Effects of hypoxia and histamine infusion on lung blood volume

Using an isolated perfused cat lung preparation we examined the effects of hypoxia and histamine infusion on the lung blood volume. Total lung blood volume was determined from the indocyanine green transit time and the ether bolus technique was used to estimate arterial and venous volumes during forward and retrograde perfusion, respectively. Changes in lung total fluid content were determined from changes in the blood volume of the perfusion system. Hypoxia increased perfusion pressure and decreased total fluid and blood volume. Histamine infusion also increased perfusion pressure and decreased blood volume. However, histamine increased total fluid volume, indicating an increase in vascular permeability. Hypoxia decreased arterial and venous volumes, and histamine decreased venous volume. The slopes of the arterial and venous volume/pressure curves were not altered by hypoxia or histamine.

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Rapid Infusion of Hydroxyethyl Starch 70/0.5 but not Acetate Ringer’s Solution Decreases the Plasma Concentration of Propofol during Target-controlled Infusion

Anesthesiology ◽

10.1097/aln.0000000000001184 ◽

2016 ◽

Vol 125 (2) ◽

pp. 304-312 ◽

Cited By ~ 8

Author(s):

Sayako Itakura ◽

Kenichi Masui ◽

Tomiei Kazama

Keyword(s):

Blood Flow ◽

Plasma Concentration ◽

Indocyanine Green ◽

Blood Volume ◽

Hydroxyethyl Starch ◽

Hepatic Blood Flow ◽

Disappearance Rate ◽

Rapid Infusion ◽

Ringer’S Solution ◽

Target Controlled Infusion

Abstract Background Rapid fluid infusion resulting in increased hepatic blood flow may decrease the propofol plasma concentration (Cp) because propofol is a high hepatic extraction drug. The authors investigated the effects of rapid colloid and crystalloid infusions on the propofol Cp during target-controlled infusion. Methods Thirty-six patients were randomly assigned to 1 of 3 interventions (12 patients per group). At least 30 min after the start of propofol infusion, patients received either a 6% hydroxyethyl starch (HES) solution at 24 ml·kg−1·h−1 or acetated Ringer’s solution at 24 or 2 ml·kg−1·h−1 during the first 20 min. In all groups, acetated Ringer’s solution was infused at 2 ml·kg−1·h−1 during the next 20 min. The propofol Cp was measured every 2.5 min as the primary outcome. Cardiac output, blood volume, and indocyanine green disappearance rate were determined using a pulse dye densitogram analyzer before and after the start of fluid administration. Effective hepatic blood flow was calculated as the blood volume multiplied by the indocyanine green disappearance rate. Results The rapid HES infusion significantly decreased the propofol Cp by 22 to 37%, compared to the Cp at 0 min, whereas the rapid or maintenance infusion of acetate Ringer’s solution did not decrease the propofol Cp. Rapid HES infusion, but not acetate Ringer’s solution infusion, increased the effective hepatic blood flow. Conclusions Rapid HES infusion increased the effective hepatic blood flow, resulting in a decreased propofol Cp during target-controlled infusion. Rapid HES infusion should be used cautiously as it may decrease the depth of anesthesia.

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Evaluation of circulating blood volume and vascular permeability in long-term hemodialysis patients

Nihon Toseki Igakkai Zasshi ◽

10.4009/jsdt.44.435 ◽

2011 ◽

Vol 44 (5) ◽

pp. 435-440 ◽

Cited By ~ 1

Author(s):

Susumu Ookawara ◽

Masayuki Suzuki ◽

Sachiko Fukase ◽

Kaoru Tabei

Keyword(s):

Vascular Permeability ◽

Blood Volume ◽

Hemodialysis Patients ◽

Circulating Blood Volume

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Relation between venous pressure and blood volume in the intestine

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.204.1.31 ◽

1963 ◽

Vol 204 (1) ◽

pp. 31-34 ◽

Cited By ~ 31

Author(s):

Paul C. Johnson ◽

Kenneth M. Hanson

Keyword(s):

Blood Volume ◽

Time Constant ◽

Time Course ◽

Venous Pressure ◽

High Viscosity ◽

Exponential Process ◽

Pressure Volume Relationship ◽

Venous Volume ◽

Volume Characteristics

The pressure volume characteristics of the intestinal venous vasculature were studied in vivo by a weight technique. The pressure-volume relationship was linear over the range 0–20 mm Hg. In a few experiments the volume increment appeared to be reduced at venous pressures above 30 mm Hg. The average compliance of the intestinal veins was 0.34 ml/mm Hg 100 g tissue. The time course of the blood volume change was also examined. Rapid elevation of venous pressure to a higher level caused blood volume to increase at an exponentially declining rate. Therefore, the phenomenon of creep in the intestinal veins appears to be a simple exponential process. The half time of the increase in venous volume averaged 7.5 sec while the time constant was 10.9 sec. The magnitude of the time constant suggests the presence of elements of rather high viscosity in the venous wall.

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Blood volume measurement with indocyanine green pulse spectrophotometry: dose and site of dye administration

Acta Neurochirurgica ◽

10.1007/s00701-009-0501-4 ◽

2009 ◽

Vol 152 (2) ◽

pp. 251-255 ◽

Cited By ~ 6

Author(s):

Menno R. Germans ◽

Philip C. de Witt Hamer ◽

Leonard J. van Boven ◽

Koos A. H. Zwinderman ◽

Gerrit J. Bouma

Keyword(s):

Indocyanine Green ◽

Blood Volume ◽

Volume Measurement ◽

Blood Volume Measurement

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Effects of graded hypotension on cerebral blood flow, blood volume, and mean transit time in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.6.h1908 ◽

1992 ◽

Vol 262 (6) ◽

pp. H1908-H1914 ◽

Cited By ~ 2

Author(s):

M. Ferrari ◽

D. A. Wilson ◽

D. F. Hanley ◽

R. J. Traystman

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Cerebral Perfusion Pressure ◽

Blood Volume ◽

Transit Time ◽

Cerebral Perfusion ◽

Pressure Range ◽

Cerebral Blood Volume ◽

Perfusion Pressure ◽

Mean Transit Time

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.

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Pulmonary vascular injury by polycations in perfused rat lungs

Journal of Applied Physiology ◽

10.1152/jappl.1987.62.5.1932 ◽

1987 ◽

Vol 62 (5) ◽

pp. 1932-1943 ◽

Cited By ~ 43

Author(s):

S. W. Chang ◽

J. Y. Westcott ◽

J. E. Henson ◽

N. F. Voelkel

Keyword(s):

Vascular Permeability ◽

Perfusion Pressure ◽

Endothelial Damage ◽

Endothelial Injury ◽

Lung Edema ◽

Vascular Effect ◽

Pulmonary Vasoconstriction ◽

Rat Lungs ◽

Hexadimethrine Bromide ◽

A Cell

Polycations, such as protamine sulfate and polylysine, have been implicated in the cause of pulmonary edema, but the mechanism is unknown. We studied the vascular effect of protamine in isolated rat lungs perfused with a cell- and plasma-free solution. Protamine (50–1,000 micrograms/ml) increased lung perfusion pressure and caused edema. Blocking the pulmonary vasoconstriction with papaverine (10(-4) M) did not prevent lung edema. In addition, lungs treated with protamine and papaverine showed increased extravascular leakage of 125I-albumin, indicating increased vascular permeability. Histological examination of these lungs showed marked endothelial injury. Functional endothelial damage was further demonstrated by the impairment of the acetylcholine-induced vascular relaxation in protamine-treated vascular rings. Antihistamines and indomethacin failed to block the pulmonary vasoconstriction and increased vascular permeability caused by protamine. In addition, we found that anionic substances, heparin and albumin, blocked the lung injury induced by protamine, whereas other polycations, polylysine and hexadimethrine bromide, caused pulmonary vasoconstriction and increased vascular permeability similar to protamine. We conclude that protamine causes pulmonary endothelial injury and lung edema and suggest that the injury may be charge mediated.

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