Optimal heating rate in constant pressure and constant flow gas chromatography

Author(s):  
Mark Merrick ◽  
Leonid M. Blumberg
1998 ◽  
Vol 201 (22) ◽  
pp. 3075-3083 ◽  
Author(s):  
T Mustafa ◽  
C Agnisola

A vasoconstrictory response to adenosine has been reported in coronary rings from fish. Since the reactivity of the large coronary arteries and the microcirculation may differ, the present study was undertaken to determine the role of adenosine in the intact coronary system of trout under constant pressure or flow using an isolated and non-working heart preparation. The involvement of nitric oxide (NO) and the interaction with noradrenaline were also studied. At 10(-9) to 10(-8 )mol l-1, adenosine caused a vasoconstrictory response, whereas between 10(-7) and 10(-5 )mol l-1 the response was predominantly vasodilative. Theophylline abolished both these responses to adenosine. The vasodilation induced by adenosine (at 10(-5 )mol l-1) was significantly reduced when the preparation was perfused under constant-flow than rather under constant-pressure conditions. The nitric oxide synthase inhibitor N-nitro-l-arginine (l-NA, 10(-4 )mol l-1) partially reduced the vasodilation induced by adenosine (at 10(-5 )mol l-1) under constant-pressure but not under constant-flow conditions. Perfusion of the intact coronary system with l-arginine or with adenosine significantly increased the rate of nitrite (NO2-) release, while perfusion with l-NA or theophylline reduced NO2- release. Chemical denudation of the coronary endothelium by CHAPS resulted in the loss of both the l-arginine- and adenosine-mediated vasodilation and the l-arginine-induced increase in the rate of NO2- release. Adenosine (10(-5 )mol l-1) offset and overrode the vasoconstriction induced by 10(-7 )mol l-1 noradrenaline. l-NA inhibited only the adenosine-induced vasodilation but not the ability to offset noradrenaline vasoconstriction, excluding the involvement of NO in the interaction between adenosine and noradrenaline.


2013 ◽  
Vol 119 (6) ◽  
pp. 1511-1519 ◽  
Author(s):  
Simone Bottan ◽  
Marianne Schmid Daners ◽  
Diane de Zelicourt ◽  
Norina Fellner ◽  
Dimos Poulikakos ◽  
...  

Object The treatment of hydrocephalus requires insight into the intracranial dynamics in the patient. Resistance to CSF outflow (R0) is a clinically obtainable parameter of intracranial fluid dynamics that quantifies the apparent resistance to CSF absorption. It is used as a criterion for the selection of shunt candidates and serves as an indicator of shunt performance. The R0 is obtained clinically by performing 1 of 3 infusion tests: constant flow, constant pressure, or bolus infusion. Among these, the bolus infusion method has the shortest examination times and provides the shortest time of exposure of patients to artificially increased intracranial pressure (ICP) levels. However, for unknown reasons, the bolus infusion method systematically underestimates the R0. Here, the authors have tested and verified the hypothesis that this underestimation is due to lack of accounting for viscoelasticity of the craniospinal space in the calculation of the R0. Methods The authors developed a phantom model of the human craniospinal space in order to reproduce in vivo pressure-volume (PV) relationships during infusion testing. The phantom model followed the Marmarou exponential PV equation and also included a viscoelastic response to volume changes. Parameters of intracranial fluid dynamics, such as the R0, could be controlled and set independently. In addition to the phantom model, the authors designed a computational framework for virtual infusion testing in which viscoelasticity can be turned on or off in a controlled manner. Constant flow, constant pressure, and bolus infusion tests were performed on the phantom model, as well as on the virtual computational platform, using standard clinical protocols. Values for the R0 were derived from each infusion test by using both a standard method based on the Marmarou PV equation and a novel method based on a system identification approach that takes into account viscoelastic behavior. Results Experiments with the phantom model confirmed clinical observations that both the constant flow and constant pressure infusion tests, but not the bolus infusion test, yield correct R0 values when they are determined with the standard method according to Marmarou. Equivalent results were obtained using the computational framework. When the novel system identification approach was used to determine the R0, all of the 3 infusion tests yielded correct values for the R0. Conclusions The authors' investigations demonstrate that intracranial dynamics have a substantial viscoelastic component. When this viscoelastic component is taken into account in calculations, the R0, is no longer underestimated in the bolus infusion test.


1964 ◽  
Vol 206 (5) ◽  
pp. 951-954 ◽  
Author(s):  
Oliver Carrier ◽  
James R. Walker ◽  
Arthur C. Guyton

The role of oxygen in control of local blood flow was investigated in isolated arterial segments 1 cm in length and 0.5–1.0 mm in diameter by perfusion with blood of various Po2 levels. A decrease in vascular resistance always occurred when the Po2 was lowered and an increase occurred when it was raised. In 20 vessels, using constant-pressure perfusion, an average increase in conductance of 2.38 times normal level was obtained when the Po2 was lowered from 100 to 30 mm Hg. When this datum was plotted according to initial flow, the smaller vessels gave the greatest response to low oxygen (2.73 times normal; sem ± 0.15), whereas the largest gave the least (1.76 times normal; sem ± 0.10). Forty-three vessels perfused under constant-flow conditions gave results which were consistent with and confirmed the constant-pressure results. In all of these experiments pH, Pco2, and temperature were monitored and kept at physiological levels. The results indicate that oxygen could well be a factor in the autoregulation of blood flow.


1989 ◽  
Vol 256 (1) ◽  
pp. H297-H301 ◽  
Author(s):  
M. W. Gorman ◽  
R. D. Wangler ◽  
H. V. Sparks

The purpose of this study was to determine the effect of vasodilation on the distribution of perfusate flow in the isolated guinea pig heart. Hearts were perfused retrogradely through the aorta with oxygenated Krebs-Henseleit buffer solution at 37 degrees C. Regional myocardial flows were measured with 15-micron radioactive microspheres. Each heart was subdivided into 45 pieces (average size 44 mg), and heterogeneity of flow was quantified as the relative dispersion (standard deviation/mean). Under control conditions at a perfusion pressure of 46 mmHg (60 cm water), the relative dispersion of left ventricular (LV) flow was 30 +/- 2% (n = 8). Vasodilation was induced via infusion of dipyridamole (10(-5) M). When flow was held constant at the resting value, relative flow dispersion increased to 43 +/- 6% (n = 8). When perfusion pressure was held constant and flow allowed to increase, relative dispersion fell to 20 +/- 5% (n = 5). Heterogeneity for the heart as a whole was higher than for the left ventricle but followed the same pattern with vasodilation. In a separate series of hearts (n = 5) equipped with LV balloons but without microsphere flow measurements, vasodilation at constant flow decreased LV pressure development, dP/dt, and O2 consumption. Vasodilation at constant pressure increased O2 consumption, but did not increase LV pressure or dP/dt. We conclude that vasodilation in this preparation will increase flow heterogeneity during constant-flow perfusion but decrease heterogeneity during constant-pressure perfusion. Furthermore, increased flow heterogeneity can compromise ventricular function.


1985 ◽  
Vol 58 (1) ◽  
pp. 206-210 ◽  
Author(s):  
M. I. Townsley ◽  
R. J. Korthuis ◽  
A. E. Taylor

In this study, 14 canine lung lobes were isolated and perfused with autologous blood at constant pressure (CP) or constant flow (CF). Pulmonary capillary pressure (Pc) was measured via venous occlusion or simultaneous arterial and venous occlusions. Arterial and venous pressures and blood flow were measured concurrently so that total pulmonary vascular resistance (RT) as well as pre- (Ra) and post- (Rv) capillary resistances could be calculated. In both CP and CF perfused lobes, 5-min arachidonic acid (AA) infusions (0.085 +/- 0.005 to 2.80 +/- 0.16 mg X min-1 X 100 g lung-1) increased RT, Rv, and Pc (P less than 0.05 at the highest dose), while Ra was not significantly altered and Ra/Rv fell (P less than 0.05 at the highest AA dose). In five CP-perfused lobes, the effect of AA infusion on the pulmonary capillary filtration coefficient (Kf,C) was also determined. Neither low-dose AA (0.167 +/- 0.033 mg X min-1 X 100 g-1) nor high-dose AA (1.35 +/- 0.39 mg X min-1 X 100 g-1) altered Kf,C from control values (0.19 +/- 0.02 ml X min-1 X cmH2O-1 X 100 g-1). The hemodynamic response to AA was attenuated by prior administration of indomethacin (n = 2). We conclude that AA infusion in blood-perfused canine lung lobes increased RT and Pc by increasing Rv and that microvascular permeability is unaltered by AA infusion.


1977 ◽  
Vol 233 (5) ◽  
pp. R222-R229 ◽  
Author(s):  
D. G. Smith

Sites of cholinergic vasoconstriction were investigated in isolated saline-perfused holobranchs of trout (Salmo gairdneri and S. trutta). Acetylcholine (ACh) always increased overall branchial vascular resistance (BVR) and, in addition, decreased the proportion of the total inflow appearing at the outflow cannula from the efferent arch artery. Since this was observed in both constant pressure and constant flow situations, it was concluded that ACh exerted most of its effect at a site downstream from the secondary lamellae, probably at the bases of the efferent filament arteries. Prussian blue dye injections indicated that, in addition, ACh caused a marked reduction in flow to the distal halves of the filaments and that flow within the proximal secondary lamellae was restricted during ACh administration to the inner and outer marginal channels of the lamellae. The results are discussed in terms of recent findings concerning the vascular anatomy of teleost gills.


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