Microvascular gas embolization clearance following perfluorocarbon administration

2003 ◽  
Vol 94 (3) ◽  
pp. 860-868 ◽  
Author(s):  
David M. Eckmann ◽  
Vladimir N. Lomivorotov

Effective treatment of vascular gas embolism may be possible with emulsified fluorocarbon compounds. We tested the hypothesis that a fluorocarbon emulsion delivered before gas embolization would enhance bubble motion through the vasculature, favoring more rapid clearance. Air microbubbles were injected into the rat cremaster microcirculation in six groups of rats receiving Perftoran, an emulsified fluorocarbon, or saline immediately before, 2 h before, or after bubble injection. Embolism dimensions and dynamics were observed by using intravital microscopy. Surface area at lodging was equal between groups. Bubbles having smaller volume embolized smaller diameter vessels in the Perftoran pretreatment groups. A higher incidence of bubble dislodgement and larger distal displacement occurred in these two groups, with a 36% decrease in the time to bubble clearance and restoration of blood flow. Intravascular emulsified fluorocarbon administration before gas embolization affected initial bubble conformation, increased bubble dislodgement, and resulted in bubble displacement further into the periphery of the microcirculation. These dynamic events did not occur if embolization preceded fluorocarbon administration.

1990 ◽  
Vol 68 (4) ◽  
pp. 1581-1589 ◽  
Author(s):  
T. Shibamoto ◽  
J. C. Parker ◽  
A. E. Taylor ◽  
M. I. Townsley

The capillary filtration coefficient (Kf,c) is a sensitive and specific index of vascular permeability if surface area remains constant, but derecruitment might affect Kf,c in severely damaged lungs with high vascular resistance. We studied the effect of high and low blood flow rates on Kf,c in papaverine-pretreated blood-perfused isolated dog lungs perfused under zone 3 conditions with and without paraquat (PQ, 10(-2) M). Three Kf,cs were measured successively at hourly intervals for 5 h. These progressed sequentially from isogravimetric blood flow with low vascular pressure (I/L) to high flow with low vascular pressure (H/L) to high flow with high vascular pressure (H/H). The blood flows of H/L and H/H were greater than or equal to 1.5 times that of I/L. There were no significant changes in Kf,c in lungs without paraquat over a 50-fold range of blood flow rates. At 3 h after PQ, I/L-Kf,c was significantly increased and both isogravimetric capillary pressure and total protein reflection coefficient were decreased from base line. At 4 and 5 h, H/L-Kf,c was significantly greater than the corresponding I/L-Kf,c (1.01 +/- 0.22 vs. 0.69 +/- 0.09 and 1.26 +/- 0.19 vs. 0.79 +/- 0.10 ml.min-1.cmH2O-1.100 g-1, respectively) and isogravimetric blood flow decreased to 32.0 and 12.0% of base line, respectively. Pulmonary vascular resistance increased to 12 times base line at 5 h after PQ. We conclude that Kf,c is independent of blood flow in uninjured lungs. However, Kf,c measured at isogravimetric blood flow underestimated the degree of increase in Kf,c in severely damaged and edematous lungs because of a high vascular resistance and derecruitment of filtering surface area.


1986 ◽  
Vol 6 (3) ◽  
pp. 338-341 ◽  
Author(s):  
Nicholas V. Todd ◽  
Piero Picozzi ◽  
H. Alan Crockard

CBF obtained by the hydrogen clearance technique and cerebral blood volume (CBV) calculated from the [14C]dextran space were measured in three groups of rats subjected to temporary four-vessel occlusion to produce 15 min of ischaemia, followed by 60 min of reperfusion. In the control animals, mean CBF was 93 ± 6 ml 100 g−1 min−1, which fell to 5.5 ± 0.5 ml 100 g−1 min−1 during ischaemia. There was a marked early postischaemic hyperaemia (262 ± 18 ml 100g−1 min−1), but 1 h after the onset of ischaemia, there was a significant hypoperfusion (51 ± 3 ml 100 g−1 min−1). Mean cortical dextran space was 1.58 ± 0.09 ml 100 g−1 prior to ischaemia. Early in reperfusion there was a significant increase in CBV (1.85 ± 0.24 ml 100 g−1) with a decrease during the period of hypoperfusion (1.33 ± 0.03 ml 100 g−1). Therefore, following a period of temporary ischaemia, there are commensurate changes in CBF and CBV, and alterations in the permeability–surface area product at this time may be due to variations in surface area and not necessarily permeability.


1990 ◽  
Vol 103 (4) ◽  
pp. 586-592 ◽  
Author(s):  
H.H. Wanamaker ◽  
M.J. Lyon

1997 ◽  
Vol 80 (5) ◽  
pp. 645-654 ◽  
Author(s):  
Carl A. Goresky ◽  
André Simard ◽  
Andreas J. Schwab

1997 ◽  
Vol 272 (1) ◽  
pp. R163-R171
Author(s):  
K. Mori ◽  
M. Maeda

Local maximal velocities of transport (Tmax) and the half-maximum transport constants (KT) for glucose transport across the blood-brain barrier have been determined in local regions of the brain in normal conscious rats. [14C]iodoantipyrine and [3H]methylglucose were infused together intravenously for 2 min in rats with plasma glucose concentrations maintained at different levels, and the time courses of the tracer levels in arterial blood were measured. Local 14C and 3H concentrations were then measured in tissue samples dissected from the frozen brains. By comparing the transport-limited uptake of [3H]methylglucose with the blood flow-limited uptake of [14C]iodoantipyrine, the value of m, a factor between 0 and 10 that accounts for diffusion and/or transport limitations, was derived, and from the equation, m = 1 - PS/F (where PS is capillary permeability-surface area product and F is cerebral blood flow), the permeability-capillary surface area for methylglucose was calculated (S. S. Kety. Pharmacol. Rev. 3: 1-41, 1951). Values for Tmax and KT for glucose were calculated by application of Michaelis-Menten kinetic relationships adapted for the competition for transport between glucose and methylglucose. Tmax was determined in three representative gray structures and one white structure of the brain: Tmax was 5.3 +/- 0.3 (SD) mumol.g-1.min-1 in the gray structures and 4.3 mumol.g-1.min-1 in the white structure. KT was 3.6 +/- 0.4 (SD) mM in the gray structures and 5.9 mM in the white structure. This approach allows the simultaneous determination of local values of Tmax and KT for glucose and the rates of blood flow in various regions of the brain in conscious animals.


1962 ◽  
Vol 202 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Hugh D. Van Liew

Uptake rate of a gas from a rat's subcutaneous gas pocket was divided by the surface area and by the apparent pocket-to-tissue tension difference to yield an exchange coefficient, K'. Values in (ml x 10–4)/(min cm2 atm) were O2, 6.6; CO2, 150; and N2, 2. Blood flow in adjacent tissue appeared to have little influence on uptakes of O2 and CO2, since the K'co2:K'o2 ratio indicated that the uptakes were governed by diffusion alone, and drastic alteration of blood flow (death of the animal) decreased K'o2 by only 10%. In contrast, blood flow apparently affected N2 uptake. Because O2 and CO2 uptakes were not blood flow limited, K'o2 and K'co2 are estimates of true permeability coefficients; the calculated permeability coefficient for N2 is 3.3 (ml x 10–4)/(min cm2 atm). Comparison shows the pocket surface to be 1/50–1/150 as effective for O2 transfer as the lung. Finally, corrections are calculated for pocket-to-tissue pO2 and pCO2 differences in gas pockets used for tissue tonometry.


1992 ◽  
Vol 12 (2) ◽  
pp. 193-203 ◽  
Author(s):  
W.-D. Heiss ◽  
M. Huber ◽  
G. R. Fink ◽  
K. Herholz ◽  
U. Pietrzyk ◽  
...  

Sixteen patients were studied by multitracer positron emission tomography (PET) within 6–48 (mean of 23) h of onset of a hemispheric ischemic stroke and again 13–25 (mean of 15.6) days later. Cerebral blood flow (CBF), cerebral blood volume (CBV), cerebral metabolic rate of oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral metabolic rate of glucose (CMRglc) were measured each time by standard methods, and the sets of brain slices obtained at the two studies were matched using a three-dimensional alignment procedure. On matched brain slices, regions of interest (ROIs) for infarct and peri-infarct tissue, contralateral mirror regions, and major brain structures were outlined. In the core of infarction, blood flow and metabolism were significantly lower than in the corresponding contralateral regions at the first study, and did not change during the observation period. In the peri-infarct tissue, CMRO2 was moderately decreased at the first measurement; over time, the CMRO2 deteriorated progressively while flow did not change. When peri-infarct regions were selected on the basis of increased OEF (25 ± 29.8% above corresponding contralateral regions) on the early scans, the CBF was significantly decreased (23 ± 6.6%) while the CMRO2 showed only a slight difference from the mirror region. Within the observation period, the CBF improved but the CMRO2, OEF, and CMRglc deteriorated. Only in a few regions with increased OEF and slightly impaired CMRO2 was metabolism preserved close to normal values. These data from repeat PET studies in reproducibly defined tissue compartments furnish evidence of viable tissue in the border zone of ischemia up to 48 h after stroke. While this viable peri-infarct tissue exhibits some potential for effective treatment of ischemic stroke, therapeutic routines available today cannot prevent subsequent metabolic derangement and progression to necrosis. Multitracer PET studies identifying viable tissue could be of value in the development of effective treatment of ischemic stroke.


1982 ◽  
Vol 52 (6) ◽  
pp. 1575-1580 ◽  
Author(s):  
R. L. Capen ◽  
W. W. Wagner

We have previously shown that airway hypoxia causes pulmonary capillary recruitment and raises diffusing capacity for carbon monoxide. This study was designed to determine whether these events were caused by an increase in pulmonary vascular resistance, which redistributed blood flow toward the top of the lung, or by an increase in cardiac output. We measured capillary recruitment at the top of the dog lung by in vivo microscopy, gas exchange surface area of the whole lung by diffusing capacity for carbon monoxide, and blood flow distribution by radioactive microspheres. During airway hypoxia recruitment occurred, diffusing capacity increased, and blood flow was redistributed upward. When a vasodilator was infused while holding hypoxia constant, these effects were reversed; i. e., capillary “derecruitment” occurred, diffusing capacity decreased, and blood flow was redistributed back toward the bottom of the lung. The vasodilator was infused at a rate that left hypoxic cardiac output unchanged. These data show that widespread capillary recruitment during hypoxia is caused by increased vascular resistance and the resulting upward blood flow redistribution.


1971 ◽  
Vol 28 (10) ◽  
pp. 1609-1614 ◽  
Author(s):  
John C. Davis

Reductions in surface area of the gill were artificially produced by ligating various gill arches and occluding their blood supply. Rainbow trout (Salmo gairdneri) responded to a 40–57% reduction in gill area, by increasing cardiac output and ventilation volume, and probably by redistributing blood within the remaining functional gill area. Fish with blood flow to gill arches one and three only, could maintain arterial PO2 at 90–100 mm Hg, whereas, in those with blood flow to arches three and four only, arterial PO2 fell to around 40 mm Hg. The presence of a chemoreceptor site for the regulation of arterial PO2 associated with the efferent blood vessels of arch number one is discussed. Such a receptor may be located in the pseudobranch or in the portion of the brain supplied with arterial blood from the first gill arch.


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