The Role of Baroreceptors and Chemoreceptors in the Regulation of the Cerebral Circulation

1975 ◽  
Vol 49 (5) ◽  
pp. 465-471 ◽  
Author(s):  
I. M. James ◽  
Lindsay A. MacDonell
Keyword(s):  
Blood Flow ◽  
Cerebral Circulation ◽  
Perfusion Pressure ◽  
Carotid Bifurcation ◽  
Arterial Perfusion ◽  
Arterial Blood ◽  
Bilateral Vagotomy ◽  
Cerebral Cortical Blood Flow ◽  
Reciprocal Change

1. Ten experiments, each using two dogs, were performed to evaluate the effect of chemoreceptor and baroreceptor activity on the cerebral circulation. 2. The carotid bifurcation areas were vascularly isolated bilaterally and perfused with arterial blood from a second animal. 3. Bilateral vagotomy interrupted stimuli from the aortic group of receptors. 4. Administration of 5% carbon dioxide to the donor animal resulted in an increase in cerebral (cortical) blood flow in the recipient. 5. A change in the arterial perfusion pressure from the donor resulted in a reciprocal change in the cerebral blood flow of the recipient. These changes were abolished by sectioning the sinus nerves.

Do vasoregulatory mechanisms in exercising human muscle compensate for changes in arterial perfusion pressure?

2007 ◽  
Vol 293 (5) ◽  
pp. H2928-H2936 ◽  
Author(s):  
Kathryn L. Walker ◽  
Natasha R. Saunders ◽  
Dennis Jensen ◽  
Jennifer L. Kuk ◽  
Suzi-Lai Wong ◽  
...  
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Perfusion Pressure ◽  
Muscle Blood Flow ◽  
Human Muscle ◽  
Isometric Handgrip ◽  
Vascular Conductance ◽  
Arterial Perfusion ◽  
Arterial Blood ◽  
Myogenic Regulation

We tested the hypothesis that vasoregulatory mechanisms completely counteract the effects of sudden changes in arterial perfusion pressure on exercising muscle blood flow. Twelve healthy young subjects (7 female, 5 male) lay supine and performed rhythmic isometric handgrip contractions (2 s contraction/ 2 s relaxation 30% maximal voluntary contraction). Forearm blood flow (FBF; echo and Doppler ultrasound), mean arterial blood pressure (arterial tonometry), and heart rate (ECG) were measured. Moving the arm between above the heart (AH) and below the heart (BH) level during contraction in steady-state exercise achieved sudden ∼30 mmHg changes in forearm arterial perfusion pressure (FAPP). We analyzed cardiac cycles during relaxation (FBFrelax). In an AH-to-BH transition, FBFrelax increased immediately, in excess of the increase in FAPP (∼69% vs. ∼41%). This was accounted for by pressure-related distension of forearm resistance vasculature [forearm vascular conductance (FVCrelax) increased by ∼19%]. FVCrelax was restored by the second relaxation. Continued slow decreases in FVCrelax stabilized by 2 min without restoring FBFrelax. In a BH-to-AH transition, FBFrelax decreased immediately, in excess of the decrease in FAPP (∼37% vs. ∼29%). FVCrelax decreased by ∼14%, suggesting pressure-related passive recoil of resistance vessels. The pattern of FVCrelax was similar to that in the AH-to-BH transition, and FBFrelax was not restored. These data support rapid myogenic regulation of vascular conductance in exercising human muscle but incomplete flow restoration via slower-acting mechanisms. Local arterial perfusion pressure is an important determinant of steady-state blood flow in the exercising human forearm.

Role of tracheal and bronchial circulation in respiratory heat exchange

1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Lung Parenchyma ◽  
Arterial Blood ◽  
Respiratory Heat Loss ◽  
Reference Flow ◽  
Pulmonary Arterial ◽  
End Tidal ◽  
Humidified Air

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.

scholarly journals Role of Perfusion Pressure in Major Organ Blood Flow during Cardiopulmonary Bypass in Canines

2000 ◽  
Vol 39 (5) ◽  
pp. 748
Author(s):  
Young Lan Kwak ◽  
Young Hwan Park ◽  
Sang Beom Nam ◽  
Young Jun Oh ◽  
Seung Ho Kim ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Perfusion Pressure ◽  
Organ Blood Flow ◽  
Major Organ

Role of reflexes following myocardial necrobiosis

1965 ◽  
Vol 209 (6) ◽  
pp. 1081-1088 ◽  
Author(s):  
G. Ascanio ◽  
F. Barrera ◽  
E. V. Lautsch ◽  
M. J. Oppenheimer
Keyword(s):  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Hemodynamic Changes ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood ◽  
Bilateral Vagotomy ◽  
Left Ventricular Systolic Pressure

Intracoronary administration of hexachlorotetrafluorobutane (Hexa) into non-thoracotomized dogs produced a statistically significant decrease in left ventricular systolic pressure (LVSP), mean femoral arterial blood pressure (MFAP), first derivative of left ventricular pressure pulse (dP/d t), total peripheral resistance (TPR), and cardiac output (C.O.) lasting up to 1 hr after injection. Femoral vascular resistance decreased during the first 3 min after production of necrobiosis. Fifty percent of the dogs died of ventricular fibrillation (VF) after Hexa infarction. Prereserpinized dogs did not show significant changes in the parameters which were significantly changed in normal dogs after Hexa necrobiosis except in the case of VF which was almost absent in this group. Bilateral vagotomy prior to Hexa administration prevented most hemodynamic changes after necrobiosis whereas atropine did not. Bilateral vagotomy and atropine 1 hr after necrobiosis increased MFAP, dP/d t, LVSP, C.O., and TPR. Apparently excitatory efferent sympathetic activity on heart and femoral arterial vessels is reflexly inhibited by the effects of intracoronary injection of Hexa. The afferent pathway is via the vagus nerve.

Use of a thermal pulse decay system to assess avian renal blood flow during reduced renal arterial perfusion pressure

1992 ◽  
Vol 262 (1) ◽  
pp. R90-R98 ◽  
Author(s):  
R. F. Wideman ◽  
R. P. Glahn ◽  
W. G. Bottje ◽  
K. R. Holmes
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Regional Differences ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Portal Flow ◽  
Arterial Perfusion ◽  
Restricted Group

Using a simplified avian kidney model, renal arterial perfusion pressure (RAPP) was reduced from 120 (control) to 70 mmHg (near the glomerular filtration rate autoregulatory limit) and then to 46 mmHg (below the glomerular filtration rate autoregulatory range) in kidneys with ambient or partially restricted renal portal flow. Renal blood flow (RBF) was measured with a thermal pulse decay (TPD) system, using TPD thermistor probes inserted at three locations to evaluate regional differences in RBF. The clearance (CPAH) and extraction of p-aminohippuric acid were used to calculate renal plasma flow (RPF). CPAH, RPF, and RBF values were consistently lower for kidneys with restricted portal flow than for kidneys with ambient portal flow. Reducing RAPP to 46 mmHg did not significantly reduce CPAH, RPF, or RBF in the ambient group but did significantly reduce CPAH and RPF (regressed on RAPP) in the restricted group. RBF was not significantly affected when RAPP was reduced in the restricted group, although significant regional differences in blood flow were recorded. Renal vascular resistance decreased significantly as RAPP was reduced to 46 mmHg in the ambient group, confirming the renal autoregulatory response. In separate validation studies, significant reductions in RBF were detected by the TPD system during acute obstructions of portal and/or arterial flow. Overall, the results support previous evidence that avian RBF remains constant over a wide range of RAPPs. Observations of nonuniform intrarenal distributions of portal blood flow suggest that the portal system maintains the constancy of RBF in regions with proportionately high portal-to-arterial flow ratios.

The adrenocorticotropic hormone and arginine vasopressin responses to hypercapnia in fetal and maternal sheep

1993 ◽  
Vol 264 (2) ◽  
pp. R324-R330 ◽  
Author(s):  
H. G. Chen ◽  
C. E. Wood
Keyword(s):  
Arginine Vasopressin ◽  
Adrenocorticotropic Hormone ◽  
Fetal Sheep ◽  
Arterial Pco2 ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Bilateral Vagotomy ◽  
Pregnant Ewe

Previous studies have demonstrated that fetal adrenocorticotropic hormone (ACTH) and arginine vasopressin (AVP) are increased during periods of acidemia produced by infusion of acid intravenously or by acidemia secondary to hypovolemia. The purpose of this study was to quantify ACTH and AVP responses to hypercapnic acidemia and to test the role of the peripheral chemoreceptors in the control of these responses. Chronically catheterized fetal sheep were subjected to carotid sinus denervation and bilateral vagotomy or were studied intact. At least 5 days after surgery, fetuses were exposed to a 60-min period of normocapnia or hypercapnia, delivered via a polyethylene bag containing 5-8% CO2 in 21% O2 fitted over the head of the pregnant ewe. Hypercapnia significantly increased fetal arterial PCO2 to 55.2 +/- 1.8 and 55.9 +/- 2.2 mmHg and decreased arterial pH to 7.257 +/- 0.011 and 7.281 +/- 0.010 in intact and denervated fetuses, respectively. Fetal mean arterial blood pressure was decreased slightly in the denervated fetuses during hypercapnia. Fetal plasma AVP was increased in both groups equally, and plasma ACTH and cortisol were increased in the denervated fetuses only. Fetal heart rate was increased significantly in intact but not denervated fetuses. We conclude that respiratory acidemia is a mild stimulus to AVP secretion and that this response is not attenuated by peripheral chemodenervation.

Glucagon inhibition of hepatic arterial responses to hepatic nerve stimulation

1977 ◽  
Vol 233 (6) ◽  
pp. H647-H654 ◽  
Author(s):  
P. D. Richardson ◽  
P. G. Withrington
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Arterial Responses ◽  
Sympathetic Discharge ◽  
Glucagon Concentration

The hepatic arterial vascular bed of the chloaralose-urethan-anesthetized dog was perfused with blood from a cannulated femoral artery. Hepatic arterial blood flow and perfusion pressure were measured. The hepatic periarterial postganglionic sympathetic nerves were stimulated supramaximally at 0.1, 0.5, 1, 2, 5, 10, and 20 Hz; this caused frequency-dependent rises in the calculated hepatic arterial vascular resistance at all frequencies above the threshold of 0.1 or 0.5 Hz. Glucagon was infused intra-arterially in dosese from 0.25 to 10 microgram/min; glucagon antagonized both the vasoconstrictor effects of hepatic nerve stimulation and of intra-arterial injections of norepinephrine. The degree of antagonism of these responses was significantly correlated with the calculated hepatic arterial glucagon concentration. It is possible that glucagon released physiologically in stress and hypoglycemia may protect the hepatic arterial vasculature from the effects of increased sympathetic discharge.

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.

Gastric microvascular actions of platelet-activating factor: role of leukocytes

1992 ◽  
Vol 262 (3) ◽  
pp. G537-G544
Author(s):  
J. G. Wood ◽  
Z. Y. Yan ◽  
L. Y. Cheung
Keyword(s):  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Ex Vivo ◽  
Platelet Activating Factor ◽  
Arterial Infusion ◽  
Edema Formation ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Alpha Chloralose

This study examined the effects of platelet-activating factor (PAF) on the gastric microcirculation. We measured changes in vascular resistance and filtration during intra-arterial infusion of graded doses of PAF and its metabolite, lyso-PAF, to an ex vivo gastric segment of alpha-chloralose-anesthetized dogs. PAF produced dose-related sustained increases in vascular resistance (2-150 nM; n = 6). Filtration and venous hematocrit were also both significantly increased by PAF. In contrast, there were no statistically significant changes in these measurements with lyso-PAF (n = 6). Filtration and venous hematocrit were not significantly changed by norepinephrine at doses that increased perfusion pressure to the same degree as PAF (n = 4). PAF also increased filtration in the absence of changes in perfusion pressure (during maximal vasodilation induced with papaverine). Finally, removal of leukocytes from gastric arterial blood significantly attenuated these responses to PAF. Our results suggest that PAF-induced mucosal ischemia is primarily due to vasoconstriction and may involve edema formation due to increased filtration as well. In addition, these responses to PAF appear to be largely dependent on circulating leukocytes.

Effect of oxygen on blood flow autoregulation in cat sartorius muscle

1981 ◽  
Vol 241 (6) ◽  
pp. H807-H815 ◽  
Author(s):  
S. M. Sullivan ◽  
P. C. Johnson
Keyword(s):  
Blood Flow ◽  
Perfusion Pressure ◽  
Important Determinant ◽  
Flow Regulation ◽  
Sartorius Muscle ◽  
Gas Mixture ◽  
Pressure Reduction ◽  
Effect Of Oxygen ◽  
Arteriolar Diameter

To assess the role of O2 in blood flow autoregulation, arteriolar diameter and erythrocyte velocity were measured in individual microvessels of the cat sartorius muscle while ambient O2 tension (PO2) and perfusion pressure were altered. The muscle surface was covered with a layer of silicone fluid equilibrated with a gas mixture containing 0—20% O2. Under control conditions (0% O2) all except the largest arterioles dilated with pressure reduction, and all showed significant blood flow autoregulation. Elevated PO2 diminished flow regulation and dilation in large and small arterioles when arterial pressure was reduced. This effect was generally more pronounced in the small arterioles where elevated PO2 caused complete cessation of blood flow. Complete blood flow stoppage was not routinely seen in larger vessels and may reflect the fact that these vessels also supply deeper tissue regions less affected by the change in ambient PO2. Our results indicate that the PO2 level of the tissue may be an important determinant in blood flow autoregulation.

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