Relation between venous pressure and blood volume in the intestine

1963 ◽  
Vol 204 (1) ◽  
pp. 31-34 ◽  
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.

Pulsatile Pressure and Flow in the Skeletal Muscle Microcirculation

1990 ◽  
Vol 112 (4) ◽  
pp. 437-443 ◽  
Author(s):  
Shou-Yan Lee ◽  
G. W. Schmid-Scho¨nbein
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Time Dependent ◽  
Physiological Importance ◽  
Pulsatile Pressure ◽  
Theoretical Predictions ◽  
Skeletal Muscle Microcirculation

Although blood flow in the microcirculation of the rat skeletal muscle has negligible inertia forces with very low Reynolds number and Womersley parameter, time-dependent pressure and flow variations can be observed. Such phenomena include, for example, arterial flow overshoot following a step arterial pressure, a gradual arterial pressure reduction for a step flow, or hysteresis between pressure and flow when a pulsatile pressure is applied. Arterial and venous flows do not follow the same time course during such transients. A theoretical analysis is presented for these phenomena using a microvessel with distensible viscoelastic walls and purely viscous flow subject to time variant arterial pressures. The results indicate that the vessel distensibility plays an important role in such time-dependent microvascular flow and the effects are of central physiological importance during normal muscle perfusion. In-vivo whole organ pressure-flow data in the dilated rat gracilis muscle agree in the time course with the theoretical predictions. Hemodynamic impedances of the skeletal muscle microcirculation are investigated for small arterial and venous pressure amplitudes superimposed on an initial steady flow and pressure drop along the vessel.

Baroreflex regulation of hindquarter vascular resistance during acute blood volume expansion

1984 ◽  
Vol 246 (1) ◽  
pp. H74-H79 ◽  
Author(s):  
G. B. Guo ◽  
D. R. Richardson
Keyword(s):  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Time Course ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Baroreflex Control ◽  
Blood Volume Expansion ◽  
Cardiopulmonary Receptors ◽  
Cardiopulmonary Baroreceptors

The baroreflex control of hindquarter vascular resistance in response to a 30% blood volume expansion (BVE) was examined in constant-flow perfused hindlimbs of chloralose-urethan-anesthetized rats. Volume expansion initially increased both systemic arterial pressure (SAP) and central venous pressure (CVP) while decreasing hindquarter vascular resistance. After these initial changes, there was a parallel return of hindquarter-vascular resistance and CVP to pre-expansion levels, suggesting that cardiopulmonary afferents play a major role in the vascular resistance adjustments to volume expansion. This notion was supported in a separate set of experiments in which CVP was elevated selectively while SAP was held constant. This manipulation elicited a decrease in hindquarter vascular resistance, which was significantly attenuated following vagal cardiopulmonary denervation. The return of hindquarter vascular resistance following BVE also occurred in the presence of elevated SAP in rats with vagotomy and aortic nerve denervation, i.e., only the carotid sinus baroreflexes intact, but the time course was much faster compared with preparations with cardiopulmonary receptors intact. No response of hindquarter vascular resistance to BVE was observed in rats with both sinoaortic and cardiopulmonary baroreceptors denervated. These findings suggest that the return of hindquarter vascular resistance following BVE involves a gradual increase in sympathetic outflow to the hindquarters resulting from both a decrease in cardiopulmonary afferent activity and a rapid adaptation of arterial baroreflexes.

Active and passive control of hepatic blood volume responses to hemorrhage at normal and raised hepatic venous pressure in cats

1980 ◽  
Vol 58 (9) ◽  
pp. 1049-1057 ◽  
Author(s):  
W. Wayne Lautt ◽  
L. Cheryle Brown ◽  
J. Scott Durham
Keyword(s):  
Blood Flow ◽  
Blood Loss ◽  
Blood Volume ◽  
Passive Control ◽  
Venous Pressure ◽  
Liver Volume ◽  
Passive Flow ◽  
Hepatic Volume ◽  
Volume Response

Hepatic blood volume decreases in response to a rapid hemorrhage (15.3 mL/min) were measured in cats anesthetized with pentobarbital or ketamine–chloralose, by use of in vivo plethysmography alone or in combination with various surgical procedures and vascular circuits. The hepatic blood volume contracts during hemorrhage to compensate for a constant proportion (26 ± 6%) of the blood loss regardless of the extent of the actual blood loss. Following denervation of the liver and α adrenoreceptor blockade (3 mg phentolamine, intraportal) the liver compensation was unaltered. After denervation, nephrectomy, hypophysectomy, and adrenalectomy the liver was still able to compensate for 20 ± 7.4% of the hemorrhage. Decreases in liver volume were linearly related to decreases in total hepatic blood flow that ensued whether the decreased blood flow was induced by hemorrhage or by clamping of the arteries supplying the splanchnic organs (superior mesenteric artery, celiac artery). The hepatic volume response to hemorrhage could be predicted accurately (97 ± 6.6%) simply from the linear passive relationship between flow and volume for a particular animal. However when hepatic venous pressure was experimentally elevated, the volume response to passive flow decrease was markedly reduced whereas the response to hemorrhage and noradrenaline infusion was unimpaired suggesting that active control factors were required to produce normal hepatic volume responses to hemorrhage at raised venous pressure. Phentolamine reduced the response at raised venous pressure but was without effect at normal venous pressure in the same animal, indicating that the hepatic nerves and (or) adrenal catecholamines are of paramount importance in control of the response at raised venous pressure when the passive flow influence is much reduced.

Dynamic synchronization analysis of venous pressure-driven cardiac output in rainbow trout

2003 ◽  
Vol 285 (4) ◽  
pp. R889-R896 ◽  
Author(s):  
Adrienne Robyn Minerick ◽  
Hsueh-Chia Chang ◽  
Todd M. Hoagland ◽  
Kenneth R. Olson
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Blood Volume ◽  
Hilbert Transform ◽  
Venous Pressure ◽  
Time Lag ◽  
Venous Compliance ◽  
Pressure Transducers ◽  
The Hilbert Transform

Measurement of venous function in vivo is inherently difficult. In this study, we used the Hilbert transform to examine the dynamic relationships between venous pressure and cardiac output (CO) in rainbow trout whose blood volume was continuously increased and decreased by ramp infusion and withdrawal (I/W). The dorsal aorta and ductus Cuvier were cannulated percutaneously and connected to pressure transducers; a flow probe was placed around the ventral aorta. Whole blood from a donor was then I/W via the dorsal aortic cannula at a rate of 10% of the estimated blood volume per minute, and the duration of I/W was varied from 40, 60, 80, 90, 120, 230, 240, 260, 300, and 340 s. Compliance [change in (Δ) blood vol/Δvenous pressure] was 2.8 ± 0.2 ml · mmHg-1 · g-1 ( N = 25 measurements; 6 fish with closed pericardium) and 2.8 ± 0.3 ml · mmHg-1 · kg-1 ( N = 19 measurements, 4 fish with open pericardium). Compliance was positively correlated with the duration of I/W, indicative of cardiovascular reflex responses at longer I/W durations. In trout with closed pericardium, CO followed venous pressure oscillations with an average time lag of 4.2 ± 1.0 s ( N = 9); heart rate (HR) was inversely correlated with CO. These studies show that CO is entrained by modulation of venous pressure, not by HR. Thus, although trout have a rigid pericardium, venous pressure (vis-a-tergo), not cardiac suction (vis-a-fronte), appears to be the primary determinant of CO. Estimation of venous compliance by ramp-modulation of venous pressure is faster and less traumatic than classical capacitance measurements and appears applicable to a variety of vertebrate species, as does the Hilbert transform, which permits analysis of signals with disparate frequencies.

Measurement of circulating blood volume in vivo after trauma-hemorrhage and hemodilution

1994 ◽  
Vol 266 (2) ◽  
pp. R368-R374 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
M. C. Lu ◽  
A. Ayala ◽  
J. M. Harkema ◽  
...  
Keyword(s):  
Indocyanine Green ◽  
Blood Volume ◽  
Fluid Resuscitation ◽  
Venous Pressure ◽  
Green Method ◽  
Reliable Technique ◽  
Circulating Blood Volume ◽  
Midline Laparotomy ◽  
Hemodynamic Variables

Although cardiac output (CO) and other hemodynamic variables are used to assess the adequacy of fluid resuscitation after hemorrhage, it is not known whether there is any correlation between restoration of CO and circulating blood volume (CBV). To determine this, rats underwent a midline laparotomy (i.e., trauma induced) and were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of maximum bleedout volume was returned in the form of Ringer lactate (RL). The animals were then resuscitated with four or five times the volume of maximum bleedout in the form of RL. CO and hepatocellular function were measured using an in vivo hemoreflectometer. CBV was monitored by using in vivo indocyanine green clearance. A good correlation between the values of blood volume obtained by this method and the 125I-albumin method indicates that the indocyanine green method is also a reliable technique for measuring CBV. Results indicate that resuscitation after hemorrhage improved the decreased CBV but did not restore it to control levels despite the fact that CO was restored and central venous pressure was more than doubled. A good correlation between depressed CBV and hepatocellular dysfunction was also observed under such conditions. Thus measurement of CBV appears to be useful for evaluating the adequacy of fluid resuscitation after trauma-hemorrhage and hemodilution.

Blood volume restitution after hemorrhage in adult sheep

1987 ◽  
Vol 253 (4) ◽  
pp. R541-R544 ◽  
Author(s):  
J. M. Grimes ◽  
L. A. Buss ◽  
R. A. Brace
Keyword(s):  
Arterial Pressure ◽  
Experimental Evidence ◽  
Blood Volume ◽  
Plasma Protein ◽  
Time Course ◽  
Venous Pressure ◽  
Adult Sheep ◽  
Protein Mass ◽  
Female Sheep ◽  
Initial Blood

Indirect experimental evidence suggested the possibility that the restoration of blood volume to normal hemorrhage in adult sheep may occur more quickly than in other species that have been studied. To test this hypothesis, we studied unanesthetized chronically catheterized adult female sheep 1-2 wk after splenectomy. An average of 19.6 +/- 1.4% (SE) of their initial blood volume was removed over 10 min. Blood volume restitution at 0.5, 1, 3, 5, 7, 24, and 48 h posthemorrhage averaged 12 +/- 3, 34 +/- 3, 41 +/- 3, 50 +/- 4, 62 +/- 10, 79 +/- 10, and 124 +/- 25%, respectively. Arterial pressure decreased during the hemorrhage and returned to normal within 2 h, whereas venous pressure did not change significantly. No change in blood osmolality occurred. There was a highly significant correlation between blood volume and plasma protein mass (r = 0.98, P less than 10(-6)) during and after the hemorrhage. Thus it appears that the posthemorrhage restoration of blood volume in adult sheep occurs over essentially the same time course as in other species and this appears to be mediated by a restoration of plasma protein mass.

Catecholaminergic regulation of venous function in the rainbow trout

1998 ◽  
Vol 274 (4) ◽  
pp. R1195-R1202 ◽  
Author(s):  
Yutong Zhang ◽  
Leroy Weaver ◽  
Andrew Ibeawuchi ◽  
Kenneth R. Olson
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Venous Compliance ◽  
Adrenoceptor Antagonist ◽  
Vascular Capacitance ◽  
Capacitance Curve ◽  
Ventral Aorta ◽  
Venous Function ◽  
The Right

The significance of the sympathetic nervous system (SNS) in regulating peripheral vascular resistance and cardiac function in fish has been well established, whereas its effect on venous function in vivo is unknown. Two protocols were employed in the present study to evaluate SNS effects on the venous system in intact, unanesthetized trout. In the first, trout were instrumented with pressure cannulas in the ventral (PVA) and dorsal (PDA) aortas and ductus Cuvier (PVEN), and cardiac output (CO) was measured with a flow probe around the ventral aorta. Heart rate, stroke volume, and gill and systemic resistances were calculated from the measured parameters. In the second group, vascular capacitance curves were obtained by monitoring mean circulatory filling pressure (PVEN) during transient interruption of CO and while blood volume was adjusted between 80 and 120% of normal. Unstressed blood volume (USBV) and vascular compliance (C) were derived from the capacitance curves. Infusion of epinephrine (Epi; 3.3 nmol ⋅ min−1 ⋅ kg body wt−1) increased PVA, PDA, and PVEN, whereas norepinephrine (NE) infusion (3.3 nmol ⋅ min−1 ⋅ kg body wt−1) increased PVA and PDA but did not affect PVEN. Epi (1.0 nmol ⋅ min−1 ⋅ kg body wt−1), but not NE (2.6 or 10.4 nmol ⋅ min−1 ⋅ kg body wt−1), displaced the capacitance curve to the right and significantly decreased USBV. Inhibition of α1-adrenoceptors with prazosin, or ganglionic nicotinic receptor blockade with hexamethonium, produced a left shift in the capacitance curve, and both treatments increased USBV and C. Conversely, the α-adrenoceptor antagonist phentolamine did not effect vascular capacitance. These results show that Epi has potent effects on trout veins in vivo and that it mobilizes blood from the unstressed into the stressed vascular compartment and augments central venous pressure by decreasing venous compliance. These results also show that the SNS is an active effector of venous tone and compliance in trout; this is the first demonstration of tonic regulation of vascular capacitance in any fish.

scholarly journals GABAB Presynaptic Inhibition Has an In Vivo Time Constant Sufficiently Rapid to Allow Modulation at Theta Frequency

2002 ◽  
Vol 87 (3) ◽  
pp. 1196-1205 ◽  
Author(s):  
Bradley J. Molyneaux ◽  
Michael E. Hasselmo
Keyword(s):  
Receptor Antagonist ◽  
Time Constant ◽  
Presynaptic Inhibition ◽  
Time Course ◽  
Theta Rhythm ◽  
Hippocampal Formation ◽  
Gabaergic Interneurons ◽  
Glutamatergic Synaptic Transmission ◽  
Theta Frequency

Cyclical activity of GABAergic interneurons during theta rhythm could mediate phasic changes in strength of glutamatergic synaptic transmission in the hippocampal formation if presynaptic inhibition from activation of GABAB receptors is sufficiently rapid to change within a theta cycle. The experiments described here analyzed the time course of GABABmodulation using a heterosynaptic depression paradigm in anesthetized rats at physiological temperatures. Heterosynaptic depression of the slope of evoked potentials decayed with a time constant that would allow significant changes in transmission across different phases of the theta cycle. This heterosynaptic depression was significantly reduced by local infusion of the GABAB receptor antagonist CGP55845A.

scholarly journals In Vivo Calcium Accumulation in Presynaptic and Postsynaptic Dendrites of Visual Interneurons

1999 ◽  
Vol 82 (6) ◽  
pp. 3327-3338 ◽  
Author(s):  
Volker Dürr ◽  
Martin Egelhaaf
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Visual Motion ◽  
Direction Selectivity ◽  
Calcium Signal ◽  
Spatial Integration ◽  
Lobula Plate ◽  
Calcium Accumulation ◽  
Low Pass

In this comparative in vivo study of dendritic calcium accumulation, we describe the time course and spatial integration properties of two classes of visual interneurons in the lobula plate of the blowfly. Calcium accumulation was measured during visual motion stimulation, ensuring synaptic activation of the neurons within their natural spatial and temporal operating range. The compared cell classes, centrifugal horizontal (CH) and horizontal system (HS) cells, are known to receive retinotopic input of similar direction selectivity, but to differ in morphology, biophysics, presence of dendrodendritic synapses, and computational task. 1) The time course of motion-induced calcium accumulation was highly invariant with respect to stimulus parameters such as pattern contrast and size. In HS cells, the rise of [Ca2+]i can be described by a single exponential with a time constant of 5–6 s. The initial rise of [Ca2+]i in CH cells was much faster (τ ≈ 1 s). The decay time constant in both cell classes was estimated to be at least 3.5 times longer than the corresponding rise time constant. 2) The voltage-[Ca2+]i relationship was best described by an expansive nonlinearity in HS cells and an approximately linear relationship in CH cells. 3) Both cell classes displayed a size-dependent saturation nonlinearity of the calcium accumulation. Although in CH cells calcium saturation was indistinguishable from saturation of the membrane potential, saturation of the two response parameters differed in HS cells. 4) There was spatial overlap of the calcium signal in response to nonoverlapping visual stimuli. Both the area and the amplitude of the overlap profile was larger in CH cells than in HS cells. Thus calcium accumulation in CH cells is spatially blurred to a greater extent than in HS cells. 5) The described differences between the two cell classes may reflect the following computational tasks of these neurons: CH cells relay retinotopic information within the lobula plate via dendritic synapses with pronounced spatial low-pass filtering. HS cells are output neurons of the lobula plate, in which the slow, local calcium accumulation may be suitable for local modulatory functions.

Effects of rapid mannitol infusion on cerebral blood volume

1986 ◽  
Vol 64 (1) ◽  
pp. 104-113 ◽  
Author(s):  
Patrick Ravussin ◽  
David P. Archer ◽  
Jane L. Tyler ◽  
Ernst Meyer ◽  
Mounir Abou-Madi ◽  
...  
Keyword(s):  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Human Subjects ◽  
Venous Pressure ◽  
Hemoglobin Concentration ◽  
Rapid Infusion ◽  
Total Blood ◽  
Content Type ◽  
Positron Emission

✓ Positron emission tomography was used to study the effect of a rapid infusion of mannitol on cerebral blood volume (CBV) in five dogs and in three human subjects. The ability of mannitol to reduce intracranial pressure (ICP) has always been attributed to its osmotic dehydrating effect. The effects of mannitol infusion include increased osmolality, total blood volume, central venous pressure (CVP), and cerebral blood flow, and decreased hematocrit, hemoglobin concentration, serum sodium level, and viscosity. Mannitol's ability to dilate the cerebral vasculature, either directly or indirectly, and thus to transiently increase ICP, is a subject of controversy. By in vivo labeling of red cells with carbon-11, the authors were able to demonstrate an early increase in CBV in dogs of 20%, 27%, and 23% (mean increase, p < 0.05) at 1, 2, and 3 minutes, respectively, after an infusion of 20% mannitol (2 gm/kg over a 3-minute period). The animals' muscle blood volume increased by 27% (mean increase, p < 0.05) 2 minutes after infusion. In the human subjects, lower doses and a longer duration of infusion (1 gm/kg over 4 minutes) resulted in an increase in CBV of 8%, 14% (p < 0.05), and 10% at 1, 2, and 3 minutes, respectively, after infusion. In dogs, ICP increased by 4 mm Hg (mean increase, p < 0.05) 1 minute after the infusion, before decreasing sharply. The ICP was not measured in the human subjects. Hematocrit, hemoglobin, sodium, potassium, osmolality, heart rate, mean arterial pressure (MAP), and CVP were measured serially. Results of these measurements, as well as the significant decrease in MAP that occurred after mannitol infusion, are discussed. This study demonstrated that rapid mannitol infusion increases CBV and ICP. The increase in muscle blood volume, in the presence of a decreased MAP and an adequate CVP, suggests that mannitol may have caused vasodilation in these experiments.

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