Modulation of bat wing venule contraction by transmural pressure changes

1992 ◽  
Vol 262 (3) ◽  
pp. H625-H634 ◽  
Author(s):  
M. J. Davis ◽  
X. Shi ◽  
P. J. Sikes

We tested the hypothesis that the frequency and amplitude of spontaneous venular contractions in the bat wing could be modulated by changes in transmural pressure. In one series of experiments, venous pressure in the wing was elevated by pressurizing a box containing the body of the animal while the wing was exposed to atmospheric pressure. During this time, venular diameters were continuously recorded using intravital microscopic techniques while venular pressures were measured through servo-null micropipettes. In another series of experiments, single venular segments were dissected from the wing, cannulated, and pressurized in vitro. The results from both experimental protocols were qualitatively similar; alterations in venous pressure over a narrow range (+/- 5 cmH2O from control) produced substantial changes in contraction frequency and amplitude. The product of frequency and cross-sectional area was maximal over the venous pressure range between 10 and 15 cmH2O. Venules demonstrated a rate-sensitive component in their reaction to rapid pressure changes, because contraction bursts occurred immediately after positive pressure steps and quiescent periods often occurred after negative pressure steps. We conclude that venular vasomotion in the bat wing is modulated by intraluminal pressure and involves a bidirectional, rate-sensitive mechanism. In addition, comparisons with arteriolar vasomotion studies suggest that venules are more sensitive to luminal pressure changes than arterioles.

1989 ◽  
Vol 256 (1) ◽  
pp. H32-H40 ◽  
Author(s):  
M. J. Davis ◽  
P. J. Sikes

The responses of three sequential branching orders of arterioles in the bat wing to rapid and slow changes in transmural pressure were studied. Arterial and venous pressures to the wing were elevated simultaneously by pressurizing a box containing the body of the animal, while the wing was exposed to atmospheric pressure. Box pressure was elevated from 0 to +48 mmHg at two rates: 24 and 0.6 mmHg/s. During this time, continuous recordings of hydrostatic pressure and diameter were made in single arterioles using intravital microscopic techniques. Second-order arterioles and arcuate arterioles from skin and skeletal muscle constricted in response to elevated transmural pressure but did not show an enhanced response to rapid pressure changes. There was a trend for terminal arterioles to show a transient peak constriction during rapid stretch, but this response was always associated with a biphasic change in arteriolar pressure. These results suggest that the transient arteriolar resistance changes associated with rapid transmural pressure increases in previous experiments may be primarily a result of transient pressure changes in small arterioles. We find no evidence that arterioles in this preparation exhibit a rate-sensitive component to their myogenic response.


1967 ◽  
Vol 22 (6) ◽  
pp. 1053-1060 ◽  
Author(s):  
Maylene Wong ◽  
Edgardo E. Escobar ◽  
Gilberto Martinez ◽  
John Butler ◽  
Elliot Rapaport

We measured the end-diastolic volume (EDV) and stroke volume (SV) in the right ventricle of anesthetized dogs during continuous pressure breathing and compared them to measurements taken during breathing at atmospheric pressure. During intratracheal positive-pressure breathing, EDV, and SV decreased and end-diastolic pressure became more positive relative to atmospheric pressure. During intratracheal negative-pressure breathing, EDV enlarged and SV tended to increase; end-diastolic pressure became more negative. During extrathoracic negative-pressure breathing SV decreased, EDV fell, though not significantly, and end-diastolic pressure rose, but insignificantly. Changes in EDV observed during intratracheal positive-pressure breathing and intratracheal negative-pressure breathing were associated with minor shifts in transmural pressure (end-diastolic pressure minus intrapleural pressure) in the expected directions, but during extrathoracic negative-pressure breathing a large increase in transmural pressure took place with the nonsignificant reduction in EDV. We believe that intrathoracic pressure influences right ventricular filling by changing the peripheral-to-central venous pressure gradient. The cause of the alteration in diastolic ventricular distensibility demonstrated during extra-thoracic negative-pressure breathing remains unexplained. positive-pressure breathing; negative-pressure breathing; extrathoracic negative-pressure breathing Submitted on August 16, 1966


2002 ◽  
Vol 93 (6) ◽  
pp. 2137-2146 ◽  
Author(s):  
Mary E. J. Lott ◽  
Michael D. Herr ◽  
Lawrence I. Sinoway

The effects of changes in transmural pressure on brachial artery mean blood velocity (MBV) were examined in humans. Transmural pressure was altered by using a specially designed pressure tank that raised or lowered forearm pressure by 50 mmHg within 0.2 s. Brachial MBV was measured with Doppler directly above the site of forearm pressure change. Pressure changes were evoked during resting conditions and after a 5-s handgrip contraction at 25% maximal voluntary contraction. The handgrip protocol selected was sufficiently vigorous to limit flow and sufficiently brief to prevent autonomic engagement. Changes in transmural pressure evoked directionally similar changes in MBV within 2 s. This was followed by large and rapid adjustments [−2.14 ± 0.24 cm/s (vasoconstriction) during negative pressure and +2.14 ± 0.45 cm/s (vasodilatation) during positive pressure]. These adjustments served to return MBV to resting levels. This regulatory influence remained operative after 5-s static handgrip contractions. Of note, changes in transmural pressure were capable of altering the timing of the peak MBV response (5 ± 0, 2 ± 0, 6 ± 1 s ambient, negative, and positive pressure, respectively) as well as the speed of MBV adjustment (−2.03 ± 0.18, −2.48 ± 0.15, −0.84 ± 0.19 cm · s−1 · s−1ambient, negative, and positive pressure, respectively) after handgrip contractions. Vascular responses, seen with changes in transmural pressure, provide evidence that the myogenic response is normally operative in the limb circulation of humans.


2001 ◽  
Vol 115 (5) ◽  
pp. 359-362 ◽  
Author(s):  
R. P. Mills ◽  
Z. G. Wang ◽  
E. W. Abel

We have developed a prototype middle-ear hearing implant which uses a multilayer piezoelectric actuator. In this series of experiments the actuator was attached to the medial wall of the attic so that it makes contact with the body of the incus. Initial in vitro evaluation has been carried out using a laser vibrometer (Polytec CLV) to measure stapes velocity. Stapes displacement is calculated by mathematical integration. The device used in this way is particularly effective at transmitting high frequency sound to the stapes. When switched off the actuator impairs the transmission of sound to the ossicular chain at low frequencies, but this effect is only 7 dB at most. The stapes displacements resulting from the action of the implant have a linear relationship with the voltages used to drive the system. The high capacitance of the present actuator means that its power requirements are higher than that of other comparable devices. An optimal method of coupling the device to the incus has yet to be identified.


2013 ◽  
Vol 16 (4) ◽  
pp. 49
Author(s):  
Allan Kenji Masuda ◽  
Mayra Fidelis Zamboni Quitero ◽  
Luciana Cardoso Espejo-Trung ◽  
Maria Aparecida Alves Cerqueira Luz

<p><strong>Objective: </strong>Early carious lesions in bovine and humanenamel developed in vitro using a pH cycling regimenwere compared. <strong>Material and Methods: </strong>Fifteencentral bovine incisors and fifteen recently extractedhuman third molars were randomly divided into twogroups: ten for the cross-sectional microhardness test(MT) and five for polarized light microscopy (PLM)analysis. Enamel blocks measuring 5 x 5 mm weremade from the buccal face of the teeth. The blocksused for the MT were sliced into two halves: “A” and“B”. “A” slices were embedded in acrylic resin, withthe face of the dentin-enamel junction left exposedfor the MT prior to pH cycling. “B” slices and wholeblocks were coated with acid-resistant varnish,except a 3 x 3 mm central window, and submitted tothe pH cycling regimen (demineralizing solution for3 h and remineralizing solution for 21 h) over fiveconsecutive days. The “B” slices were then submittedto the MT and the whole blocks were processed forthe PLM study. <strong>Results: </strong>The PLM analysis revealedshallow, extensive lesions in the bovine enamel,hardly showing the superficial, dark and translucentzones, as well as deep cavity lesions in the humanenamel, with the body of the lesion and the darkzone evident. The MT revealed a significant decreasein microhardness in the superficial levels of thebovine enamel caries and at all depth levels of thehuman enamel caries. <strong>Conclusion: </strong>The pH cyclingregimen adopted led to the development of deeperand more demineralized carious lesions in humanenamel than bovine enamel</p><p>Keywords<br />Dental caries; Dental enamel; Microhardness tests; Polarization microscopy.</p>


1993 ◽  
Vol 264 (4) ◽  
pp. H1174-H1186 ◽  
Author(s):  
M. J. Davis

The hypothesis that spontaneous contractions of bat wing venules could be modulated by luminal flow was tested. Single venules (114 +/- 5 microns diam) from the wings of anesthetized pallid bats were dissected, cannulated, and pressurized in vitro. A dual reservoir system was used to independently control luminal pressure and flow. In the absence of flow, and with pressure set to 10 cmH2O, all venules contracted spontaneously at rates between 20 and 40 cycles/min. Pressure elevation over the range of 3-10 cmH2O caused a rapid increase in contraction frequency and decrease in amplitude; pressure reduction caused a rapid decrease in contraction frequency and increase in amplitude. In contrast, initiation of flow resulted in a delayed and gradual reduction of contraction amplitude and/or frequency (sometimes to zero). The net effect of flow was to increase mean diameter and decrease the product of frequency x cross-sectional area. Flow-induced inhibition of venular contraction was eliminated by endothelial denudation but persisted in the presence of NG-monomethyl-L-arginine (10(-4) M) or indomethacin (10(-5) M) in concentrations that blocked the effects of exogenously applied ATP or arachidonic acid, respectively. The flow-induced venular response also persisted in the presence of superoxide dismutase (55 U/ml). Denuded venules responded to flow when placed downstream (i.e., perfused in series) from venules with intact endothelium. These results indicate that luminal flow can modulate the contractile function of bat wing venules via release of a transferable substance from the endothelium. The exact nature of the substance is not yet known but it does not appear to be classical endothelium-derived relaxing factor, a prostaglandin, or an oxygen radical.


1988 ◽  
Vol 255 (6) ◽  
pp. H1558-H1562 ◽  
Author(s):  
L. Kuo ◽  
M. J. Davis ◽  
W. M. Chilian

The goal of this study was to examine myogenic responses of isolated porcine subepicardial and subendocardial arterioles (80–100 micron in diameter) within physiological ranges of intraluminal pressure. Arterioles were located by perfusion with india ink-gelatin solution then dissected and cannulated with glass micropipettes. Intraluminal pressure was altered in 20-cmH2O steps over the range of 20–140 cmH2O. IN physiological salt solution (36–37 degrees C), the coronary arterioles developed spontaneous tone and exhibited myogenic responses. At the lower pressures (20–60 cmH2O), subendocardial arterioles responded passively (diameter decreased from a control diameter at 60 cmH2O), whereas subepicardial arterioles maintained their diameters. At higher pressures (100–140 cmH2O), both subepicardial and subendocardial arterioles demonstrated myogenic constriction, but subepicardial arterioles demonstrated greater myogenic constriction than subendocardial arterioles. This implies that myogenic autoregulation in subepicardial arterioles is better than that in the subendocardial arterioles at both low and high pressures. In the presence of nitroprusside (10(-4) M), all arterioles responded to pressure changes passively, and there were no differences between subepicardial and subendocardial vessels. The functional integrity of the endothelium was verified by relaxation to substance P (10(-7) M). This is the first in vitro study to demonstrate coronary myogenic activity and transmural differences in these arteriolar responses. Our data support the concept that myogenic mechanisms in 80 to 100-micron arterioles may actively contribute to autoregulation of coronary blood flow.


1990 ◽  
Vol 68 (6) ◽  
pp. 2581-2587 ◽  
Author(s):  
J. C. Leiter ◽  
J. A. Daubenspeck

In anesthetized or decerebrate animals, negative pressure applied to the upper airway selectively activates the hypoglossal nerve compared with the phrenic nerve. Conversely, positive pressure reduces hypoglossal nerve activity out of proportion to any change in the phrenic neurogram. We have tested the hypothesis that analogous pressure changes applied to awake humans would selectively inhibit or activate genioglossal electromyographic (EMGge) activity relative to diaphragmatic electromyographic activity (EMGdi). We studied seven normal subjects in a head-out body plethysmograph. Pressure at the mouth was either atmospheric, +10 cmH2O, or -10 cmH2O, and lung volume was held constant by applying an identical pressure to the body surface. Thus the transmural pressure distorting the respiratory system was applied only to the upper airway. Subjects breathed CO2-enriched (2-3%) room air to stimulate phasic respiratory EMGge activity. We found that -10 cmH2O pressure applied selectively to the upper airway resulted in a 49% enhancement of peak-integrated EMGge activity, but EMGdi activity remained at control levels. Positive pressure did not result in any changes in EMGge or EMGdi activity. Neither pressure resulted in significant changes in the magnitude or pattern of ventilation. We conclude that reflex mechanisms maintaining upper airway patency are demonstrable in awake humans and probably have an important role in moment-to-moment modulation of upper airway muscle activity in normal awake humans.


1993 ◽  
Vol 265 (6) ◽  
pp. H1847-H1855 ◽  
Author(s):  
J. C. Falcone ◽  
H. J. Granger ◽  
G. A. Meininger

The purpose of this study was to determine whether the vascular myogenic response is enhanced in hypertension. Experiments were conducted in the intact cremaster muscle microcirculation as well as in isolated arterioles of hypertensive (SHR) and normotensive (WKY) rats. Increasing venous pressure in vivo by approximately 5 mmHg had no effect on normotensive first- (1A) or third-order arteriolar (3A) diameters; in contrast, hypertensive 1A diameter decreased 4% (89 +/- 2 to 85 +/- 3 microns) with an 8% decrease in 3A (24 +/- 2 to 22 +/- 2 microns). To further examine this enhanced constriction to elevated intravascular pressure in SHR, diameter was monitored in isolated 1A during step increases and decreases in intraluminal pressure. Normotensive arterioles displayed myogenic responses between pressures of 50 and 170 cmH2O; in contrast, hypertensive arterioles demonstrated myogenic responses over an extended pressure range (50–210 cmH2O). In addition, the change in diameter for each step change in pressure was greater in the arterioles from SHR, indicating an increased myogenic responsiveness. The myogenic reactions were unaffected by alpha-receptor blockade with phentolamine (10(-6) M), indicating that adrenergic hypersensitivity was not involved in the enhanced response to stretch. Morphometric analysis of the vascular wall revealed no differences in wall thickness, cross-sectional wall area, or wall-to-lumen ratio between normotensive and hypertensive rats. The length-tension relationships for normotensive and hypertensive rats demonstrated that peak active tension occurred at nearly the same vascular smooth muscle length. In addition, SHR arterioles were capable of maintaining higher levels of active tension that WKY arterioles, indicating an altered length-tension curve in chronic arterial hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)


Blood ◽  
1984 ◽  
Vol 63 (2) ◽  
pp. 335-341
Author(s):  
CA Hall ◽  
JA Begley ◽  
PD Green-Colligan

Hydroxocobalamin (OH-Cbl), when used to treat vitamin B12 deficiency, is better retained by the body than is cyanocobalamin (CN-Cbl), but the availability to cells has not been studied systematically. In a series of experiments, we compared the uptake and internalization of OH-Cbl and CN-Cbl bound to transcobalamin II (TCII) by a human cell model, the HeLa cell. TCII-OH-Cbl was: (1) taken up in larger amounts per unit time, (2) the greater uptake was not a consequence of more effective attachment to receptors of TCII-Cbl nor to a more rapid regeneration of receptors, (3) the difference was expressed during the phase of internalization of TCII-Cbl, (4) with CN-Cbl, the stages of binding to receptors plus internalization were more readily reversed, and (5) larger amounts of OH-Cbl were internalized and converted to active coenzyme forms of Cbl. When injected into a healthy person, 200 micrograms of OH-Cbl was better retained in the circulation than 200 micrograms of CN-Cbl. When added in vitro in equivalent amounts, more OH-Cbl was bound to nonspecific plasma proteins. This greater and broader binding neither enhanced nor interfered with the uptake of Cbl by cells, which was determined by the amount of Cbl bound physiologically to TCII. It was concluded that OH-Cbl is a more efficient form of treatment of the common types of Cbl deficiency, principally because of the better retention, which requires less frequent injections, but also because of greater availability to cells.


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