Arteriolar responses to elevation of venous and arterial pressures in cat mesentery

1983 ◽  
Vol 245 (5) ◽  
pp. H796-H807 ◽  
Author(s):  
M. E. Burrows ◽  
P. C. Johnson
Keyword(s):  
Volume Flow ◽  
Myogenic Response ◽  
Wall Tension ◽  
Local Regulation ◽  
Pressure Elevation ◽  
Cell Velocity ◽  
Red Blood Cell Velocity ◽  
Flow Dependency ◽  
Arteriolar Diameter ◽  
Intravascular Pressure

These studies were undertaken to determine the importance of metabolic (flow-dependent) and myogenic (pressure-dependent) factors in the response of arterioles to changes in intravascular pressure. The response of 26 arterioles in the isolated cat mesentery to increased venous and arterial pressure was studied by measuring changes of arteriolar diameter, red blood cell velocity, and intravascular pressure. Circumferential wall tension and volume flow in the arterioles were calculated. The fraction of the arteriolar responses to intravascular pressure elevation that could be attributed only to a myogenic response in which wall tension is regulated varied from 20 to 56%, depending on the method of pressure elevation. The largest fraction of the response attributable to a myogenic mechanism (ignoring the contributions of flow) varied from 50 to 93%. The fraction of the responses attributable only to flow dependency varied from 0 to 23%, whereas the largest fraction attributable to this mechanism varied from 18 to 73%, depending on the method of pressure elevation. It is concluded that, in cat mesentery, both metabolic and myogenic mechanisms appear to contribute to local regulation of flow with elevation of intravascular pressure, but other factors cannot be excluded.

Diameter, wall tension, and flow in mesenteric arterioles during autoregulation

1981 ◽  
Vol 241 (6) ◽  
pp. H829-H837 ◽  
Author(s):  
M. E. Burrows ◽  
P. C. Johnson
Keyword(s):  
Arterial Pressure ◽  
Average Diameter ◽  
Vessel Diameter ◽  
Flow Regulation ◽  
Blood Velocity ◽  
Volume Flow ◽  
Wall Tension ◽  
Pressure Data ◽  
Dependent Mechanism ◽  
Intravascular Pressure

The effect of arterial pressure on vessel diameter, blood velocity, and intravascular pressure was examined in cat mesenteric arterioles in the arterial pressure range of 120—40 mmHg. Circumferential wall tension and volume flow in individual vessels were calculated. Twenty-nine arterioles with an average diameter of 25.1 micrometers were studied. Twenty-six reactive vessels dilated by an average of 6.5 micrometers with arterial pressure reduction, whereas three nonreactive arterioles narrowed by an average of 5.9 micrometers. When pressure was reduced, circumferential wall tension in reactive arterioles tended to be maintained, whereas in nonreactive vessels tension decreased more than pressure. Data from 25 of 26 reactive arterioles were consistent with the hypothesis that regulation of wall tension accounts for the autoregulatory response; however, in 18 of these vessels a flow-dependent mechanism could also account for the response. Thus the hypothesis that wall tension is a controlled variable responsible for autoregulation is supported, but an important role for flow regulation in local control is also supported.

Contribution of hyperosmolality to glucose-induced intestinal hyperemia

1985 ◽  
Vol 248 (5) ◽  
pp. G521-G525 ◽  
Author(s):  
K. G. Proctor
Keyword(s):  
Blood Flow ◽  
Time Course ◽  
Glucose Absorption ◽  
Intestinal Tissue ◽  
Bicarbonate Buffer ◽  
Cell Velocity ◽  
Red Blood Cell Velocity ◽  
Tissue Osmolality ◽  
Arteriolar Diameter ◽  
Related Increase

To test the hypothesis that changes in tissue osmolality participate in glucose-induced absorptive hyperemia, the mucosa of the rat jejunum was suffused with isotonic or hypertonic glucose solutions. Blood flow was calculated from the product of a constant, arteriolar diameter, and red blood cell velocity, which were measured in the submucosal microcirculation. Isotonic glucose solutions (293 +/- 2 mosmol/kg) were prepared by diluting 5, 10, or 20 ml of 5% glucose, which is isotonic with plasma, to 100 ml with Ringer-bicarbonate buffer to concentrations of 250, 500, and 1,000 mg/100 ml. Glucose was added directly to Ringer-bicarbonate buffer to increase osmolality. The osmolalities of the 250, 500, and 1,000 mg/100 ml hypertonic solutions were 305 +/- 3,319 +/- 3, and 353 +/- 1 mosmol/kg, respectively. Glucose caused a concentration-related increase in estimated submucosal arteriolar blood flow that averaged 18-21% (n = 14), 24-27% (n = 14), and 34-45% (n = 14) at 250, 500, and 1,000 mg/100 ml glucose, respectively. There was no effect of solution osmolality on either the time course or the magnitude of the hyperemia at a given glucose concentration. Whereas the magnitude of the glucose-induced hyperemia averaged less than 50%, the application of 10(-2) M adenosine caused a fivefold increase in calculated blood flow (492 +/- 67%, n = 24). Thus, glucose caused relatively small increases in intestinal blood flow. If changes in luminal osmolality caused changes in intestinal tissue osmolality, then it is unlikely that hyperosmolality participates in the functional hyperemia associated with glucose absorption.

Relationship between microvascular blood velocity and pressure distribution

1977 ◽  
Vol 232 (4) ◽  
pp. H400-H405 ◽  
Author(s):  
H. N. Mayrovitz ◽  
R. F. Tuma ◽  
M. P. Wiedeman
Keyword(s):  
Blood Pressure ◽  
Shear Rate ◽  
Pressure Distribution ◽  
Blood Velocity ◽  
Volume Flow ◽  
Myotis Lucifugus ◽  
Velocity Shear ◽  
Cell Velocity ◽  
Red Blood Cell Velocity ◽  
Good Agreement

Red blood cell velocity and diameter were measured in vessels of the wing of the unanesthetized bat (Myotis lucifugus) from the supplying artery to the capillaries. These data were used to determine the manner in which velocity, shear rate, volume flow, and blood pressure depend on the vessel's hierarchical position within the vascular network. The results show that velocity decreases in an almost linear fashion as the capillary is approached but that the shear rate increases as one progresses distally from the supplying artery. Blood volume flow was found to decrease as an exponential function of the branching order. Comparison with available date in some animal species, including man, indicates some agreement in capillary velocity, although significantly lower values have been reported in some preparations. Using a method whereby blood pressure distribution could be obtained from anatomical data and center-line blood velocity, the rheologic alterations accompanying consecutive vessel branching were deduced and found to be in good agreement with data available in the literature.

Venular-arteriolar diffusion of adenosine in hamster cremaster microcirculation

1990 ◽  
Vol 258 (6) ◽  
pp. H1918-H1924 ◽  
Author(s):  
R. L. Hester
Keyword(s):  
Blood Flow ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Cell Velocity ◽  
Red Blood Cell Velocity ◽  
A Site ◽  
Arteriolar Diameter ◽  
Rule Out

During increases in blood flow, both the terminal and the proximal arterioles dilate. The mechanism behind the dilation of the proximal arterioles is not known but may be the result of the diffusion of a vasoactive metabolite from adjacent venules. To determine whether an increase in venous adenosine (ADO) concentration could affect an adjacent arteriole, venules were perfused using a micropipette containing 10(-7)-10(-4) M ADO. During the venular perfusion, arteriolar diameter and red blood cell velocity were measured at a site 0.5 to 6 mm from the micropipette tip. The adjacent arteriole of the venular arteriolar pair dilated 29 +/- 3% with a 5-s 10(-4) M ADO perfusion, 32 +/- 4% with a 10-s 10(-4) M ADO perfusion, and 85 +/- 22% with a 60-s 10(-4) M ADO perfusion. One and 2-min perfusions with 10(-5) M ADO resulted in a 36 +/- 6% and 33 +/- 4% increase in diameter of the paired arteriole, respectively. The red blood cell velocity responses were variable, yet, on average, calculated blood flow increased in each group of experiments. Venular perfusions with saline resulted in a 2% change in arteriolar diameter. To rule out nondiffusional effects, venular perfusions were performed when the arteriole was not paired with the venule but crossed the venule. Venular perfusion with 10(-6) and 10(-7) M ADO resulted in a significant increase in diameter of the crossing arteriole of 19 +/- 3% and 6 +/- 2%, respectively. Therefore, the diffusion of a vasoactive metabolite from a venule to an arteriole may provide a mechanism by which the tissue can send a signal to cause a dilation of the more proximal arterioles.

Capillary and arteriolar responses to local vasodilators are impaired in a rat model of sepsis

1998 ◽  
Vol 84 (3) ◽  
pp. 837-844 ◽  
Author(s):  
Karel Tyml ◽  
Jingcheng Yu ◽  
David G. McCormack
Keyword(s):  
Vascular Function ◽  
Vascular Reactivity ◽  
Control Level ◽  
Cecal Ligation ◽  
Cell Velocity ◽  
Longus Muscle ◽  
Significant Difference ◽  
Red Blood Cell Velocity ◽  
Arteriolar Diameter

Although sepsis is known to affect vascular function, little is known about changes at the capillary level. We hypothesized that sepsis attenuates the “upstream” arteriolar response to vasoactive agents applied locally to capillaries. Sepsis in rats was induced by cecal ligation and perforation. After 24 h, extensor digitorum longus muscle was prepared for intravital microscopy. Phenylephrine (PE, 10 mM) and acetylcholine (ACh, 10 mM) were applied iontophoretically on terminal arterioles and on their downstream daughter capillaries (300 μm from arteriole). There was no significant difference between control and septic rats in baseline arteriolar diameters [8.0 ± 0.6 vs. 9.8 ± 0.8 (SE) μm] or baseline red blood cell velocity ( V RBC) in perfused daughter capillaries (255 ± 10 vs. 264 ± 13 μm/s). Application of PE onto arterioles resulted in comparable constrictions (i.e., −22% diameter change) and V RBC reductions (−100%) in control and septic rats. In contrast, arteriolar diameter and V RBCincreases after application of ACh were attenuated in sepsis (diameter: from 41 to 14%; V RBC: from 67 to 24%). Application of PE onto the capillary reduced V RBC to the same level (−100%) in both groups, whereas application of ACh increased V RBCless in septic than in control rats (20 vs. 73%). On the basis of arteriolar-capillary pair stimulations, sepsis affected V RBC responses to ACh more in the capillary than in the arteriole. When the adenosine analog 5′- N-ethylcarboxamidoadenosine (0.1 mM) was used instead of ACh, similar effects of sepsis were seen. To test for a possible involvement of inducible NO synthase (iNOS) in sepsis-induced attenuated ACh responses, arterioles and capillaries in septic animals were locally pretreated with the iNOS blocker aminoguanidine (10 mM). In both microvessels, aminoguanidine restored the ACh response to the control level. We conclude that impaired capillary V RBCand arteriolar diameter responses to vasodilators applied to capillaries in septic rat skeletal muscle were due to dysfunction at arteriolar and capillary levels. The study underscores the significant role iNOS/NO may play in sepsis-induced alteration of vascular reactivity in vivo.

Microcirculatory responses in cat sartorius muscle to hemorrhagic hypotension

1989 ◽  
Vol 257 (5) ◽  
pp. H1647-H1655 ◽  
Author(s):  
I. P. Torres Filho ◽  
M. A. Boegehold ◽  
E. Bouskela ◽  
S. D. House ◽  
P. C. Johnson
Keyword(s):  
Blood Cell ◽  
Vascular Resistance ◽  
Red Blood Cell ◽  
Volume Flow ◽  
Sartorius Muscle ◽  
Hemorrhagic Hypotension ◽  
Cell Velocity ◽  
Calculated Volume ◽  
Red Blood Cell Velocity

The purpose of this study was to examine changes in the microcirculation that might explain the rise in vascular resistance during hemorrhagic hypotension. Diameter and red blood cell velocity of microcirculatory vessels in exteriorized cat sartorius muscles were studied during 4 h of hemorrhagic hypotension at 60 mmHg. During hypotension, vascular resistance of the muscles rose approximately 70% while calculated volume flow in arterioles and venules fell to about the same degree. Average red blood cell velocity for all capillaries showed a comparable decline. Red blood cell flow stopped in approximately 60% of capillaries, but the extent of stoppage varied greatly among capillary fields. Arterioles larger than 45 microns constricted 9-29%, with the largest arterioles showing the greatest constriction. Arterioles smaller than 45 microns dilated 34-56%, with the smallest arterioles showing the greatest dilation. Venular diameter did not change with hemorrhage. The predominance of arteriolar dilation, especially in the later stages of hypotension, should lead to a fall in vascular resistance of the muscle. This effect may be offset by constriction of arteries outside the microcirculatory field observed and blockage of capillaries or venules by formed elements.

Activation of brain adenosine receptors evokes vasodilation in skin arterioles

1991 ◽  
Vol 261 (2) ◽  
pp. H457-H462 ◽  
Author(s):  
K. G. Proctor ◽  
I. Stojanov ◽  
S. L. Bealer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Depressor Response ◽  
Arterial Blood ◽  
Cell Velocity ◽  
Red Blood Cell Velocity ◽  
Cutaneous Perfusion ◽  
Arteriolar Diameter

Metabolically stable adenosine (ADO) agonists were infused into cannulas chronically implanted in the lateral cerebral ventricle intracerebroventricularly (icv) while responses in skin microcirculation of pentobarbital-anesthetized hamsters were observed with intravital microscopy. Cyclohexyladenosine (CHA; A1-receptor selective; 0.0001-1 pmol) and N-ethylcarboxoamidoadenosine (NECA; A2-receptor selective; 0.01-0.05 pmol) were delivered in 10 microliters of bicarbonate-buffered Ringer vehicle. Mean systemic arterial blood pressure, heart rate, skin arteriolar diameter, and red blood cell velocity were continuously monitored. Blood flow was calculated from measurements of arteriolar diameter (20-40 microns) and red blood cell velocity. CHA icv caused dose-related decreases in blood pressure and heart rate, as well as increases in cutaneous perfusion. Comparable amounts of CHA administered intravenously evoked no response. Pretreatment with an A1-selective antagonist xanthine amine congener (XAC, 5 pmol icv or 1 mg/kg iv) had no effect on the depressor response but antagonized the bradycardia. In contrast, a nonselective antagonist 8-phenyltheophylline (8pTHEO, 5 pmol icv or 0.3 mg/kg iv) had no effect on the bradycardia but attenuated the depressor response. By either route, both antagonists prevented the cutaneous microcirculatory responses evoked by icv CHA. NECA icv produced hypotension but no change in the skin, and the depressor response was not altered by icv XAC. These observations provide direct evidence that chemical stimulation of central nervous system (CNS) ADO receptors is linked to a cutaneous vascular response that can be dissociated from other cardiorespiratory depressant actions of CNS ADO.

Coronary artery myogenic response in a genetic model of hypertrophic cardiomyopathy

2002 ◽  
Vol 283 (6) ◽  
pp. H2244-H2249 ◽  
Author(s):  
Henrik H. Petersen ◽  
Jonathan Choy ◽  
Brian Stauffer ◽  
Farzad Moien-Afshari ◽  
Christian Aalkjaer ◽  
...  
Keyword(s):  
Transgenic Mouse ◽  
Genetic Model ◽  
Morphological Characteristics ◽  
Myogenic Tone ◽  
Chain Gene ◽  
Myogenic Response ◽  
Cardiac Phenotype ◽  
First Time ◽  
Pressure Myograph ◽  
Intravascular Pressure

Hypertrophic cardiac myopathy (HCM) is the leading cause of mortality in young athletes. Abnormalities in small intramural coronary arteries have been observed at autopsy in such subjects. The walls of these intramural vessels, especially in the ventricular septum, are thickened, and the lumen frequently appears narrowed. Whether these morphological characteristics have functional correlates is unknown. We studied coronary myogenic tone in a transgenic mouse model of HCM that has mutations in the cardiac α-myosin heavy chain gene. This transgenic mouse has a cardiac phenotype that resembles that occurring in humans. We examined the possible vascular contributions to the pathology of HCM. Septal arteries from 3- and 11-mo-old wild-type (WT) and transgenic (TG) mice were studied on a pressure myograph. The myogenic response to increased intravascular pressure in older animals was significantly reduced [maximal constriction: 32 ± 4% (TG) and 46 ± 4% (WT), P < 0.05]. After inhibition of endothelin receptors with bosentan, both WT and TG mice had similar increases in myogenic constriction. The sensitivity to exogenous endothelin was significantly reduced in TG mice, suggesting that the reduced myogenic constriction in HCM was due to reduced receptor sensitivity. In conclusion, we show for the first time that 1) myogenic tone in the coronary septal artery of the mouse is regulated by a basal release of endothelin, and 2) pressure-induced myogenic activation is attenuated in HCM, possibly consequent to a reduction in endothelin responsiveness. The associated reduction in coronary vasodilatory reserve may increase susceptibility to ischemia and arrhythmias.

Characteristics and origin of myogenic response in isolated gracilis muscle arterioles

1994 ◽  
Vol 266 (3) ◽  
pp. H1177-H1183 ◽  
Author(s):  
D. Sun ◽  
G. Kaley ◽  
A. Koller
Keyword(s):  
Pressure Range ◽  
Perfusion Pressure ◽  
Gracilis Muscle ◽  
Tetraacetic Acid ◽  
Flow Conditions ◽  
Third Order ◽  
Before And After ◽  
Physiological Pressure ◽  
Arteriolar Diameter ◽  
Intravascular Pressure

Responses to changes in intravascular pressure of isolated rat gracilis muscle arterioles were investigated under no-flow conditions. First-, second-, and third- order arterioles were isolated and cannulated. Vascular diameters were measured with an image-shearing device and then recorded. In response to the step increases in perfusion pressure (from 20 to 160 mmHg, by 10- or 20-mmHg steps) arterioles constricted and developed active tone. For example, at 100, 80, and 50 mmHg pressure the steady-state active diameters of 1st-, 2nd-, and 3rd-order arterioles were 76.9 +/- 1.6, 32.3 +/- 1.1 and 22.3 +/- 3.2 microns, respectively. At the same perfusion pressure, by use of a Ca(2+)-free solution (ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid; 1 mM) containing sodium nitroprusside (SNP; 10(-4) M), the passive diameters (PD) of these vessels were 161.8 +/- 3.2, 76.0 +/- 1.7, and 47.6 +/- 2.2 microns. The negative slopes of the pressure-diameter curves indicate that in the physiological pressure range an inverse relationship exists between the arteriolar diameter and intravascular pressure. The maximum constriction expressed as a percent of PD was similar in the various sized arterioles (approximately 60%) but was reached at lower pressures in the smaller vessels. The vasoactive function of endothelium and vascular smooth muscle was assessed by the responses of arterioles to acetylcholine (ACh; 10(-6) M) and SNP (5 x 10(-8) M) before and after removal of the endothelium with air. After removal of the endothelium, dilation to ACh was abolished while dilation to SNP was retained.(ABSTRACT TRUNCATED AT 250 WORDS)

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