the endothelial layer of the vessel wall resulted in a decrease in the oxygen gradient across the vessel. SUMMARY: The vascular wall is a sink for oxygen. The modulation of vessel wall oxygen consumption can substantially impact the amount of oxygen released to the tissue.

Arteries↗

PubMed2004

Microvascular oxygen delivery and consumption following treatment with verapamil.

The microvascular distribution of oxygen was studied in the arterioles and venules of the awake hamster window chamber preparation to determine the contribution of vascular smooth muscle relaxation to oxygen consumption of the microvascular wall during verapamil-induced vasodilatation. Verapamil HCl delivered in a 0.1 mg/kg bolus injection followed by a continuous infusion of 0.01 mg.kg(-1).min(-1) caused significant arteriolar dilatation, increased microvascular flow and functional capillary density, and decreased arteriolar vessel wall transmural Po(2) difference. Verapamil caused tissue Po(2) to increase from 25.5 +/- 4.1 mmHg under control condition to 32.0 +/- 3.7 mmHg during verapamil treatment. Total oxygen released by the microcirculation to the tissue remained the same as at baseline. Maintenance of the same level of oxygen release to the tissue, increased tissue Po(2), and decreased wall oxygen concentration gradient are compatible if vasodilatation significantly lowers vessel wall oxygen consumption, which in this model appears to constitute an important oxygen-consuming compartment. These findings show that treatment with verapamil, which increases oxygen supply through vasodilatation, may further improve tissue oxygenation by lowering oxygen consumption of the microcirculation.

Animals↗

PubMed2004

Oxygen distribution and respiration by the microcirculation.

Longitudinal and radial oxygen gradients in the microcirculation due to oxygen release from arterioles show that in some tissues oxygen is primarily supplied by arterioles and secondarily by capillaries. In several tissues, the arteriolar rate of oxygen exit is too large to be explained by diffusion alone, indicating that in these tissues oxygen consumption of the arteriolar wall in vivo is much greater than that shown in in vitro studies of endothelium and vascular smooth muscle, a phenomenon that may be related to the synthesis autocoids by the endothelium in vivo. The functional significance of the high metabolic rate of the arteriolar vessels may be related to the need of providing a metabolic barrier for protecting the parenchymal tissue from high oxygen levels in arterial blood, thus reducing formation of oxygen free radicals in the perivascular tissue, a supposition supported by the finding that the radial oxygen gradient at the microvascular wall and therefore its rate of oxygen consumption are proportional to local blood oxygen partial pressure (pO(2)). Oxygen consumption by the endothelium and/or smooth muscle is also a factor in causing terminal lymphatic pO(2) to have the lowest oxygen level in the tissue, rendering this compartment most vulnerable in hypoxic conditions.

Animals↗

PubMed2003

Microlymphatic and tissue oxygen tension in the rat mesentery.

Oxygen phosphorescence quenching was used to measure tissue Po(2) of lymphatic vessels of 43.6 +/- 23.1 microm (mean +/- SD) diameter in tissue locations of the rat mesentery classified according to anatomic location. Lymph and adipose tissue Po(2) were 20.6 +/- 9.1 and 34.1 +/- 7.8 mmHg, respectively, with the difference being statistically significant. Rare microlymphatic vessels in connective tissue not surrounded by microvessels had a Po(2) of 0.8 +/- 0.2 mmHg, whereas the surrounding tissue Po(2) was 3.0 +/- 3.2 mmHg, with both values being significantly lower than those of adipose tissue. Lower of lymph fluid Po(2) relative to the surrounding tissue was also evident in paired measurements of Po(2) in the lymphatic vessels and perilymphatic adipose tissue, which was significantly lower than the Po(2) in paired adipose tissue. The Po(2) of the lymphatic fluid of the mesenteric microlymphatics is consistently lower than that of the surrounding adipose tissue by approximately 11 mmHg; therefore, lymph fluid has the lowest Po(2) of this tissue. The disparity between lymph and tissue Po(2) is attributed to the microlymphatic vessel wall and lymphocyte oxygen consumption.

Adipose Tissue↗