scholarly journals Changes in Pial Arteriolar Diameter and CSF Adenosine Concentrations during Hypoxia

1993 ◽  
Vol 13 (2) ◽  
pp. 214-220 ◽  
Author(s):  
Joseph R. Meno ◽  
Al C. Ngai ◽  
H. Richard Winn
Keyword(s):  
Vessel Diameter ◽  
Sprague Dawley ◽  
Extracellular Adenosine ◽  
Moderate Hypoxia ◽  
Adenosine Receptor Antagonist ◽  
Sprague Dawley Rats ◽  
Pial Arterioles ◽  
Pial Vessel ◽  
Arteriolar Vasodilation ◽  
Arteriolar Diameter

We measured the changes in pial arteriolar diameter and CSF concentrations of adenosine, inosine, and hypoxanthine during hypoxia in the absence and presence of topically applied dipyridamole (10−6 M) and erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA; 10−5 M). Closed cranial windows were implanted in halothane-anesthetized adult male Sprague–Dawley rats for the observation of the pial circulation and collection of CSF. The mean resting arteriolar diameter in mock CSF was 31.2 ± 5.9 μm. Topically applied dipyridamole and EHNA, in combination, caused a slight but significant ( p < 0.05) increase in resting arteriolar diameter (33.8 ± 4.3 μm). With mock CSF, moderate hypoxia caused a 22.1 ± 9.7% increase in pial vessel diameter. Topically applied dipyridamole and EHNA significantly ( p < 0.01) potentiated pial arteriolar vasodilation in response to hypoxia. Moreover, the potentiating effects of dipyridamole and EHNA during hypoxia were completely abolished by theophylline (0.20 μmol/g, i.p.; p < 0.05), an adenosine receptor antagonist. Resting concentrations of adenosine, inosine, and hypoxanthine in the subwindow CSF were 0.18 ± 0.09, 0.35 ± 0.21, and 0.62 ± 0.12 μ M, respectively. In the absence of dipyridamole and EHNA, these levels were not affected by sustained moderate hypoxia (Pao2 = 36 ± 6 mm Hg). However, in the presence of dipyridamole and EHNA, the concentration of adenosine in the CSF during hypoxia was significantly ( p < 0.05) increased. Our data indicate that dipyridamole and EHNA potentiate hypoxic vasodilation of pial arterioles while simultaneously increasing extracellular adenosine levels, thus supporting the hypothesis that adenosine is involved in the regulation of cerebral blood flow.

Effect of inosine on pial arterioles: potentiation of adenosine-induced vasodilation

1989 ◽  
Vol 256 (3) ◽  
pp. H603-H606 ◽  
Author(s):  
A. C. Ngai ◽  
M. R. Monsen ◽  
S. Ibayashi ◽  
K. R. Ko ◽  
H. R. Winn
Keyword(s):  
Vessel Diameter ◽  
Uptake Inhibitor ◽  
Adenosine Uptake ◽  
Pial Arterioles ◽  
Significant Change ◽  
Pial Vessel ◽  
Arteriolar Vasodilation ◽  
Arteriolar Diameter

We examined the cerebral vasoactivity of inosine and its effect on pial arteriolar vasodilation induced by adenosine. Pial circulation was observed through cranial windows implanted in rats anesthetized with halothane. No significant change in venous or arteriolar diameter was apparent when inosine (10(-6) to 10(-3) M) was superfused. In contrast, adenosine in concentrations of 10(-7) and 10(-6) M dilated pial arterioles by 9.0 +/- 1.2 and 17.7 +/- 1.7%, respectively. Addition of 10(-5) M inosine had no effect, whereas 10(-4) M inosine enhanced the vasodilation induced by 10(-7) M adenosine to 19.4 +/- 1.7% and that by 10(-6) M adenosine to 23.3 +/- 2.3%. When theophylline (5 X 10(-5) M) was perfused together with 10(-7) M adenosine and 10(-4) M inosine, the vasodilation was almost completely abolished. The present study indicates that inosine alone does not affect pial vessel diameter but potentiates the response of pial arterioles to exogenous adenosine. This potentiating action of inosine may be attributed to an increase in perivascular adenosine and may be explained by the action of inosine as an adenosine uptake inhibitor.

L-NNA decreases cortical hyperemia and brain cGMP levels following CO2 inhalation in Sprague-Dawley rats

1994 ◽  
Vol 267 (2) ◽  
pp. H837-H843 ◽  
Author(s):  
K. Irikura ◽  
K. I. Maynard ◽  
W. S. Lee ◽  
M. A. Moskowitz
Keyword(s):  
Blood Flow ◽  
Vessel Diameter ◽  
Sprague Dawley ◽  
Doppler Flowmetry ◽  
Cranial Window ◽  
Sprague Dawley Rats ◽  
Acetylcholine Inhalation ◽  
Flow Changes ◽  
Pial Vessel

The role of nitric oxide (NO) in the response to 5% CO2 inhalation was investigated by measuring 1) regional cerebral blood flow (rCBF) by laser-Doppler flowmetry and pial vessel diameter through a closed cranial window after topical NG-nitro-L-arginine (L-NNA, 1 mM), and 2) the time-dependent changes in brain guanosine 3',5'-cyclic monophosphate (cGMP) levels after L-NNA (10 mg/kg ip). When L-NNA (but not NG-nitro-D-arginine) was applied topically for 30 or 60 min, the response to hypercapnia was significantly attenuated. A correlation was found between inhibition of brain NO synthase (NOS) activity and the rCBF response (r = 0.77; P < 0.01). However, L-NNA applied 15 min before hypercapnia did not attenuate the increase in rCBF but did attenuate the dilation to topical acetylcholine. Inhalation of CO2 (5%) elevated brain cGMP levels by 20–25%, and L-NNA reduced this response. These data from the rat suggest that 1) a product of NOS activity is associated with hypercapnic hyperemia and the attendant increase in brain cGMP levels, and 2) hypercapnic blood flow changes may not be dependent on endothelial NOS activity within pial vessels.

scholarly journals Basic Fibroblast Growth Factor Dilates Rat Pial Arterioles

1994 ◽  
Vol 14 (1) ◽  
pp. 70-74 ◽  
Author(s):  
Sami Rosenblatt ◽  
Katsumi Irikura ◽  
Cornelio G. Caday ◽  
Seth P. Finklestein ◽  
Michael A. Moskowitz
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Vessel Diameter ◽  
Fibroblast Growth ◽  
Sprague Dawley ◽  
Cranial Window ◽  
Sprague Dawley Rats ◽  
Pial Arterioles ◽  
Synthase Inhibitor

Basic fibroblast growth factor (bFGF) is a polypeptide that promotes the survival and differentiation of brain neurons, glia, and endothelial cells. It has been shown recently that intravenously administered bFGF lowers blood pressure by systemic vasodilation; this effect is mediated, in part, by nitric oxide (NO)-dependent mechanisms. In the current study, we directly evaluated the effect of bFGF on pial arterioles of pentobarbital-anesthetized Sprague-Dawley rats (n = 18) using the closed cranial window technique. Basic FGF (5–200 ng/ml) produced dose-dependent vasodilation; maximal vessel diameter (∼120% of control) was reached at 100 ng/ ml. No vasodilation was found when bFGF was heat inactivated, or preincubated with blocking antibody. Moreover, bFGF-induced vasodilation was attenuated by coadministration of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), consistent with an NO-dependent mechanism. These results suggest that bFGF may play an important role in the regulation of cerebrovascular tone and cerebral blood flow.

Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats

2007 ◽  
Vol 292 (6) ◽  
pp. H2737-H2744 ◽  
Author(s):  
Masahito Kajiya ◽  
Masanori Hirota ◽  
Yousuke Inai ◽  
Takahiko Kiyooka ◽  
Taro Morimoto ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Pressure Overload ◽  
Suppressive Effect ◽  
Protective Role ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Small Arteries ◽  
Sprague Dawley Rats ◽  
Endothelial Nitric Oxide ◽  
Arteriolar Vasodilation

Pulmonary hypertension (PH) causes right ventricular (RV) hypertrophy and, according to the extent of pressure overload, eventual heart failure. We tested the hypothesis that the mechanical stress in PH-RV impairs the vasoreactivity of the RV coronary microvessels of different sizes with increased superoxide levels. Five-week-old male Sprague-Dawley rats were injected with monocrotaline ( n = 126) to induce PH or with saline as controls ( n = 114). After 3 wk, coronary arterioles (diameter = 30–100 μm) and small arteries (diameter = 100–200 μm) in the RV were visualized using intravital videomicroscopy. We evaluated ACh-induced vasodilation alone, in the presence of Nω-nitro-l-arginine methyl ester (l-NAME), in the presence of tetraethylammonium (TEA) or catalase with or without l-NAME, and in the presence of SOD. The degree of suppression in vasodilation by l-NAME and TEA was used as indexes of the contributions of endothelial nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), respectively. In PH rats, ACh-induced vasodilation was significantly attenuated in both arterioles and small aretries, especially in arterioles. This decreased vasodilation was largely attributable to reduced NO-mediated vasoreactivity, whereas the EDHF-mediated vasodilation was relatively robust. The suppressive effect on arteriolar vasodilation by catalase was similar to TEA in both groups. Superoxide, as measured by lucigenin chemiluminescence, was significantly elevated in the RV tissues in PH. SOD significantly ameliorated the impairment of ACh-induced vasodilation in PH. Robust EDHF function will play a protective role in preserving coronary microvascular homeostasis in the event of NO dysfunction with increased superoxide levels.

Acute cyclosporine-induced renal vasoconstriction: lack of effect of theophylline

1990 ◽  
Vol 258 (1) ◽  
pp. F41-F45
Author(s):  
P. C. Churchill ◽  
N. F. Rossi ◽  
M. C. Churchill ◽  
A. K. Bidani ◽  
F. D. McDonald
Keyword(s):  
Renal Plasma Flow ◽  
Left Kidney ◽  
Chronic Administration ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Adenosine Receptor Antagonist ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Group 1

Both acute and chronic administration of cyclosporine A (CSA) lead to renal vasoconstriction, but the mechanism is not fully understood. The present studies were designed to explore the possible role of adenosine in acute CSA-induced renal vasoconstriction in rats. Six groups of anesthetized Sprague-Dawley rats were studied using standard clearance techniques: group 1 rats were controls; groups 2, 4, and 6 received CSA intravenously at 20, 30, and 40 mg.h-1.kg body wt-1, respectively; groups 3 and 5 were identical to groups 2 and 4 except that a priming injection of theophylline was given (56 mumol/kg body wt) and theophylline was included in the intravenous infusate (0.56 mumol.min-1.kg body wt-1). CSA produced acute and concentration-dependent reductions in renal plasma flow (left kidney) and in the clearances of p-aminohippuric acid and inulin (both kidneys). Except in group 6, these changes were observed in the absence of a decrease in arterial blood pressure, demonstrating that CSA produced an acute and concentration-dependent increase in renovascular resistance. Theophylline not only failed to block CSA-induced renal vasoconstriction, if anything, it potentiated it. Because theophylline is an adenosine receptor antagonist, these findings contradict the hypothesis that adenosine mediates acute CSA-induced renal vasoconstriction.

Hypoglycemia selectively abolishes hypoxic reactivity of pial arterioles in piglets: role of adenosine

1995 ◽  
Vol 268 (2) ◽  
pp. H871-H878 ◽  
Author(s):  
T. S. Park ◽  
E. R. Gonzales ◽  
A. R. Shah ◽  
J. M. Gidday
Keyword(s):  
Arterial Pco2 ◽  
Adenosine Receptor Antagonist ◽  
Cranial Window ◽  
Newborn Piglets ◽  
Window Technique ◽  
Pial Arterioles ◽  
Cerebrovascular Regulation ◽  
Arterial Po2 ◽  
Arteriolar Diameter

Episodes of hypoxia often occur in hypoglycemic newborns, but it is not known whether dysfunctions in cerebrovascular regulation contribute to brain injury incurred by these affected neonates. We tested the hypotheses that 1) perinatal hypoglycemia impairs cerebrovascular responses to hypoxia and 2) a reduced vascular smooth muscle sensitivity to adenosine accounts for this impairment. Responses of 25- to 50-mu m-diam pial arterioles were determined using the cranial window technique in isoflurane-anesthetized newborn piglets < 5 days of age. Hypoxia (arterial PO2 = 28 +/- 1 mmHg) caused a 47 +/- 5% increase (P = 0.0008) in arteriolar diameter, 89% of which could be blocked by prior superfusion of the window space with the preferential A2-adenosine receptor antagonist 3,7-dimethyl-1-propargylxanthine (DMPX; 50 microM). Insulin-induced hypoglycemia (blood glucose = 18 +/- 1 mg/dl without isoelectric electroencephalogram) caused a 31 +/- 5% increase (P = 0.002) in arteriolar diameter; however, no additional dilatative response to hypoxia (arterial PO2 = 28 +/- 1 mmHg) could be elicited in these animals. Arteriolar dilation of 41 +/- 6% (P = 0.002) induced by superfusion of 20 microM adenosine under normoglycemic conditions was also completely abolished after the animals were rendered hypoglycemic. Unlike the response to hypoxia and adenosine, hypoglycemia only attenuated prostanoid-dependent dilations to hypercapnia (arterial PCO2 = 68 +/- 3 mmHg) by 55 +/- 9%. These results indicate that, in the newborn, hypoglycemia selectively abolishes hypoxic reactivity through an impairment in adenosine-mediated cerebrovascular dilation.

Cholinergic vasodilation of intracerebral arterioles in rats

1987 ◽  
Vol 253 (5) ◽  
pp. H1253-H1260 ◽  
Author(s):  
R. G. Dacey ◽  
J. E. Bassett
Keyword(s):  
Vessel Diameter ◽  
Sprague Dawley ◽  
Cholinergic Mechanisms ◽  
Smooth Muscle Contractility ◽  
Cholinergic Mechanism ◽  
In Situ Data ◽  
Prostaglandin F2 Alpha ◽  
Sprague Dawley Rats ◽  
Long Acting

Much morphological and physiological evidence indicates that cholinergic mechanisms play a significant role in the control of cerebral blood flow. Despite in situ data suggesting that an intrinsic cholinergic mechanism produces vasodilation in the intracerebral microcirculation, there is no direct information on the effect of acetylcholine (ACh) on intracerebral arterioles. We investigated cholinergic mechanisms in isolated perfused intracerebral arterioles from pentobarbital sodium-anesthetized Sprague-Dawley rats. In arterioles with resting diameters of 46.8 +/- 6.6 microns (mean +/- SE) ACh produced no significant dilation at pH 7.30. At pH 7.60, however, a significant dose-dependent dilation to a maximum of 119.0 +/- 1.0% of control diameter was observed. Carbachol, a long-acting cholinergic agonist, similarly failed to dilate vessels at pH 7.30 but significantly dilated vessels at pH 7.60. Prostaglandin F2 alpha produced a maximum contraction to 68.3 +/- 2.7% of control diameter (n = 8). ACh at concentrations of 10(-4) and 2 X 10(-4) M induced a significant dilation of this prostaglandin-induced contraction. In vessels similarly preconstricted with serotonin, 10(-4) M ACh produced significant dilation. Atropine, having no effect on vessel diameter when administered alone, blocked cholinergic vasodilation of intracerebral arterioles at pH 7.60. Attempts at endothelial removal, although successful in eliminating endothelial cells from the preparation, significantly impaired smooth muscle contractility. ACh has no significant effect on the spontaneous cerebrovascular tone in this preparation, but in vessels preconstricted by a variety of means it produced vasodilation mediated by atropine sensitive receptors.

Modulation of Rat Pial Arteriolar Responses to Flow by Glucose

2002 ◽  
Vol 97 (2) ◽  
pp. 471-477 ◽  
Author(s):  
Michael E. Ward ◽  
Lu Yan ◽  
Mark R. Angle
Keyword(s):  
Shear Stress ◽  
High Glucose ◽  
Glucose Concentration ◽  
Muscle Tone ◽  
Transmural Pressure ◽  
Intraluminal Pressure ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Pial Arterioles ◽  
Physiologic Saline

Background Pial arteriolar responses to flow contribute to regulation of cerebral perfusion and vary according to the transmural pressure to which the vessel is exposed. This study determined the effect of increased glucose concentration on the flow responses of pial arterioles at low and high levels of transmural pressure. Methods Pial arterioles from Sprague-Dawley rats were mounted in a perfusion myograph. In some arterioles, the endothelium was removed by perfusion with air. Diameters were recorded at transmural pressures of 60 and 120 mmHg during superfusion with physiologic saline containing 5 mm D-glucose, 20 mm D-glucose, or 5 mm D-glucose and 15 mm L-glucose. Diameters during superfusion with saline containing 44 mm D-glucose were measured at an intraluminal pressure of 60 mmHg. Flow-diameter relationships (5-30 microl/min) were recorded during perfusion with the same solutions. Results Increasing D-glucose concentration caused constriction (P &lt; 0.05) in endothelium-denuded but not in endothelium-intact arterioles. Addition of L-glucose caused constriction in endothelium-intact and -denuded vessels (P &lt; 0.05 for both). At a D-glucose concentration of 5 mm and at low intraluminal pressure, flow elicits endothelium-dependent dilation such that shear stress remains constant. At a D-glucose concentration of 20 or 44 mm, after addition of L-glucose (15 mm), and at high intraluminal pressures, flow elicits constriction and shear stress is unregulated. Conclusions High glucose concentrations elicit increased basal arteriolar smooth muscle tone that is counteracted by release of endothelium-derived relaxing factors. Endothelium-dependent relaxation to flow (shear stress) is inhibited at high glucose concentrations.

Proper Choice of Vessels for Supermicrosurgery Training: An Experimental Animal study

2018 ◽  
Vol 34 (09) ◽  
pp. 742-748
Author(s):  
Yooseok Ha ◽  
Seung Song ◽  
Nak Kang ◽  
Sang-Ha Oh
Keyword(s):  
Experimental Animal ◽  
Animal Studies ◽  
Free Flaps ◽  
Vessel Diameter ◽  
Sprague Dawley ◽  
Epigastric Vessel ◽  
Sprague Dawley Rats ◽  
Pedicle Length ◽  
Experimental Animal Study ◽  
Arteries And Veins

Background Reconstruction using supermicrosurgery, a technique of microneurovascular anastomosis for smaller vessels (< 0.8 mm), has become popular. Experimental animal studies for supermicrosurgery training have been reported; however, there have been few studies performed according to vessel diameter and pedicle length. In this study, the external diameters of four vessels (femoral, superficial epigastric, axillary, and common thoracic) and pedicle length of two flaps (superficial epigastric and common thoracic–long thoracic) were measured. Methods The inguinal and pectoral regions of Sprague-Dawley rats (n = 19) were dissected anatomically, and the external diameters of the four vessels were measured (right and left, artery and vein measured separately). After elevating the superficial epigastric and common thoracic–long thoracic flaps, the pedicle length of the flaps was also measured. Results Among the 16 vessels examined, the external diameters of 11 and 5 vessels were above and below 0.8 mm, respectively. The external diameters of the superficial epigastric vessel and common thoracic vessel (both arteries and veins) were below 0.8 mm. The external diameters of the femoral and axillary vessels (veins) were above 0.8 mm. The length of the common thoracic–long thoracic pedicle was approximately10 mm longer than that of the superficial epigastric pedicle. Conclusions The external diameters of the superficial epigastric vessel and common thoracic vessel are small enough for supermicrosurgery training. The pedicle lengths of both the superficial epigastric and common thoracic–long thoracic flaps are sufficient to perform free flap experiments. Supermicrosurgical free flaps using these two vessels and a study of the physiology and pharmacology of the flaps will likely be possible in the future.

Interaction between hypoxia and hypercapnia in regulating canine diaphragm arteriolar diameter

1996 ◽  
Vol 80 (3) ◽  
pp. 802-809 ◽  
Author(s):  
M. E. Ward
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Sodium Nitroprusside ◽  
Vessel Diameter ◽  
Additive Effect ◽  
Severe Hypoxia ◽  
Moderate Hypoxia ◽  
Arterial Blood ◽  
Venous Pco2 ◽  
Arteriolar Diameter

In alpha-chloralose-anesthetized mongrel dogs, the microvascular responses to hypoxia and hypercapnia were studied in the vascularly isolated ex vivo left hemidiaphragm. The diaphragm was perfused with arterial blood diverted from the femoral artery by a pump. A series of membrane oxygenators was used to adjust the blood gas composition of the blood perfusing the diaphragm. Arteriolar diameters were measured by intravital microscopy during an infusion of sodium nitroprusside, moderate hypoxia (phrenic venous PO2 25 Torr), severe hypoxia (phrenic venous PO2 13 Torr), hypercapnia (phrenic venous PCO2 100 Torr), and a simultaneous presentation of hypoxia and hypercapnia. Recordings were made after 15 min under each condition when a steady state had been established for vessel diameter and flow. Pump speed was adjusted manually under each condition to ensure that the steady-state perfusion pressure was the same as that under the control condition. Moderate hypoxia generally resulted in dilation; however, vasoconstriction was seen in some arterioles. Severe hypoxia caused vasodilation that was inversely related to baseline vessel diameter and paralleled the response to sodium nitroprusside. Hypercapnia resulted in vasodilation of the diaphragmatic circulation at values of phrenic venous PCO2 = 80 Torr. The arteriolar response to hypercapnia was also inversely related to baseline vessel diameter. Hypoxia and hypercapnia in combination exerted an additive effect on arteriolar diameter but produced a greater than additive effect on blood flow. Both PO2 and PCO2 may contribute to the local regulation of diaphragmatic blood flow. The vasodilator effects of both hypoxia and hypercapnia are greater in smaller than in larger arterioles. The interaction between PO2 and PCO2 on arteriolar diameter is additive. An apparent synergistic effect on blood flow results from the power function relating diameter to flow.

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