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1.
Experiments on anesthetized dogs and on vascular test-preparations demonstrated that reactive hyperemia (RH) was accompanied by the appearance of vasodilator in the blood, and that the level increased with the duration of occlusion of the artery. Removal of the endothelium of the part of the vascular bed studied using saponin, decreased the RH and relaxation of a test-preparation. A rise of pressure in the vascular bed, and a decrease in the deformability of the endothelium resulting from pretreatment with dimerized glutaraldehyde, affected both the hyperemia and the reaction of the vascular preparation in a similar way. It was concluded that the RH resulted from the secretion of vasoactive substances by the endothelium in response to a fall in intravascular pressure. 相似文献
2.
Summary The noradrenaline, adrenaline and acetylcholine-induced vasoregulatory escape was demonstrated in the vascular bed of intact or skinned and denervated dog's hind limb. Escape effect disappeared or decreased markedly under elevation tissue pressure in the examined hind limb. These data indicate that tissue pressure factor may take part in the mechanism of the escape phenomenon. 相似文献
3.
Reactive hyperemia was induced in hindlimbs of rats by occlusion of the femoral artery. Using fluorescein dye as a peripheral vascular marker, we observed that there was an increase in the number of flowing capillaries supplying the muscle fibres following release of the occlusion. The results indicate that the number of flowing capillaries is not dependent on the duration of occlusion (2-10 min). 相似文献
4.
Summary Reactive hyperemia was induced in hindlimbs of rats by occlusion of the femoral artery. Using fluorescein dye as a peripheral vascular marker, we observed that there was an increase in the number of flowing capillaries supplying the muscle fibres following release of the occlusion. The results indicate that the number of flowing capillaries is not dependent on the duration of occlusion (2–10 min). 相似文献
5.
An increase in venous pressure in the rat tail is known to result in acute edema. Acute venous stasis edema of the rat tail was induced by applying a force-controlled banding of standard tension (200 g) proximally for a period of 6-12 h. The hemodynamic changes of acute venous stasis edema were evaluated using non-invasive plethysmography, fluorescence angiography, computer thermography and invasive radioactive microsphere techniques. It is shown here that reduction of tail circulation to 40% of the control value is followed by prolonged vascular disorder characterized by genesis of reversible edema, increased total blood flow to the tail and decreased local cutaneous blood flow, without affecting the general hemodynamics. The cutaneous circulation (decreased blood flow) seems to be principally involved in the edemogenic response, whereas the deeper vessels (hyperemia) may or may not play a determinant role in acute experimental venous stasis edema in rats. 相似文献
6.
Endothelial cells as part of a vascular oxygen-sensing system: hypoxia-induced release of autacoids 总被引:2,自引:0,他引:2
U Pohl 《Experientia》1990,46(11-12):1175-1179
Higher developed organisms are equipped with many central and local control mechanisms, which enable an adequate blood and oxygen supply to tissues over a wide range of demands. Global adaptive responses include changes in the circulatory and ventilatory system as well as increases in the oxygen carrying capacity of the blood. At the level of the specialized organs there exist additional control systems for the regulation of local blood flow. Most systems make use of highly specialized cells which are able to sense the oxygen partial pressure of the transport medium, blood, and within the tissues. In the past years, it has been shown that the vascular endothelium lining the entire circulatory system can actively modulate the vascular tone and platelet functions by the release of autacoids, among them prostacyclin and endothelium-derived nitric oxide (EDRF). Recent experiments demonstrate that the release of EDRF is PO2-dependent, which suggests that endothelial cells may act as functional local oxygen sensors within the vascular system. 相似文献
7.
The vasculature is one of the most dynamic tissues that encounter numerous mechanical cues derived from pulsatile blood flow, blood pressure, activity of smooth muscle cells in the vessel wall, and transmigration of immune cells. The inner layer of blood and lymphatic vessels is covered by the endothelium, a monolayer of cells which separates blood from tissue, an important function that it fulfills even under the dynamic circumstances of the vascular microenvironment. In addition, remodeling of the endothelial barrier during angiogenesis and trafficking of immune cells is achieved by specific modulation of cell–cell adhesion structures between the endothelial cells. In recent years, there have been many new discoveries in the field of cellular mechanotransduction which controls the formation and destabilization of the vascular barrier. Force-induced adaptation at endothelial cell–cell adhesion structures is a crucial node in these processes that challenge the vascular barrier. One of the key examples of a force-induced molecular event is the recruitment of vinculin to the VE-cadherin complex upon pulling forces at cell–cell junctions. Here, we highlight recent advances in the current understanding of mechanotransduction responses at, and derived from, endothelial cell–cell junctions. We further discuss their importance for vascular barrier function and remodeling in development, inflammation, and vascular disease. 相似文献
8.
T. Koyama Y. Kakiuchi T. Sasajima S. Makinoda T. Arai M. Ishikawa Ch. Nagashima 《Cellular and molecular life sciences : CMLS》1977,33(9):1169-1170
Summary Colloid osmotic pressure (COP) of blood from the great cardiac vein was continuously measured by the use of a membrane colloid osmometer during reactive hyperemia resulting from temporary occlusion of the anterior descending branch of left coronary artery. The COP increased sharply but transiently after the release, then it decreased below the initial level and gradually recovered. It was concluded that a measurable amount of water moved from the capillary blood into the myocardial tissue and then flowed back slowly into the capillary blood. 相似文献
9.
Summary An increase in venous pressure in the rat tail is known to result in acute edema. Acute venous stasis edema of the rat tail was induced by applying a force-controlled banding of standard tension (200 g) proximally for a period of 6–12 h. The hemodynamic changes of acute venous stasis edema were evaluated using non-invasive plethysmography, fluorescence angiography, computer thermography and invasive radioactive microsphere techniques. It is shown here that reduction of tail circulation to 40% of the control value is followed by prolonged vascular disorder characterized by genesis of reversible edema, increased total blood flow to the tail and decreased local cutaneous blood flow, without affecting the general hemodynamics. The cutaneous circulation (decreased blood flow) seems to be principally involved in the edemogenic response, whereas the deeper vessels (hyperemia) may or may not play a determinant role in acute experimental venous stasis edema in rats.Acknowledgment. The authors thank Mr G. Ponard for his technical assistance. 相似文献
10.
Summary Reactive hyperemic responses of the coronary arterial bed, provoked by asphyxia or clamping of the coronary artery, were compared in alloxan-diabetic and metabolically healthy dogs. In alloxan-diabetic dogs the response of the coronary arterial bed lasted longer, and its reactivity to hypoxia was lower. Treatment with adenosine caused less vasodilation in diabetic animals than in controls. These changes may be due to the altered reactivity of diabetic vascular smooth muscle. 相似文献
11.
Reactive hyperemic responses of the coronary arterial bed, provoked by asphyxia or clamping of the coronary artery, were compared in alloxan-diabetic and metabolically healthy dogs. In alloxan-diabetic dogs the response of the coronary arterial bed lasted longer, and its reactivity to hypoxia was lower. Treatment with adenosine caused less vasodilation in diabetic animals than in controls. These changes may be due to the altered reactivity of diabetic vascular smooth muscle. 相似文献
12.
R S Tuttle 《Experientia》1986,42(7):817-819
Pressor responses evoked by stimulation of the preganglionic sympathetic trunk of the feline superior cervical ganglion have been recorded in vivo from the vascular bed perfused by one external carotid and the vertebral artery. When vasoconstrictor activity is blocked and potential vasodilator activity enhanced by close, intracarotid injection of guanethidine and prostaglandin F2 alpha respectively, stimulation evokes a weak pressor response followed, on cessation of stimulation, by a prolonged vasodilation lasting for 6-8 min. The magnitude and duration of the poststimulation vasodilation was reduced significantly by atropine. Due to the prolonged nature of the vasodilation, it is unlikely that a sympathetic cholinergic vasodilation in the classical sense is involved. 相似文献
13.
Endothelial nitric oxide synthase: insight into cell-specific gene regulation in the vascular endothelium 总被引:2,自引:0,他引:2
The vascular endothelium plays a crucial role in regulating normal blood vessel physiology. The gene products responsible
are commonly expressed exclusively, or preferentially, in this cell type. However, despite the importance of regulated gene
expression in the vascular endothelium, relatively little is known about the mechanisms that restrict endothelial-specific
gene expression to this cell type. While significant progress has been made towards understanding the regulation of endothelial
genes through cis/trans paradigms, it has become apparent that additional mechanisms must also be operative. For example,
chromatin-based mechanisms, including cell-specific DNA methylation patterns and post-translational histone modifications,
have recently been demonstrated to play important roles in the cell-specific expression of endothelial nitric oxide synthase
(eNOS). This review investigates the involvement of epigenetic regulatory mechanisms in vascular endothelial cell-specific
gene expression using eNOS as a prototypical model, and will address the possible contributions of these pathways to diseases
of the vasculature.
Received 13 September 2005; received after revision 13 October 2005; accepted 19 October 2005 相似文献
14.
The distribution of histamine receptors was studied in the isolated perfused vascular bed of the cat terminal ileum. The results indicated that the depressor effect of histamine is mediated through the stimulation of metiamide-sensitive H2-receptors, while the pressor effect of the amine is mediated by the stimulation of mepyramine-sensitive H1-receptors. 相似文献
15.
Deepak Atri Bruno Larrivée Anne Eichmann Michael Simons 《Cellular and molecular life sciences : CMLS》2014,71(5):867-883
Arteriovenous malformations occur when abnormalities of vascular patterning result in the flow of blood from arteries to veins without an intervening capillary bed. Recent work has revealed the importance of the Notch and TGF-β signaling pathways in vascular patterning. Specifically, Notch signaling has an increasingly apparent role in arterial specification and suppression of branching, whereas TGF-β is implicated in vascular smooth muscle development and remodeling under angiogenic stimuli. These physiologic roles, consequently, have implicated both pathways in the pathogenesis of arteriovenous malformation. In this review, we summarize the studies of endothelial signaling that contribute to arteriovenous malformation and the roles of genes implicated in their pathogenesis. We further discuss how endothelial signaling may contribute to vascular smooth muscle development and how knowledge of signaling pathways may provide us targets for medical therapy in these vascular lesions. 相似文献
16.
R. S. Tuttle 《Cellular and molecular life sciences : CMLS》1986,42(7):817-819
Summary Pressor responses evoked by stimulation of the preganglionic sympathetic trunk of the feline superior cervical ganglion have been recorded in vivo from the vascular bed perfused by one external carotid and the vertebral artery. When vasoconstrictor activity is blocked and potential vasodilator activity enhanced by close, intracarotid injection of guanethidine and prostaglandin F2 respectively, stimulation evokes a weak pressor response followed, on cessation of stimulation, by a prolonged vasodilation lasting for 6–8 min. The magnitude and duration of the poststimulation vasodilation was reduced significantly by atropine. Due to the prolonged nature of the vasodilation, it is unlikely that a sympathetic cholinergic vasodilation in the classical sense is involved. 相似文献
17.
Adenosine 5'-triphosphate (ATP) was released into the perfusate of rat isolated mesenteric arterial beds during each of two consecutive increases in flow. There was no significant difference between the amounts of ATP released on each occasion. Substance P was also released into the perfusate by increased flow, although its release was more variable. Removal of the endothelium of the mesenteric vessels with sodium deoxycholate led to a significant reduction (74%) in the amount of ATP released compared with the release before the endothelium had been removed. This suggests that the ATP released into the mesenteric arterial perfusate during increased flow arises from endothelial cells. 相似文献
18.
Sergio Claudio Saccà Alberto Izzotti 《Cellular and molecular life sciences : CMLS》2014,71(12):2197-2218
Primary open-angle glaucoma is a multifactorial disease that affects the retinal ganglion cells, but currently its therapy is to lower the eye pressure. This indicates a definite involvement of the trabecular meshwork, key region in the pathogenesis of glaucoma. This is the first target of glaucoma, and its functional complexity is a real challenge to search. Its functions are those to allow the outflow of aqueous humor and not the reflux. This article describes the morphological and functional changes that happen in anterior chamber. The “primus movens” is oxidative stress that affects trabecular meshwork, particularly its endothelial cells. In these develops a real mitochondriopaty. This leads to functional impotence, the trabecular meshwork altering both motility and cytoarchitecture. Its cells die by apoptosis, losing barrier functions and altering the aqueous humor outflow. All the morphological alterations occur that can be observed under a microscope. Intraocular pressure rises and the malfunctioning trabecular meshwork endotelial cells express proteins that completely alter the aqueous humor. This is a liquid whose functional proteomics complies with the conditions of the trabecular meshwork. Indeed, in glaucoma, it is possible detect the presence of proteins which testify to what occurs in the anterior chamber. There are six classes of proteins which confirm the vascular endothelium nature of the anterior chamber and are the result of the morphofunctional trabecular meshwork decay. It is possible that, all or in part, these proteins can be used as a signal to the posterior pole. 相似文献
19.
D. Evéquoz E. Grouzmann A. G. Beck-Sickinger H. -R. Brunner B. Waeber 《Cellular and molecular life sciences : CMLS》1994,50(10):936-938
Neuropeptide Y (NPY) increases blood pressure either directly or indirectly by potentiating the effect of various vasoconstrictors. Only one (the Y1-receptor) of two subtypes of receptors (Y1 and Y2) is thought to mediate the vascular smooth muscle contraction. To test this hypothesis we challenged isolated rat mesenteric arteries that had a functional endothelium with (1–36) NPY and with specific Y1-receptor ([Leu31, Pro34] NPY) and Y2-receptor ([Ahx5–24, -Glu2--Lys30] NPY) agonists. The Y1-receptor agonist elicited a contractile response similar to that of NPY, whereas the Y2-receptor agonist had no effect on wall tension. We also found that the presence of a functional endothelium has no influence on the contractile response to NPY. From these data we conclude that the direct contractile effect of NPY in the mesenteric artery is mediated by stimulation of Y1-receptors and is not endothelium-dependent. 相似文献
20.
Larrucea S Butta N Rodriguez RB Alonso-Martin S Arias-Salgado EG Ayuso MS Parrilla R 《Cellular and molecular life sciences : CMLS》2007,64(22):2965-2974
Podocalyxin (PODXL) is a mucin protein of the CD34 family expressed in kidney glomerular podocytes, vascular endothelium,
progenitor bone marrow and tumor cells. It is assumed that PODXL plays an anti-adherent role in kidney podocytes. CHO cells
stably expressing human PODXL (CHO-PODXL) or human tumor cells (Tera-1) inherently expressing PODXL showed increased adherence
to platelets. The adherence of cells was inhibited (70%) by blockers of platelet P-selectin, prevented by the soluble ectodomain
of human PODXL (PODXL-Δ) or by the arginine-glycine-aspartate (RGDS) peptide and partially impeded by inhibition of integrin
αVβ3/αVβ5, suggesting a coordinated action of P-selectin and integrins. Colocalization of platelet P-selectin and PODXL expressed
on CHO cells was demonstrated by confocal immunofluorescence. No adherence to platelets was observed when PODXL was expressed
in glycomutant CHO cells deficient in sialic acid.
Received 14 August 2007; received after revision 12 September 2007; accepted 13 September 2007 相似文献