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PubMed2005

Effect of erythrocyte aggregation at normal human levels on functional capillary density in rat spinotrapezius muscle.

Previous studies have shown that functional capillary density (FCD) is substantially reduced by erythrocyte aggregation. However, only supranormal levels of aggregability were studied. To investigate the effect of erythrocyte aggregability at the level seen in healthy humans, the FCD of selected capillary fields in rat spinotrapezius muscle was determined with high-speed video microscopy under normal (nonaggregating) conditions and after induction of erythrocyte aggregation with Dextran 500 (200 mg/kg). To examine shear rate dependence, the effect was studied both at normal and reduced arterial pressures (50 and 25 mmHg), the latter achieved by short periods of hemorrhage. In a separate study, volume flow was determined in arterioles (52.1 +/- 3.7 microm) under the same conditions. Before Dextran 500 infusion, FCD fell to 91% and 76% of control values, respectively, when arterial pressure was reduced to 50 and 25 mmHg. After Dextran 500 infusion, FCD was 96% at normal arterial pressure and fell to 79% and 37% of normal control values at 50 and 25 mmHg. All FCD values were significantly lower after dextran infusion. FCD reduction after lowering arterial pressure or dextran infusion appeared to be due to plasma skimming rather than capillary plugging. Reduction of FCD by dextran at reduced pressure was compensated by increased red blood cell flux in capillaries with red blood cell flow. We conclude that the level of aggregability seen in healthy humans is an important determinant of FCD only at reduced arterial pressure.

Animals↗
PubMed2005

Synchronous progression of calcium transient-dependent beating and sarcomere destruction in apoptotic adult cardiomyocytes.

During early apoptosis, adult cardiomyocytes show unusual beating, suggesting possible participation of abnormal Ca(2+) transients in initiation of apoptotic processes in this cell type. Simultaneously with the beating, these cells show dynamic structural alteration resulting from cytoskeletal disintegration that is quite rapid. Because of the specialized structure and extensive cytoskeleton of cardiomyocytes, we hypothesized that its degradation in so short a time would require a particularly efficient mechanism. To better understand this mechanism, we used serial video microscopy to observe beta-adrenergic stimulation-induced apoptosis in isolated adult rat cardiomyocytes while simultaneously recording intracellular Ca(2+) concentration and cell length. Trains of Ca(2+) transients and corresponding rhythmic contractions and relaxations (beating) were observed in apoptotic cells. Frequencies of Ca(2+) transients and beating gradually increased with time and were accompanied by cellular shrinkage. As the cells shrank, amplitudes of Ca(2+) transients declined and diastolic intracellular Ca(2+) concentration increased until the transients were lost. Beating and progression of apoptosis were significantly inhibited by antagonists against the L-type Ca(2+) channel (nifedipine), ryanodine receptor (ryanodine), inositol 1,4,5-trisphosphate receptor (heparin), sarco(endo)plasmic Ca(2+)-ATPase (thapsigargin), and Na(+)/Ca(2+) exchanger (KB-R7943). Electron-microscopic examination of beating cardiomyocytes revealed progressive breakdown of Z disks. Immunohistochemical analysis and Western blot confirmed that disappearance of Z disk constituent proteins (alpha-actinin, desmin, and tropomyosin) preceded degradation of other cytoskeletal proteins. It thus appears that, in adult cardiomyocyte apoptosis, Ca(2+) transients mediate apoptotic beating and efficient sarcomere destruction initiated by Z disk breakdown.

Adrenergic beta-Agonists↗
PubMed2003

A new method for assessing arteriolar diameter and hemodynamic resistance using image analysis of vessel lumen.

To characterize the nonuniform diameter response in a blood vessel after a given stimulus (e.g., arteriolar conducted response), frequent serial diameter measurements along the vessel length are required. We used an advanced image analysis algorithm (the "discrete dynamic contour") to develop a quick, reliable method for serial luminal diameter measurements along the arteriole visualized by intravital video microscopy. With the use of digitized images of the arteriole and computer graphics, the method required an operator to mark the image of the two inner edges of the arteriole at several places along the arteriolar length. The algorithm then "filled in" these marks to generate two continuous contours that "hugged" these edges. A computer routine used these contours to determine luminal diameters every 20 microm. Based on these diameters and on Poiseuille's law, the routine also estimated the hemodynamic resistance of the blood vessel. To demonstrate the usefulness of the method, we examined the character of spatial decay of KCl-induced conducted constriction along approximately 500-microm-long arteriolar segments and the KCl-induced increase in hemodynamic resistance computed for these segments. The decay was only modestly fitted by a simple exponential, and the computed increase in resistance (i.e., 5- to 70-fold) was only modestly predicted by resistance increase based on our mathematical model involving measurements at two arteriolar sites (Tyml K, Wang X, Lidington D, and Oullette Y. Am J Physiol Heart Circ Physiol 281: H1397-H1406, 2001). We conclude that our method provides quick, reliable serial diameter measurements. Because the change in hemodynamic resistance could serve as a sensitive index of conducted response, use of this index in studies of conducted response may lead to new mechanistic insights on the response.

Animals↗
PubMed1984

Effect of aminophylline on adenosine and exercise dilation of rat cremaster arterioles.

The present study was undertaken to evaluate the role that adenosine may play in exercise vasodilation. Responses of rat cremaster muscle arterioles to either topically applied adenosine or muscle exercise were recorded via video-microscopy before and after topical administration of aminophylline (10(-4) M). In all experiments, alpha-adrenergic receptors were blocked by pretreatment with phentolamine. Under control conditions the average concentration of adenosine required to produce a 50% dilation response (ED50) was 1.9 X 10(-6) M, and the full dose-response curve spanned 2 log units from threshold to near maximum responses. Topical aminophylline increased the ED50 for adenosine dilation to 9.1 X 10(-6) M. Stepwise increases in muscle twitch rate produced a progressive arteriolar dilation, and the dilation associated with 2-Hz exercise approached the maximal dilation observed with adenosine. Topical aminophylline, however, had no effect on the arteriolar dilation response to cremaster muscle exercise. It is unlikely that our results can be explained by any influence that exercise might have on the arteriolar sensitivity to adenosine or on the efficacy of aminophylline blockade because aminophylline had no effect on the arteriolar response to even the lowest rates of exercise tested. We conclude either that adenosine does not mediate exercise dilation in rat cremaster muscle or that interstitial adenosine levels during exercise in the presence of 10(-4) M aminophylline are significantly higher (5X) than during exercise without aminophylline.

Adenosine↗
PubMed1985

Differential effect of cyclooxygenase inhibitors on absorptive hyperemia.

To test whether the hydrolytic products of digestion could stimulate vasoactive prostaglandin synthesis in the intestine, the muscularis and mucosa of the rat jejunum were suffused with a bicarbonate-buffered Ringer vehicle containing cyclooxygenase inhibitors (meclofenamate or indomethacin; 3 X 10(-5) M). To evoke blood flow changes, either glucose (56 mM), oleic acid (20 or 40 mM), or sodium arachidonate was added to the mucosal vehicle. Bile salt (taurocholic acid, 10 mM) was added to emulsify oleic acid. Blood flow was calculated (BFc) in submucosal arterioles by use of video microscopy. Neither bile salt nor cyclooxygenase inhibitors altered resting BFc. Neither oleic acid concentration nor solution osmolality altered the magnitude of absorptive hyperemia. After 10 min of glucose, BFc increased 36 +/- 6% with vehicle (n = 16) and 39 +/- 8% with meclofenamate (n = 10). After 10 min of oleic acid, BFc increased 21 +/- 5% with vehicle (n = 17) and 34 +/- 6% with inhibitors (n = 17). In animals exposed twice to the same concentration of oleic acid, the paired difference between the vehicle and inhibitors (19 +/- 7%; n = 9) was significant. Arachidonate alone produced no dose-related (0.06-1.9 mM) effect on BFc (n = 41), but arachidonate (0.3 mM) combined with cyclooxygenase inhibitors (6 X 10(-5) M) produced a significant BFc increase of 35 +/- 7% (n = 6). These observations suggest that the absorption of oleic acid, but not glucose, stimulates the synthesis of a vasoactive metabolite of arachidonate. The mechanism for the differential effect of cyclooxygenase inhibitors is unknown but could involve nonprostaglandin metabolites of arachidonate, such as lipoxygenase or cytochrome P-450 products.

Animals↗
PubMed1986

Skeletal muscle vasodilation during electrical stimulation of the preoptic recess.

Transverse (3rd-order) arterioles (diam 12 +/- 2 micron, n = 6) in rat spinotrapezius muscle were observed with video microscopy during electrical stimulation of preoptic recess in periventricular region of hypothalamus (AV3V region) to test whether active skeletal muscle vasodilation was mediated by a beta-adrenergic mechanism. Bipolar wire electrodes were implanted in AV3V 3-7 days before an experiment. Continuous superfusion of propranolol (10(-5) M) caused steady-state reduction (3 +/- 1 microns) in arteriolar diameter and reduced steady-state vasodilation (26 +/- 2 vs. 11 +/- 2 microns) caused by a continuous superfusion of isoproterenol (10(-6) M). Six arterioles were observed with and without propranolol during four frequencies of AV3V stimulation (8-15 V, 0.2-0.5 ms pulse duration; 10, 15, 20, and 25 Hz; 1 min stimulus duration). Stimulation caused frequency-related reductions in arterial blood pressure (10-20 mmHg), which were sustained and not altered by propranolol. Transient peak diameters were observed after 30 +/- 7 s; the time was not related to stimulus frequency or affected by propranolol. Peak diameters averaged 14-17 microns during vehicle and 11-12 micron during propranolol (maximum diam 32 +/- 3). Peak vasodilations were significant but identical with vehicle or propranolol (avg 3 +/- 1 microns) and not related to stimulus frequency. Diameters stabilized at steady-state values above base line only during 15 and 20 Hz with vehicle and only during 20 Hz with propranolol. We conclude that AV3V stimulation causes transient vasodilation in spinotrapezius muscle that is probably not mediated by beta-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Shunting of leukocytes in rabbit tenuissimus muscle.

Leukocyte distribution was studied in 58 arterioles and capillaries constituting eight networks in the fascia adjacent to the rabbit tenuissimus muscle. Fluorescence video microscopy (acridine red) and digital image processing were used to visualize the leukocytes. Leukocyte concentration in the transverse arterioles leaving the muscle proper to irrigate the fascia was significantly elevated to 143 +/- 13% (mean +/- SE) of the systemic count. Leukocytes were found to further accumulate along the arteriolar tree, reaching 244 +/- 16% of systemic in the most remote branches. Leukocyte accumulation in the connective tissue can be calculated to lead to a decrease of leukocyte concentration in muscle capillaries to 89% of the systemic value. This shunting effect may be important in preventing leukocyte-induced capillary obstruction. At individual arteriolar bifurcations, leukocytes were found to preferentially enter the downstream branch with higher flow rate (regression coefficient 1.11 +/- 0.04, n = 100). This preferential distribution is quantitatively sufficient to account for the observed leukocyte distribution in the network.

Algorithms↗
PubMed1989

Propagation of vasomotor responses coordinates arteriolar resistances.

We tested the hypothesis that a conduction pathway intrinsic to the arteriolar wall possesses the properties necessary to coordinate vasomotor responses in the microcirculation. Acetylcholine (ACh) or norepinephrine (NE) was iontophoresed onto cheek pouch arterioles (15-35 microns diam) of pentobarbital-anesthetized hamsters, and diameter responses were observed using intravital video microscopy. ACh and NE induced vasodilation and vasoconstriction, respectively, that propagated both upstream and downstream from the site of application. Propagated vasomotor responses decayed with distance along the arterioles; this decay was characterized by mechanical length constants of 1.9 and 1.8 mm for ACh and NE, respectively. Vasodilations and vasoconstrictions initiated on daughter vessels of a branch propagated into parent arterioles that were approximately twice the diameter of the daughter vessels. Iontophoretic stimuli applied simultaneously to paired daughter vessels induced propagated responses that summed linearly in the parent vessel. We conclude that the arteriolar network functions as a highly coordinated syncytium and that diverse vasomotor stimuli can be summed and integrated within the peripheral microvasculature.

Acetylcholine↗
PubMed1989

Effects of endothelial impairment on arteriolar dilator responses in vivo.

In pentobarbital-anesthetized rats we investigated the role of the endothelium in the dilation of third-order arterioles of cremaster muscle to acetylcholine, adenosine, and sodium nitroprusside in vivo. Responses to the topical administration of these agents were measured with image shearing and recorded with video microscopy before and after light-dye (L-D) treatment of a 50- to 100-microns segment of the arteriole under study. L-D treatment consisted of intravascular administration of sodium fluorescein and the illumination of a discrete area of the arteriole under study with its excitation light from a mercury lamp. Before L-D treatment, acetylcholine (10(-7) to 10(-5) M) and adenosine (10(-6) to 10(-4) M) produced dose-dependent increases in arteriolar diameter (vasodilation). After L-D treatment of the arteriolar segment, administration of 10(-7) M acetylcholine evoked a vasoconstriction (-19% from control), and the dilator responses to 10(-6) and 10(-5) M were inhibited by 91 and 77%, respectively. In contrast, the arteriolar dilator responses to all doses of adenosine and sodium nitroprusside (2 x 10(-7) M) were not altered by this treatment. In addition, the dilator responses to acetylcholine were not changed in the nonilluminated, distal, and proximal segments of the arterioles. These findings suggest that L-D treatment selectively alters the function of the endothelium resulting in the loss of vasodilation to acetylcholine, whereas arteriolar smooth muscle function does not appear to be affected.

Acetylcholine↗
PubMed1989

Arteriolar oxygen reactivity is inhibited by leukotriene antagonists.

Experiments were performed to test the hypothesis that the arteriolar constriction produced by elevated oxygen tensions in the hamster cheek pouch is mediated by a leukotriene. To test this hypothesis, the diameter response of arterioles in superfused hamster cheek pouch preparations to stepwise increases in superfusion solution oxygen content was measured by video microscopy in the absence and 30 min after superfusion with solutions containing inhibitors of the synthesis or actions of leukotrienes. Oxygen-induced constrictions were inhibited in a dose-dependent fashion by two structurally distinct 5-lipoxygenase inhibitors (U 60257 and SC 43251) and two different leukotriene receptor antagonists (SKF 102922 and FPL 55712). Also, all four inhibitors tended to dilate the arterioles under low PO2 conditions. The inhibition of oxygen reactivity appeared to be selective in that arteriolar constrictions induced by topical application of phenylephrine were unaffected (SC 43251, SKF 102922, FPL 55717, and 30 microM U 60257) or only modestly reduced (100 microM U 60257) by the inhibitors. These data are consistent with the hypothesis that a leukotriene, or related compound, mediates arteriolar oxygen reactivity in the hamster cheek pouch.

Animals↗
PubMed1989

Endothelial impairment inhibits prostaglandin and EDRF-mediated arteriolar dilation in vivo.

The role of endothelium in the vasodilation of third order arterioles of cremaster muscle to a variety of vasoactive agents was investigated in pentobarbital-anesthetized rats. Changes in diameter to topical administration of agents were measured with image shearing, before and after mercury light/sodium fluorescein (light/dye) treatment of a 50- to 100-microns segment of the arteriole under study and were recorded with video microscopy. Before light/dye treatment, arachidonic acid (10(-5) M), prostaglandin E2 (5 x 10(-6) M), A23187 (2 x 10(-6) M), acetylcholine (10(-5) M), and adenosine (10(-4) M) elicited dilation between 75 and 106% of basal diameter. After light/dye treatment, dilations to arachidonic acid, A23187, and acetylcholine were completely eliminated; however, the responses to prostaglandin E2 and adenosine were not altered. These results indicate that light/dye treatment interferes with the production of or response to prostaglandins as well as other endothelial mediators, like endothelium-derived relaxing factor (EDRF). In a second series of experiments, bradykinin, in concentrations of 10(-9), 10(-8), and 10(-7) M elicited dose-dependent dilations, which were partially inhibited by indomethacin and completely abolished after additional light/dye treatment. Dilation of arterioles to adenosine was maintained throughout these experiments. These data suggest that vasodilation to bradykinin is mediated partly via prostaglandin production and partly via other endothelium-derived factor(s).

Acetylcholine↗
PubMed1990

Cyclooxygenase inhibition potentiates myogenic activity in skeletal muscle arterioles.

The proposition that arteriolar constriction to increased intravascular pressure is mediated through either the increased local production of an eicosanoid constrictor factor or decreased production of a dilating factor was examined. The myogenic response of arterioles was studied by enclosing anesthetized rats in an airtight Plexiglas box with the cremaster muscle exteriorized into a tissue bath containing Krebs solution. Microvascular responses were observed by video microscopy. The arteriolar response to a 20-mmHg increase in intravascular pressure was examined in the absence or presence of cyclooxygenase inhibition. In the absence of cyclooxygenase inhibition, second-order arterioles (2As) responded passively to increased pressure by distending to 107 +/- 1% of control diameter. In the presence of the indomethacin, 2As constricted to 79 +/- 5% of control. Third-order arterioles (3As) constricted to 47 +/- 8% of control without indomethacin and similarly to 33 +/- 4% with indomethacin. To test whether inhibitors of endothelium-derived relaxation factor would potentiate the myogenic response of 3As, methylene blue or gossypol was topically applied to the cremaster muscle. Neither inhibitor was found to augment the myogenic vasoconstriction; however, these inhibitors were observed to significantly reduce basal vascular tone. In comparison, the tonic local production of dilating prostaglandins appears to attenuate myogenic activity as demonstrated by the appearance of myogenic activity in the normally passive 2As when exposed to cyclooxygenase inhibitors.

Animals↗
PubMed1990

Analysis of vasomotion waveform changes during pressure reduction and adenosine application.

Changes in the vasomotion waveform were studied in transverse arterioles (TAs) and their first-order side branches (FOSs) in the tenuissimus muscle of 14 young, anesthetized rabbits during stepwise arterial pressure reduction and local application of adenosine using intravital video microscopy. Pressure reduction resulted in a systematic increase in vasomotion cycle length (CL) and amplitude (A) concomitant with an increase in effective vascular diameter (Deff) and maximum diameter and a decrease in blood flow (Q). During adenosine application Deff and maximum diameter also increased, but CL and A did not change systematically. At moderate pressure reductions and during adenosine application CL changes were limited (less than 1.5 s) and nonsystematic, agreeing with an earlier study (D. W. Slaaf, G. J. Tangelder, H. C. Teirlinck, and R. S. Reneman. Microvasc. Res. 33: 71-80, 1987). In TAs these changes resulted from changes in both the dilation and the constriction phase. In FOSs, however, changes in CL were caused by prolongation of the dilation phase alone. At greatly reduced pressure levels, the CL increase was more pronounced and in both TAs and FOSs was caused by plateau formation in the dilation phase. Stretch of the arteriolar wall does not seem to play a role in control of the vasomotion waveform. Because the onsets of dilation always occur synchronously in TAs and FOSs, but the onsets of constriction do not, vasomotion seems to be a series of rhythmic dilations.

Adenosine↗
PubMed1990

Hepatic microvascular changes associated with development of liver fibrosis and cirrhosis.

Quantitative data defining basic microvascular parameters are needed for better understanding of the relationship between liver blood flow and function under normal and pathological conditions. The present study was undertaken to quantitate the following microvascular parameters: flow velocities in sinusoids and terminal hepatic venules; the range of sizes of terminal hepatic vessels; and acinar sizes in both normal rat livers and during the development of liver cirrhosis. Fibrosis and cirrhosis were induced by either weekly administration of carbon tetrachloride (CCl4) or by choline-deficient diet. Microcirculation was observed using intravital epifluorescent video microscopy and recorded on a videotape for subsequent analysis. It was found that even early stages of liver disease, when only mild hepatic fibrosis was present, are associated with profound changes in the hepatic microvasculature. These changes include the appearance of highly fluorescent cells in the liver parenchyma (mainly in the areas where collagen is being deposited), a marked dilatation of the terminal hepatic venules, an increase in hepatic venous outflow, and appearance of sinusoids with very high flow velocities. As fibrosis progresses to cirrhosis, the proportion of these "fast sinusoids" increases from 7% in fibrotic livers to 33% in cirrhotic livers. These results demonstrate the presence of functional intrahepatic shunts in cirrhotic livers and support the hypothesis that hyperdynamic splanchnic circulation may be an important factor in the etiology of portal hypertension in liver disease.

Animals↗
PubMed1990

Microcirculatory responses to exogenous endothelial cell-derived relaxing factor.

Endothelium-derived relaxing factor (EDRF) plays an important role in the vasodilatory responses of large blood vessels. However, such a role has yet to be conclusively shown for the microvasculature. In this study we tested the sensitivity of arterioles in the cheek pouch of pentobarbital-anesthetized hamsters to the EDRF-dependent agonists bradykinin and A23187, as well as to exogenous EDRF from cultured bovine aortic endothelial cells. The pouch superfusion fluid was arranged to first pass through a column containing endothelial cells and then on to the tissue. Bradykinin (10-30 nM) or A23187 (0.3 microM) was introduced either upstream or downstream to the endothelial cells, and the resultant responses were measured with video microscopy. Bradykinin and A23187 both caused a dose-dependent release of a microvessel dilator from cultured endothelial cells. We take this dilator to be EDRF based on the characteristics of the responses to the stimuli. Indomethacin (7.7 microM) was present in the superfusate to eliminate the production of cyclooxygenase products from the endothelial cells, and the magnitude of the response was diminished if the superfusate was first passed through a 3-min delay coil before arrival at the pouch. The arterioles dilated to the direct application of bradykinin in a dose-dependent fashion. They did not respond however to the direct application of A23187. These studies demonstrate that arteriolar smooth muscle is able to respond to exogenous EDRF and support the premise that EDRF may play an active role in the regulation of blood flow in the microcirculation.

Animals↗
PubMed1991

Adrenergic facilitation of myogenic response in skeletal muscle arterioles.

The myogenic response was studied in large skeletal muscle arterioles in the presence of varying degrees of constriction with norepinephrine (NE; 3 x 10(-8) to 1 x 10(-5) M) or potassium chloride (KCl, 40-120 mM). The cremaster muscle of anesthetized rats was exteriorized into a Krebs-filled tissue bath chamber for observation of the microvasculature using a video microscopy system. The body of the rats was enclosed in an airtight Plexiglas box that was pressurized from 0 to +30 mmHg to raise intravascular pressure and elicit the myogenic response. All experiments were performed in acutely denervated muscles with propranolol (1 x 10(-6) M) present to produce beta-receptor blockade. Diameter responses of the first-order arteriole (1A) were measured with a videoimage caliper and intravascular pressure with the servo-null micropipette technique. Under basal conditions, without NE, 1A diameter increased in a passivelike fashion from 122 +/- 5.4 to 130 +/- 5.1 microns as box pressure was elevated from 0 to +30 mmHg, respectively. Addition of NE to the cremaster bath produced a dose-dependent constriction of the 1A (EC50 2 x 10(-7) M). In the presence of this adrenergic tone the 1A exhibited myogenic constriction in response to increases in box pressure. For example, topical application of 3 X 10(-7) M NE caused the 1A to constrict from 122 +/- 5.4 to 70 +/- 5.3 microns. In the presence of this adrenergic tone elevating box pressure from 0 to +30 mmHg caused additional constriction to 55 +/- 6.6 microns.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

EDRF released from microvascular endothelial cells dilates arterioles in vivo.

Microvascular endothelial cells (MECs) from rat epididymal fat pad were isolated and cultured in vitro on Cytodex 3 microcarrier beads. In Krebs-suffused cremaster muscle of pentobarbital-anesthetized rats arteriolar diameters (mean control diam 20.9 +/- 0.9 micron) were measured using image shearing video microscopy. Two lines of suffusate (1.5 ml/min each) were established; one contained a column of microcarrier beads only (no cells in line; NC) the other contained a 1-ml column of MECs grown on beads (through cells; TC). The muscle preparation and the MECs were first treated with indomethacin (Indo; 28 microM). Indo treatment blocked arteriolar dilation to A23187 (1 microM) and arachidonic acid (AA; 0.25 microM) administered into the NC line. A 4.0 +/- 0.6 micron increase in arteriolar diameter was observed, however, when A23187 (but not AA) was infused through the TC line containing Indotreated MECs on beads. The A23187-elicited dilation was abolished by the introduction of NG-monomethyl-L-arginine (L-NMMA; 200 microM) into the TC line. Administration of atropine (2 microM) onto the cremaster muscle via the NC line inhibited the dilations in response to acetylcholine (ACh; 2.7 microM) given through the NC line. Infusion of ACh through the TC line onto the atropine-treated cremaster muscle, however, elicited a 5.8 +/- 1.3 micron increase in arteriolar diameter, a response that was blocked by prior administration of L-NMMA into the TC line. Arteriolar dilation induced by adenosine (0.5 microM) or sodium nitroprusside (0.5 microM) applied via the NC or TC line was unaffected by L-NMMA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Microvascular recruitment in hamster striated muscle: role for conducted vasodilation.

The influence of conducted vasodilation upon arteriolar diameter and capillary red blood cell (rbc) perfusion was investigated in the cremaster muscle of male hamsters anesthetized with pentobarbital. The muscle was surgically exposed, superfused with physiological saline solution (pH 7.4; 34 degrees C), and transilluminated for observation of microvessels using intravital video microscopy. The tip (2 microns ID) of a glass micropipette filled with acetylcholine (ACh; 1.0 M) was positioned adjacent to an arteriole. Microiontophoretic delivery of an ACh stimulus (200-1,000 nA; 200-750 ms) caused vasodilation at the pipette tip, which conducted rapidly along the arteriole and decayed with distance; this was characterized by length constants of 2.1 and 2.4 mm (P greater than 0.05) for arterioles with maximal diameters of 32 +/- 2 (means +/- SE; n = 8) and 63 +/- 2 microns (n = 5), respectively. When applied to the distal end of a terminal arteriole (TA) devoid of flow, ACh triggered a dilation that was conducted proximally (greater than 1,000 microns upstream) into the parent vessel (terminal arteriole feed, TAF) containing rbc flow, thereby inducing flow into the TA; stimulation of the TAF also induced rbc flow into TA. In capillaries fed by TA, rbc flux (rbc/s) increased from zero at rest to 23 +/- 6 during the peak of the TA dilation (n = 9); calculated tube hematocrit increased from 4 +/- 2 to 28 +/- 3%. Findings demonstrate that conduction of vasodilation can coordinate vasomotor responses between terminal and parent arterioles and promote rbc delivery to capillaries supplying striated muscle fibers.

Acetylcholine↗