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.

Blood flow, volume, and transit time in the pulmonary microvasculature using laser-Doppler

1994 ◽  
Vol 76 (6) ◽  
pp. 2643-2650 ◽  
Author(s):  
T. S. Hakim ◽  
E. Gilbert ◽  
E. M. Camporesi
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Transit Time ◽  
Flow Rate ◽  
Venous Pressure ◽  
Laser Doppler ◽  
Flow Volume ◽  
Doppler Flowmetry ◽  
Blood Flow Volume ◽  
Wide Range

Capillary transit time is determined by the ratio of capillary volume to flow rate. Exercise-induced hypoxemia is thought to occur because of the short transit time of erythrocytes in capillaries. The effect of flow rate on capillary volume (recruitment vs. distension) is controversial. In a perfused left lower lobe preparation in canine lungs, we used laser-Doppler flowmetry (model ALF21R) to monitor changes in blood flow, volume, and transit time in the microvasculature near the subpleural surface. Changes in total flow, blood volume, and total transit time (tt) were also measured. The results showed that microvascular volume approached maximum when flow rate was at resting value (0.4 l/min) and pressure in the pulmonary artery was > 6 mmHg relative to the level of the capillaries. In contrast, the total blood volume increased gradually over a wide range of flow rates. When flow increased 4.2 times (from 155 to 650 ml/min), tt decreased from 7.32 to 3.53 s; meanwhile, microvascular flow increased from 6.0 to 12.7 units and microvascular transit time decreased from 3.14 to 1.81 units. The changes in microvascular volume and transit time were essentially independent of whether the venous pressure was higher or lower than alveolar pressure. At very high flow (6–10 times resting value), tt fell gradually to approximately 1 s. Direct monitoring of transit time with the laser-Doppler also revealed a gradual decline in microvascular transit time as flow rate increased from 2 to 10 times the normal flow. (ABSTRACT TRUNCATED AT 250 WORDS)

Antiadrenergic and Antihistaminic Therapy in Hemorrhagic Shock in Dog and Rat

1956 ◽  
Vol 186 (1) ◽  
pp. 79-84 ◽  
Author(s):  
S. Jacob ◽  
Edward W. Friedman ◽  
Sabin Levenson ◽  
Philip Glotzer ◽  
H. A. Frank ◽  
...  
Keyword(s):  
Blood Flow ◽  
Survival Rate ◽  
Blood Loss ◽  
Pressure Gradient ◽  
Protective Effect ◽  
Hemorrhagic Shock ◽  
Venous Pressure ◽  
Survival Period ◽  
Effect Of Treatment ◽  
Antihistaminic Drugs

The influence of pretreatment with dibenamine on the development and course of hemorrhagic shock, and the effect of treatment with dibenamine, rapidly acting antiadrenergic drugs, or antihistaminic drugs after hemorrhagic shock had been allowed to become unresponsive to replacement transfusion, were tested in dogs prepared in advance to permit measurement of portal-caval venous pressure gradient. Preliminary dibenamine administration was also tested in rats submitted to hemorrhagic shock. The conclusions were as follows: 1) The protective effect of dibenamine prior to the induction of hemorrhagic shock in the dog consists mainly of a reduction of the bleeding volume. Intrahepatic vasoconstriction is not reduced. A dog which is not under the influence of dibenamine can tolerate a greater degree of blood loss than a dibenaminized dog. After hemorrhagic shock has been allowed to become refractory to replacement transfusion, antiadrenergic and antihistaminic drugs do not reduce intrahepatic vasoconstriction or increase the survival period or the survival rate. 2) Dibenamine given prior to hemorrhage enables the rat to survive a degree of blood loss which is lethal to the untreated rat. This, in part, appears to be due to better blood flow to the respiratory center.

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.

scholarly journals Blood flow augmentation by intrinsic venular contraction in vivo

2012 ◽  
Vol 302 (12) ◽  
pp. R1436-R1442 ◽  
Author(s):  
Ranjeet M. Dongaonkar ◽  
Christopher M. Quick ◽  
Jonathan C. Vo ◽  
Joshua K. Meisner ◽  
Glen A. Laine ◽  
...  
Keyword(s):  
Blood Flow ◽  
Animal Models ◽  
Venous Pressure ◽  
Vessel Diameter ◽  
Peristaltic Pump ◽  
Passive Resistance ◽  
Functional Roles ◽  
Cyclic Contractions ◽  
Contraction Cycle

Venomotion, spontaneous cyclic contractions of venules, was first observed in the bat wing 160 years ago. Of all the functional roles proposed since then, propulsion of blood by venomotion remains the most controversial. Common animal models that require anesthesia and surgery have failed to provide evidence for venular pumping of blood. To determine whether venomotion actively pumps blood in a minimally invasive, unanesthetized animal model, we reintroduced the batwing model. We evaluated the temporal and functional relationship between the venous contraction cycle and blood flow and luminal pressure. Furthermore, we determined the effect of inhibiting venomotion on blood flow. We found that the active venous contractions produced an increase in the blood flow and exhibited temporal vessel diameter-blood velocity and pressure relationships characteristic of a peristaltic pump. The presence of valves, a characteristic of reciprocating pumps, enhances the efficiency of the venular peristaltic pump by preventing retrograde flow. Instead of increasing blood flow by decreasing passive resistance, venular dilation with locally applied sodium nitroprusside decreased blood flow. Taken together, these observations provide evidence for active venular pumping of blood. Although strong venomotion may be unique to bats, venomotion has also been inferred from venous pressure oscillations in other animal models. The conventional paradigm of microvascular pressure and flow regulation assumes venules only act as passive resistors, a proposition that must be reevaluated in the presence of significant venomotion.

Sequential changes in intrarenal hemodynamics during saline infusion in the dog

1975 ◽  
Vol 228 (6) ◽  
pp. 1663-1668 ◽  
Author(s):  
MT Velasquez ◽  
AV Notargiacomo ◽  
JN Cohn
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Venous Pressure ◽  
Indicator Dilution ◽  
Saline Infusion ◽  
Kidney Volume ◽  
Dilution Technique ◽  
Filtration Fraction ◽  
Anesthetized Dogs ◽  
Intrarenal Blood Flow

Intrarenal blood flow and volume (indicator-dilution technique), kidney volume (mercury-in-rubber resistance gage), intr-renal venous pressure, filtration fraction, and sodium excretion were determined dequentially before and during a l-h infusion of isotonicsaline 80 ml/kg in anesthetized dogs. The cortical fraction of renal blood flow roseduring the first 20 min of infusion from an average of 70 to 77%, butreturned nearly to control levels during the last 20 min of infusion because ofa low rise in noncortical flow. During the first 20 min a 23% increase in cortical blood volume accounted for one-third of the 8.5% increase in kidney volume, whereasin the last 20 min cortical blood volume had fallen nearly to control values and kidneyvolume was increased by 17.2%. Intrarenal resistances calculated from intrarenalpressure and flow indicated persistent cortical prevenous dilatation, progressive cortical venous constriction, and only a slight late reduction in noncortical resistance.These data indicate that hemodynamics are shanging continuously during saline infusion and the natriuresis probably is multifactorial.

Renal Denervation in Combination With Angiotensin Receptor Blockade Prolongs Blood Pressure Trough During Hemorrhage

Hypertension ◽  
2021 ◽  
Author(s):  
Reetu R. Singh ◽  
Zoe McArdle ◽  
Lindsea C. Booth ◽  
Clive N. May ◽  
Geoff A. Head ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Blood Loss ◽  
Renal Blood Flow ◽  
Blood Volume ◽  
Antihypertensive Medication ◽  
Renal Denervation ◽  
Organ Damage ◽  
Antihypertensive Medications ◽  
Hemodynamic Responses

Majority of patients with hypertension and chronic kidney disease (CKD) undergoing renal denervation (RDN) are maintained on antihypertensive medication. However, RDN may impair compensatory responses to hypotension induced by blood loss. Therefore, continuation of antihypertensive medications in denervated patients may exacerbate hypotensive episodes. This study examined whether antihypertensive medication compromised hemodynamic responses to blood loss in normotensive (control) sheep and in sheep with hypertensive CKD at 30 months after RDN (control-RDN, CKD-RDN) or sham (control-intact, CKD-intact) procedure. CKD-RDN sheep had lower basal blood pressure (BP; ≈9 mm Hg) and higher basal renal blood flow (≈38%) than CKD-intact. Candesartan lowered BP and increased renal blood flow in all groups. 10% loss of blood volume alone caused a modest fall in BP (≈6–8 mm Hg) in all groups but did not affect the recovery of BP. 10% loss of blood volume in the presence of candesartan prolonged the time at trough BP by 9 minutes and attenuated the fall in renal blood flow in the CKD-RDN group compared with CKD-intact. Candesartan in combination with RDN prolonged trough BP and attenuated renal hemodynamic responses to blood loss. To minimize the risk of hypotension-mediated organ damage, patients with RDN maintained on antihypertensive medications may require closer monitoring when undergoing surgery or experiencing traumatic blood loss.

scholarly journals Energy of blood circulation during blood loss

2020 ◽  
Vol 86 (1) ◽  
pp. 87-93
Author(s):  
K.G. Mykhnevych ◽  
O.V. Kudinova ◽  
S.A. Lutsik
Keyword(s):  
Blood Loss ◽  
Blood Volume ◽  
Blood Circulation ◽  
Venous Pressure ◽  
Intensive Therapy ◽  
Venous Blood ◽  
Peripheral Resistance ◽  
Blood Parameters ◽  
Compensatory Mechanisms ◽  
Energy Indicators

The state of circulatory energy in blood loss has been studied in 44 patients with spleen injury. Kinetic (final diastolic and systolic volumes of the left ventricle, heart rate), dynamic (effective arterial and central venous pressure, total peripheral resistance), hemic (oxygen content in arterial and venous blood) parameters of blood circulation, as well as the level of lactate reflecting the degree of hypoxia were studied. The energy indicators of blood circulation were determined: the power consumed by tissues, the oxygen reserve (reflecting the correspondence of the oxygen consumed by tissues to their needs) and the integral energy indicator - circulatory reserve. It has been determined that with an increase in blood loss, the energy indicators of blood circulation decrease: the power consumed by tissues decrease to (48.0±6.1); (41.1±8.7) and (23.5±9.3) mW/m2, the oxygen reserve decrease to (0.43±0.04); (0.37±0.05) and(0.27+0.07), the circulatory reserve decrease to (229+93); (180±41) and (47±25) mW/m2 respectively at blood loss 20 %, 30 % and 40 % of blood volume. Apparently 20 % blood loss is the maximum amount of blood loss in relation to compensatory possibilities of autoregulation of blood circulation. 30 % blood loss causes more strain on the compensatory mechanisms, at 40 % blood loss the possibility of autoregulation is exhausted. All patients with blood loss up to 20 and up to 30 % of the blood volume survived in the future, with 40 % blood loss 30 % of patients could not be saved. In all deceased patients the circulatory reserve was below 50 mW/m2. It has been determined that a decrease in the circulatory reserve to 100 mW/m2 or lower is a serious threat to life and requires great intensive therapy for blood loss, the level of the circulatory reserve of 50 mW/m2 is not compatible with life, that is, it corresponds to irreversible hemorrhagic shock. Keywords: blood loss, hypovolemia, circulatory energy, blood flow power, oxygen reserve, circulatory reserve.

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