Autoregulation of diaphragmatic blood flow in dogs

1988 ◽  
Vol 64 (1) ◽  
pp. 329-336 ◽  
Author(s):  
S. N. Hussain ◽  
C. Roussos ◽  
S. Magder
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Muscular Activity ◽  
Work Load ◽  
Quiet Breathing ◽  
Transdiaphragmatic Pressure ◽  
Arterial Blood ◽  
Normal Ranges ◽  
Phrenic Artery ◽  
Spontaneously Breathing

In eight anesthetized spontaneously breathing dogs, we determined whether diaphragmatic blood flow is dependent on arterial blood pressure (Pa) or whether it is autoregulated. We also determined whether diaphragmatic muscular activity affects the degree of autoregulation. We measured blood flow through the left phrenic artery (Qphr) with an electromagnetic flow probe and decreased Pa in steps by controlled hemorrhage. Phrenic venous blood was sampled to allow the calculation of diaphragmatic O2 consumption (VO2phr). Diaphragmatic energy demands were varied by using three inspiratory resistances (R1, R2, and R3), which increased peak transdiaphragmatic pressure two-, three-, and fourfold, respectively. During quiet breathing, Qphr was independent of Pa between Pa of 90 and 120 mmHg (i.e., plateau of pressure-flow relation), but at lower Pa, Qphr was directly related to Pa. During inspiratory loading, the Qphr plateau ended at a higher Pa than with quiet breathing, but within the normal ranges of Pa there still was a plateau. VO2phr at a given work load was constant between Pa of 70 and 120 mmHg, but at Pa of 50-55 mmHg, VO2phr declined with all work loads. We conclude that in spontaneously breathing dogs 1) Qphr is autoregulated over the normal range of blood pressures and 2) VO2phr is maintained over wider ranges of Pa than Qphr.

Diaphragmatic blood flow in the dog

1986 ◽  
Vol 60 (2) ◽  
pp. 554-561 ◽  
Author(s):  
H. Bark ◽  
S. M. Scharf
Keyword(s):  
Blood Flow ◽  
Duty Cycle ◽  
Stimulus Frequency ◽  
Phase Flow ◽  
Transdiaphragmatic Pressure ◽  
Relaxation Phase ◽  
Duty Cycles ◽  
Tension Time ◽  
Phrenic Artery ◽  
Electromagnetic Flow Probe

In anesthetized mongrel dogs we measured the blood flow in the left phrenic artery (Qdi), using an electromagnetic flow probe, before and during supramaximal phrenic nerve stimulation (pacing). This was done at constant respiratory rate (24/min) but at three different stimulation frequencies at a duty cycle of 0.4 (20, 50, and 100 Hz) and at three different duty cycles at a stimulation frequency of 50 Hz (duty cycle = 0.2, 0.4, and 0.8). Qdi was unchanged during diaphragm contraction until transdiaphragmatic pressure (Pdi) was greater than approximately 11 cmH2O, whereafter it began to decrease, reaching zero at Pdi approximately 20 cmH2O. Thus, when Pdi was greater than 21 cmH2O, all flow occurred during relaxation. Qdi averaged over the entire respiratory cycle (Qt) was less at duty cycle = 0.8 than under the other conditions. This was because of decreasing length of relaxation phase rather than a difference of relaxation phase flow (Qr), which was maximal during all conditions of phrenic stimulation. During pacing-induced fatigue, Qt actually rose slightly as Pdi fell. This was due to an increase in contraction phase flow while Qr remained constant. The relationship between Qt and tension-time index was not unique but varied according to the different combinations of duty cycle and stimulus frequency.

scholarly journals The Contribution of Arterial Blood Gases in Cerebral Blood Flow Regulation and Fuel Utilization in Man at High Altitude

2015 ◽  
Vol 35 (5) ◽  
pp. 873-881 ◽  
Author(s):  
Christopher K Willie ◽  
David B MacLeod ◽  
Kurt J Smith ◽  
Nia C Lewis ◽  
Glen E Foster ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Cerebral Metabolism ◽  
Venous Blood ◽  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Cerebrovascular Function

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H+ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.

Role of glucagon in splanchnic hyperemia of chronic portal hypertension

1986 ◽  
Vol 251 (5) ◽  
pp. G674-G677 ◽  
Author(s):  
J. N. Benoit ◽  
B. Zimmerman ◽  
A. J. Premen ◽  
V. L. Go ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Venous Blood ◽  
Reference Sample ◽  
Venous Hypertension ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Portal Vein Stenosis ◽  
Arterial Blood

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.

Systemic and hepatic hemodynamic changes in acute liver injury

1997 ◽  
Vol 272 (3) ◽  
pp. G617-G625 ◽  
Author(s):  
A. J. Makin ◽  
R. D. Hughes ◽  
R. Williams
Keyword(s):  
Blood Flow ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Venous Blood ◽  
Marked Change ◽  
Arterial Blood Flow ◽  
Venous Flow ◽  
Subsequent Increase ◽  
Arterial Blood

Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subsequent increase in portal venous flow resulted in an overall increase in total hepatic blood flow of 500%. At this point the oxygen delivery by the hepatic arterial and portal venous systems was equal. These circulatory changes returned to control values by 72 h with recovery of liver function. These results demonstrate the development of a hyperdynamic circulation and a marked change in the normal relationship between portal venous and hepatic arterial blood flows that occur during hepatic injury.

Adrenal catecholamines in E. coli endotoxin shock

1961 ◽  
Vol 16 (2) ◽  
pp. 348-350 ◽  
Author(s):  
Florian Nykiel ◽  
Vincent V. Glaviano
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Venous Blood ◽  
Endotoxin Shock ◽  
Mean Blood Pressure ◽  
E Coli ◽  
Arterial Blood ◽  
Splanchnic Nerves

In dogs with left adrenal cannulation, administration of 1 mg/kg of purified E. coli endotoxin resulted in a decrease in mean blood pressure and adrenal blood flow. These changes were accompanied by significant increases in levels of epinephrine in adrenal venous blood. Release of epinephrine by the adrenals in endotoxin shock was due to a neurogenic mechanism, since sectioning of the splanchnic nerves prevented secretion of epinephrine. The rise in epinephrine output from an intact adrenal was noted to occur only in the presence of a significant decrease in arterial blood pressure; therefore endotoxin causes adrenal stimulation from reflexes initiated by the hypothalamus or peripheral baroreceptors. Submitted on September 20, 1960

Correlation of left phrenic arterial flow with regional diaphragmatic blood flow

1988 ◽  
Vol 64 (5) ◽  
pp. 2230-2235 ◽  
Author(s):  
D. G. Nichols ◽  
S. M. Scharf ◽  
R. J. Traystman ◽  
J. L. Robotham
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Blood Flow ◽  
Phrenic Nerve Stimulation ◽  
Flow Probe ◽  
Mechanically Ventilated ◽  
Doppler Flow ◽  
Arterial Blood ◽  
Phrenic Artery ◽  
Crural Diaphragm

Previous work has assumed that left phrenic arterial blood flow (Qpa) reflects diaphragmatic blood flow. We have tested this assumption in four anesthetized mechanically ventilated dogs by measuring Qpa with a Doppler flow probe and regional diaphragmatic blood flow with radiolabeled microspheres. Flows were examined during control 1 (diaphragm at rest), pacing (phrenic pacing: rate 20/min, duty cycle 0.33), control 2, hypotension (rest with mean arterial pressure reduced by 45% of the control 1 value), and hypotension and pacing. As a percent of the control 1 value, Qpa was 511 +/- 107% during pacing, 139 +/- 12% during control 2, 40 +/- 13% during hypotension, and finally 347 +/- 31% during hypotension and pacing. Similarly, percent left hemidiaphragmatic blood flow (Qlh) was 362 +/- 91% during pacing, 91 +/- 10% during control 2, 14 +/- 2% during hypotension, and finally 213 +/- 50% during hypotension and pacing. The changes in flow to the left costal and crural diaphragm were similar to those recorded for Qlh. We conclude that Qpa correlates with total and regional diaphragmatic blood flow (r = 0.77–0.81, P less than 0.001) under conditions of supramaximal phrenic nerve stimulation in which the metabolic demands of the region perfused by the phrenic artery are presumed to be similar to the metabolic demands of the rest of the diaphragm.

Response to cold of Eskimos of the eastern Canadian Arctic

1963 ◽  
Vol 18 (5) ◽  
pp. 970-974 ◽  
Author(s):  
G. Malcolm Brown ◽  
Robert E. Semple ◽  
C. S. Lennox ◽  
G. S. Bird ◽  
C. W. Baugh
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Canadian Arctic ◽  
The Body ◽  
Arterial Blood ◽  
Acute Cold Exposure ◽  
Body Core ◽  
Average Skin ◽  
Skin Temperatures ◽  
Eastern Canadian Arctic

Skin, muscle, and rectal temperatures, and O2 consumption of Eskimos and Caucasians have been compared during an acute cold exposure involving immersion of one hand and forearm in a 5 C water bath. The Eskimos consumed less O2, maintained their rectal temperatures at a higher level, and gave up less heat from the muscles of the limbs. Though the Eskimos had significantly more adipose tissue, average skin temperatures were the same in the two groups. The pattern of temperatures noted now and the previously observed higher blood flow in the hand and forearm of Eskimos point to increased cooling of arterial blood by returning venous blood in the extremities with resultant preservation of heat in the body core. Submitted on August 6, 1962

Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs

2001 ◽  
Vol 280 (5) ◽  
pp. G819-G827 ◽  
Author(s):  
S. M. Jakob ◽  
J. J. Tenhunen ◽  
S. Laitinen ◽  
A. Heino ◽  
E. Alhava ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Tamponade ◽  
Venous Blood ◽  
Liver Blood Flow ◽  
Hepatic Function ◽  
Arterial Blood Flow ◽  
Cellular Damage ◽  
Aortic Blood Flow ◽  
Venous Blood Flow ◽  
Arterial Blood

The hepatic arterial buffer response (HABR) tends to maintain liver blood flow under conditions of low mesenteric perfusion. We hypothesized that systemic hypoperfusion impairs the HABR. In 12 pigs, aortic blood flow was reduced by cardiac tamponade to 50 ml · kg−1 · min−1 for 1 h (short-term tamponade) and further to 30 ml · kg−1 · min−1 for another hour (prolonged tamponade). Twelve pigs without tamponade served as controls. Portal venous blood flow decreased from 17 ± 3 (baseline) to 6 ± 4 ml · kg−1 · min−1 (prolonged tamponade; P = 0.012) and did not change in controls, whereas hepatic arterial blood flow decreased from 2 ± 1 (baseline) to 1 ± 1 ml · kg−1 · min−1 (prolonged tamponade; P = 0.050) and increased from 2 ± 1 to 4 ± 2 ml · kg−1 · min−1in controls ( P = 0.002). The change in hepatic arterial conductance (Δ C ha) during acute portal vein occlusion decreased from 0.1 ± 0.05 (baseline) to 0 ± 0.01 ml · kg−1 · min−1 · mmHg−1(prolonged tamponade; P = 0.043). In controls, Δ C ha did not change. Hepatic lactate extraction decreased, but hepatic release of glutathione S-transferase A did not change during cardiac tamponade. In conclusion, during low systemic perfusion, the HABR is exhausted and hepatic function is impaired without signs of cellular damage.

Effect of norepinephrine on diaphragm contractility and blood flow

1990 ◽  
Vol 69 (6) ◽  
pp. 2019-2028 ◽  
Author(s):  
G. S. Supinski ◽  
A. F. DiMarco ◽  
J. Gonzalez ◽  
M. D. Altose
Keyword(s):  
Blood Flow ◽  
Group Iv ◽  
Arterial Flow ◽  
Force Frequency ◽  
Group Iii ◽  
Arterial Blood ◽  
Group I ◽  
Intramuscular Electrodes ◽  
Phrenic Artery ◽  
Group Ii

Recent studies have shown that diaphragm fatigue can be reversed by mechanical augmentation of phrenic arterial flow. The purpose of the present experiment was to determine whether it was possible to pharmacologically augment diaphragm blood flow and reverse fatigue by the administration of norepinephrine. Four groups of studies were performed, all employing our previously described in situ isometric canine diaphragm strip preparation (Supinski et al., J. Appl. Physiol. 60: 1789-1796, 1986). Group I studies examined the effects of norepinephrine on the contractility of the nonfatigued diaphragm in normotensive dogs, group II studies examined the effects of this drug on the contractility of the fatigued diaphragm in normotensive animals, and group III studies examined the effect of this drug on the contractility of the fatigued diaphragm in hypotensive animals. Group IV studies examined the effect of norepinephrine in normotensive animals in which the phrenic artery was cannulated and pump perfused at constant flow. Fatigue was induced in group II, III, and IV studies by rhythmically stimulating the diaphragm via intramuscular electrodes. Norepinephrine had no effect on the contractility of the nonfatigued diaphragm (group I). In normotensive (group II) and hypotensive animals (group III), norepinephrine elicited dramatic increases in arterial blood pressure and phrenic arterial flow and produced a significant upshift in the force-frequency curve of the fatigued diaphragm. However, when phrenic flow was held constant (group IV experiments), norepinephrine failed to augment the contractility of the fatigued diaphragm. These results indicate that 1) norepinephrine can increase phrenic blood flow and augment the contractility of the fatigued diaphragm in both normotensive and hypotensive conditions and 2) this effect of norepinephrine to partially reverse fatigue is secondary to its action to augment diaphragmatic blood flow.

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