Spleen volume and blood flow response to repeated breath-hold apneas

2003 ◽  
Vol 95 (4) ◽  
pp. 1460-1466 ◽  
Author(s):  
Darija Baković ◽  
Zoran Valic ◽  
Davor Eterović ◽  
Ivica Vuković ◽  
Ante Obad ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cold Water ◽  
Splenic Vein ◽  
Arterial Blood Flow ◽  
Breath Hold ◽  
Spleen Volume ◽  
Blood Flows ◽  
Arterial Blood ◽  
Active Contraction ◽  
Spleen Contraction

The purpose of this study was 1) to answer whether the reduction in spleen size in breath-hold apnea is an active contraction or a passive collapse secondary to reduced splenic arterial blood flow and 2) to monitor the spleen response to repeated breath-hold apneas. Ten trained apnea divers and 10 intact and 7 splenectomized untrained persons repeated five maximal apneas (A1-A5) with face immersion in cold water, with 2 min interposed between successive attempts. Ultrasonic monitoring of the spleen and noninvasive cardiopulmonary measurements were performed before, between apneas, and at times 0, 10, 20, 40, and 60 min after the last apnea. Blood flows in splenic artery and splenic vein were not significantly affected by breath-hold apnea. The duration of apneas peaked after A3 (143, 127, and 74 s in apnea divers, intact, and splenectomized persons, respectively). A rapid decrease in spleen volume (∼20% in both apnea divers and intact persons) was mainly completed throughout the first apnea. The spleen did not recover in size between apneas and only partly recovered 60 min after A5. The well-known physiological responses to apnea diving, i.e., bradycardia and increased blood pressure, were observed in A1 and remained unchanged throughout the following apneas. These results show rapid, probably active contraction of the spleen in response to breath-hold apnea in humans. Rapid spleen contraction and its slow recovery may contribute to prolongation of successive, briefly repeated apnea attempts.

Relationship between portal venous and hepatic arterial blood flows: spectrum of response

1990 ◽  
Vol 259 (6) ◽  
pp. G1010-G1018 ◽  
Author(s):  
T. Kawasaki ◽  
F. J. Carmichael ◽  
V. Saldivia ◽  
L. Roldan ◽  
H. Orrego
Keyword(s):  
Blood Flow ◽  
Arterial Blood Flow ◽  
Portal Vein Ligation ◽  
Artery Ligation ◽  
Blood Flows ◽  
Arterial Blood ◽  
Group A ◽  
Group B ◽  
The Relationship ◽  
Group D

The relationship between portal tributary blood flow (PBF) and hepatic arterial blood flow (HAF) was studied in awake, unrestrained rats with the radiolabeled microsphere technique. Six distinct patterns of response emerged. In group A (PBF+, HAF 0), ethanol, acetate, glucagon, prostacyclin, and a mixed diet increased PBF without a change in HAF; in group B (PBF+, HAF+), adenosine and histamine increased both PBF and HAF; in group C (PBF 0, HAF+), isoflurane and triiodothyronine did not change PBF but increased HAF; and in group D (PBF-, HAF+), halothane and vasopressin decreased PBF and increased HAF. Acute partial portal vein ligation decreased PBF (56%) and increased HAF (436%). Hypoxia (7.5% O2) decreased PBF (28%) and increased HAF (110%). In group E (PBF+, HAF-), acute hepatic artery ligation increased PBF (35%) and reduced HAF (74%), while in group F (PBF-, HAF-), thyroidectomy reduced PBF and HAF (36 and 47%, respectively). All blood flow responses were accompanied by the expected changes in both portal tributary and hepatic arterial vascular resistances. The data suggest that the portal and hepatic arterial vascular territories have regulatory mechanisms that allow for independent changes.

Pulmonary blood flow, pressure and resistance following tetraethylammonium and aminophylline

1961 ◽  
Vol 200 (2) ◽  
pp. 287-291 ◽  
Author(s):  
M. Harasawa ◽  
S. Rodbard
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Arterial Blood Flow ◽  
Tetraethylammonium Chloride ◽  
Blood Flows ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Flow Pressure

The effects of tetraethylammonium chloride (TEAC) and aminophylline on the pulmonary vascular resistance were studied in thoracotomized dogs. Pulmonary arterial blood flow and pressure, and systemic blood pressure were measured simultaneously. Both drugs showed marked hypotensive effects on the systemic vessels. In every instance pulmonary arterial pressures and blood flows were reduced by TEAC given via the pulmonary artery and increased by aminophylline. However, the calculated pulmonary vascular resistance remained essentially unchanged in all experiments. These data challenge the concept that the pulmonary vessels respond to these drugs by active vasodilatation

Increase in hepatic blood flow during early sepsis is due to increased portal blood flow

1991 ◽  
Vol 261 (6) ◽  
pp. R1507-R1512 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
I. H. Chaudry
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Hepatic Blood Flow ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow ◽  
Early Sepsis

Although hepatic blood flow increases significantly during early sepsis [as produced by cecal ligation and puncture (CLP)], it is not known whether this is due to the increase in portal or hepatic arterial blood flows. To study this, rats were subjected to CLP, after which they and sham-operated rats received either 3 or 6 ml normal saline/100 g body wt subcutaneously (i.e., all rats received crystalloid therapy). Blood flow in various organs was determined by using a radioactive microsphere technique at 5 and 20 h after CLP or sham operation. Portal blood flow was calculated as the sum of blood flows to the spleen, pancreas, gastrointestinal tract, and mesentery. Total hepatic blood flow was the sum of portal blood flow and hepatic arterial blood flow. A significant increase in portal blood flow and in total hepatic blood flow was observed at 5 h after CLP (i.e., early sepsis), and this was not altered by doubling the volume of crystalloid resuscitation after the induction of sepsis. In contrast, hepatic arterial blood flow during early sepsis was found to be similar to control; however, it was significantly reduced in late sepsis (i.e., 20 h after CLP). Cardiac output was significantly higher than the control in early sepsis. However, even in late sepsis, cardiac output and total hepatic blood flow were not significantly different from controls. These results indicate that the increased total hepatic blood flow during early hyperdynamic sepsis is solely due to the increased portal blood flow.

Splenic baroreceptors control splenic afferent nerve activity

2006 ◽  
Vol 290 (2) ◽  
pp. R352-R356 ◽  
Author(s):  
Karli Moncrief ◽  
Susan Kaufman
Keyword(s):  
Blood Flow ◽  
Venous Pressure ◽  
Venous Blood ◽  
Splenic Vein ◽  
Afferent Nerve ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Nerve Activity ◽  
Vein Occlusion ◽  
Arterial Blood

Stenosis of either the portal or splenic vein increases splenic afferent nerve activity (SANA), which, through the splenorenal reflex, reduces renal blood flow. Because these maneuvers not only raise splenic venous pressure but also reduce splenic venous outflow, the question remained as to whether it is increased intrasplenic postcapillary pressure and/or reduced intrasplenic blood flow, which stimulates SANA. In anesthetized rats, we measured the changes in SANA in response to partial occlusion of either the splenic artery or vein. Splenic venous and arterial pressures and flows were simultaneously monitored. Splenic vein occlusion increased splenic venous pressure (9.5 ± 0.5 to 22.9 ± 0.8 mmHg, n = 6), reduced splenic arterial blood flow (1.7 ± 0.1 to 0.9 ± 0.1 ml/min, n = 6) and splenic venous blood flow (1.3 ± 0.1 to 0.6 ± 0.1 ml/min, n = 6), and increased SANA (1.7 ± 0.4 to 2.2 ± 0.5 spikes/s, n = 6). During splenic artery occlusion, we matched the reduction in either splenic arterial blood flow (1.7 ± 0.1 to 0.7 ± 0.05, n = 6) or splenic venous blood flow (1.2 ± 0.1 to 0.5 ± 0.04, n = 5) with that seen during splenic vein occlusion. In neither case was there any change in either splenic venous pressure (−0.4 ± 0.9 mmHg, n = 6 and +0.1 ± 0.3 mmHg, n = 5) or SANA (−0.11 ± 0.15 spikes/s, n = 6 and −0.05 ± 0.08 spikes/s, n = 5), respectively. Furthermore, there was a linear relationship between SANA and splenic venous pressure ( r = 0.619, P = 0.008, n = 17). There was no such relationship with splenic venous ( r = 0.371, P = 0.236, n = 12) or arterial ( r = 0.275, P = 0.413, n = 11) blood flow. We conclude that it is splenic venous pressure, not flow, which stimulates splenic afferent nerve activity and activates the splenorenal reflex in portal and splenic venous hypertension.

Relationship between vascular reactivity in vitro and blood flows in rats with cirrhosis

1999 ◽  
Vol 97 (3) ◽  
pp. 313-318 ◽  
Author(s):  
Dominique PATERON ◽  
Frédéric OBERTI ◽  
Pascale LEFILLIATRE ◽  
Nary VEAL ◽  
Khalid A. TAZI ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Reactivity ◽  
Regional Blood Flow ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Vascular Responsiveness ◽  
Microsphere Method ◽  
Radioactive Microsphere Method

In cirrhosis there is a hyperdynamic circulation, which occurs mainly in the systemic and splanchnic regions. Using isolated-vessel models, previous studies have shown reduced aortic reactivity to vasoconstrictors in rats with cirrhosis. The aim of the present study was to evaluate and compare the vascular responsiveness to phenylephrine in arterial rings and the blood flows from different regions in rats with cirrhosis and controls. Reactivity was studied in isolated thoracic aortic, superior mesenteric arterial and carotid arterial rings from sham-operated and bile-duct-ligated rats by measuring the cumulative concentration-dependent tension induced by phenylephrine (10-9–10-4 M). Blood flows were measured by the radioactive microsphere method. In rats with cirrhosis, a significant hyporeactivity to phenylephrine was observed in both the aorta and the superior mesenteric artery compared with the corresponding arteries of normal rats. This hyporesponsiveness was corrected by Nω-nitro-l-arginine (0.1 mM). In contrast, carotid artery reactivity and the responses to Nω-nitro-l-arginine were similar in the cirrhotic and control groups. In each case, cardiac output and mesenteric arterial blood flow were significantly higher in cirrhotic than in normal rats. Cerebral blood flows were not significantly different between the two groups. In cirrhotic rats, arterial hyporeactivity may be a consequence of increased regional blood flow and increased production of nitric oxide.

scholarly journals Effect of Electrical Stimulation on Blood Flow in Calf Muscles in Different Body Positions

2018 ◽  
Vol 1 (96) ◽  
Author(s):  
Julius Dovydaitis ◽  
Albinas Grūnovas
Keyword(s):  
Blood Flow ◽  
Body Position ◽  
Venous Blood ◽  
The Body ◽  
Arterial Blood Flow ◽  
Reserve Capacity ◽  
Horizontal Position ◽  
Blood Flows ◽  
Arterial Blood ◽  
Electrical Muscle

Background.  In  most  studies  on  cardiovascular  system,  testing  of  subjects  was  performed  in  a  horizontal position. With the change of the body position, certain functional changes occur in the cardiovascular system. The aim of this study was to analyze the effect of electrical muscle stimulation (EMS) on arterial and venous blood flows.Methods. Eighteen athletes aged 19–23 performed two sessions of tests in horizontal and sitting positions. Changes in arterial and venous blood flows were recorded before and after EMS. In each session two occlusions were performed. In the horizontal position, the initial occlusion pressure of 20 mmHg was applied and as the balance in arterial and venous blood flow rates was reached, the additional pressure of 20 mmHg (40  mmHg in total). In the sitting position, the occlusion pressure of 40 and 20 mmHg was applied respectively (60 mmHg in total). In both sessions EMS was performed using the electrical stimulator Mioritm 021.Results. In both horizontal and vertical positions, the effect of EMS on arterial blood flow, venous reserve capacity and venous elasticity was insignificant. Arterial and venous blood flows was affected significantly by the change of the body position. In the sitting position, arterial blood flow was significantly (p < .05) lower compared to the horizontal position. Similar results were recorded in venous reserve capacity.Conclusion.  The  study  suggests  that  blood  flow  in  the  calf  muscles  is  affected  by  the  body  position  and hydrostatic pressure; arterial blood flow increases in the horizontal body position.Keywords:  electrical muscle stimulation (EMS), arterial blood flow, venous reserve capacity, venous elasticity

scholarly journals Brief asphyxial state following immediate cord clamping accelerates onset of left-to-right shunting across the ductus arteriosus after birth in preterm lambs

2020 ◽  
Vol 128 (2) ◽  
pp. 429-439
Author(s):  
Joseph J. Smolich ◽  
Kelly R. Kenna ◽  
Michael M. H. Cheung ◽  
Jonathan P. Mynard
Keyword(s):  
Blood Flow ◽  
Ductus Arteriosus ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cord Clamping ◽  
Umbilical Cord Clamping ◽  
Left Ventricular Output ◽  
Transition Study

Reversal of shunting across the ductus arteriosus from right-to-left to left-to-right is a characteristic feature of the birth transition. Given that immediate cord clamping (ICC) followed by an asphyxial cord clamp-to-ventilation (CC-V) interval may augment left ventricular (LV) output and central blood flows after birth, we tested the hypothesis that an asphyxial CC-V interval accelerates the onset of postnatal left-to-right ductal shunting. High-fidelity central blood flow signals were obtained in anesthetized preterm lambs (gestation 128 ± 2 days) after ICC followed by a nonasphyxial (∼40 s, n = 9) or asphyxial (∼90 s, n = 9) CC-V interval before mechanical ventilation for 30 min after birth. Left-to-right ductal flow segments were related to aortic isthmus and descending aortic flow profiles to quantify sources of ductal shunting. In the nonasphyxial group, phasic left-to-right ductal shunting was initially minor after birth, but then rose progressively to 437 ± 164 ml/min by 15 min ( P < 0.001). However, in the asphyxial group, this shunting increased from 24 ± 21 to 199 ± 93 ml/min by 15 s after birth ( P < 0.001) and rose further to 471 ± 190 ml/min by 2 min ( P < 0.001). This earlier onset of left-to-right ductal shunting was supported by larger contributions ( P < 0.001) from direct systolic LV flow and retrograde diastolic discharge from an arterial reservoir/windkessel located in the descending aorta and its major branches, and associated with increased pulmonary arterial blood flow having a larger ductal component. These findings suggest that the duration of the CC-V interval after ICC is an important modulator of left-to-right ductal shunting, LV output and pulmonary perfusion at birth. NEW & NOTEWORTHY This birth transition study in preterm lambs demonstrated that a brief (∼90 s) asphyxial interval between umbilical cord clamping and ventilation onset resulted in earlier and greater left-to-right shunting across the ductus arteriosus after birth. This greater shunting 1) resulted from an increased left ventricular output associated with a higher systolic left-to-right ductal flow and increased retrograde diastolic discharge from a lower body arterial reservoir/windkessel, and 2) was accompanied by greater lung perfusion after birth.

Hand arterial blood flow responses to local venous congestion

1981 ◽  
Vol 240 (6) ◽  
pp. H980-H983
Author(s):  
B. I. Levy ◽  
Y. Oliva ◽  
J. P. Martineaud
Keyword(s):  
Blood Flow ◽  
Venous Occlusion ◽  
Middle Part ◽  
Venous Congestion ◽  
Arterial Blood Flow ◽  
Cuff Inflation ◽  
Blood Flows ◽  
Arterial Blood ◽  
Hand Control ◽  
Occlusion Cuff

Hand and forearm blood flows were measured in 12 subjects by means of a range-gated Doppler velocimeter, in basal conditions and after inflation (30, 50, 60, 70, and 90 mmHg) of a venous occlusion cuff on the middle part of the forearm. In basal conditions, there were significant decreases in radial, ulnar, and brachial blood flow after cuff inflation (up to -78, -69, and -31%, respectively). Minimal values were reached in less than 7 s. After occlusion of the circulation of the hand, control brachial blood flow was lowered but not significantly affected by venous distension. The results must be considered and accounted where venous occlusion plethysmography is used to measure segmental blood flow.

Glucagon increases hepatic oxygen supply-demand ratio in pigs

1987 ◽  
Vol 252 (5) ◽  
pp. G648-G653
Author(s):  
S. Gelman ◽  
E. Dillard ◽  
D. A. Parks
Keyword(s):  
Blood Flow ◽  
Oxygen Supply ◽  
Venous Blood ◽  
Portal Blood Flow ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Young Pigs ◽  
Hepatic Venous Blood ◽  
Pentobarbital Sodium Anesthesia

The present study was performed on eight young pigs to test the hypothesis that glucagon increases hepatic oxygen supply to a greater extent than hepatic oxygen uptake, providing a better hepatic oxygen supply-demand relationship. The experiments were performed under pentobarbital sodium anesthesia and controlled ventilation. Splanchnic blood flow was studied using radioactive microspheres. Glucagon was administered in doses of 1 and 5 micrograms X kg-1 X min-1. During glucagon infusion, hepatic arterial blood flow substantially increased, splenic and pancreatic blood flows increased moderately, while stomach and intestinal blood flows, as well as portal blood flow did not change significantly. Shunting of both 9- and 15-micron spheres through preportal tissues did not change significantly. Oxygen content in arterial or portal venous blood did not change significantly, while it increased in hepatic venous blood by 30%. There were no differences in the effects between the doses of glucagon administered. There was no correlation found between changes in hepatic oxygen supply and cardiac output or blood pressure. The changes observed during glucagon administration resulted in an increase in oxygen delivery to the liver and hepatic oxygen supply-uptake ratio.

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