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61.
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63.
PURPOSE: (1) Describe a new methodology that permits the comprehensive assessment of retinal arteriolar vascular reactivity in response to a sustained and stable hypercapnic stimulus. (2) Determine the magnitude of the vascular reactivity response of the retinal arterioles to hypercapnic provocation in healthy, young subjects. METHODOLOGY: Eleven healthy subjects of mean age 27 years (SD 3.43) participated in the study and one eye was randomly selected. A mask attached to a sequential rebreathing circuit, and connected to a gas delivery system, was fitted to the face. To establish baseline values, subjects breathed bottled air for 15 min and at least 6 blood flow measurements of the supero-temporal arteriole were acquired using the Canon Laser Blood Flowmeter (CLBF). Air flow was then decreased until a stable increase in fractional end-tidal CO(2) concentration (F(ET)CO(2)) of 10-15% was achieved. CLBF measurements were acquired every minute (minimum of 6 measurements) during the 20-minute period of elevated F(ET)CO(2). F(et)CO(2) was then reduced to baseline levels, and 6 further CLBF measurements were acquired. Respiratory rate, blood pressure, pulse rate and oxygen saturation were monitored continuously. RESULTS: Retinal arteriolar diameter, blood velocity and blood flow increased during hypercapnia relative to baseline (p=0.0045, p<0.0001 and p<0.0001, respectively). Group mean F(ET)CO(2) showed an increase of 12.0% (SD 3.6) relative to baseline (p<0.0001). CONCLUSIONS: This study describes a new methodology that permits the comprehensive assessment of retinal arteriolar vascular reactivity in response to a sustained and stable hypercapnic stimulus. Retinal arteriolar diameter, blood velocity and blood flow increased significantly in response to a hypercapnic provocation in young, healthy subjects. 相似文献
64.
Angiotensin-converting enzyme inhibitors (ACEi) provide renoprotection. A low sodium diet enhances their efficacy. However, the added effect of sodium restriction on proteinuria and blood pressure is not invariably associated with better preservation of renal morphology, suggesting that the combination of ACEi with a low sodium diet can elicit renal structural abnormalities. To test this hypothesis, the effects of ACEi in combination with a control (CS) or a low sodium (LS) diet were investigated in healthy rats and in adriamycin nephrotic rats. After 3 weeks of treatment, rats were sacrificed and kidneys examined for renal structural abnormalities. In healthy rats, ACEi reduced blood pressure: the fall in blood pressure was significantly greater in the ACEi/LS group. Renal morphology was normal in the ACEi/CS group but severe interstitial damage was found in the ACEi/LS group. This was associated with increased interstitial macrophage influx and up-regulation of osteopontin, alpha-smooth muscle actin, and collagen III expression. In addition, ACEi/LS induced an increase in the total medial area of afferent arterioles. In nephrotic rats, ACEi/LS reduced both blood pressure and proteinuria, whereas only blood pressure was reduced in the ACEi/CS group. Mild interstitial damage was present in the ACEi/CS group but, strikingly, pronounced tubulo-interstitial abnormalities occurred in the ACEi/LS group, similar to those seen in ACEi/LS healthy rats, with similar changes in afferent arteriolar walls. In conclusion, the combination of ACEi/LS elicits pronounced renal interstitial abnormalities in healthy and nephrotic rats, despite a significant reduction of proteinuria in the latter. Considering their occurrence in healthy rats, these renal adverse effects cannot be due to specific characteristics of adriamycin nephrosis. Further studies should elucidate the mechanisms underlying these observations and their impact on long-term renoprotection. 相似文献
65.
Birgitte L. Justesen Paresh Mistry Nish Chaturvedi Simon A. Thom Nicholas Witt Dennis Köhler Alun D. Hughes Anne Katrin Sjølie 《Acta ophthalmologica. Supplement》2010,88(4):453-457
Purpose: Diabetes has adverse effects on the retinal microvasculature. The purpose of this study was to compare the effects of inhalation of hypoxic, hyperoxic and normoxic–hypercapnic gas mixtures on retinal vessel diameter in people with and without diabetes. Methods: Sixty‐one participants (aged 24–50 years) 29 with (male : female ratio 2.6 : 1) and 32 without (male : female ratio 0.7 : 1) diabetes, inhaled hypoxic, hyperoxic and normoxic–hypercapnic gas mixtures for 3–5 mins. The diameters of arterioles and venules were measured using digital retinal images taken before and after gas inhalation. Results: There was no significant difference in the diameters of arterioles and venules prior to gas inhalation in people with and without diabetes. Inhalation of the hyperoxic gas mixture caused a statistically significant decrease in arteriolar and venular diameters without altering mean arterial pressure significantly. Arteriolar vasoconstriction in response to the hyperoxic gas mixture was significantly reduced in people with diabetes (3.95% versus 7.75%; p = 0.04), but venular vasoconstriction did not differ significantly. A hypoxic gas mixture caused increased arteriolar and venular diameter and a normoxic–hypercapnic gas mixture had no significant effect on vessel diameter. Responses to hypoxic and normoxic–hypercapnic gas did not differ significantly between diabetes and non‐diabetes subjects. Conclusions: Type 1 diabetes impairs retinal arteriolar responses to hyperoxia. Abnormalities in retinal arteriolar reactivity in response to oxygen may play a role in the development of diabetic retinopathy and this technique may represent a simple means of identifying early abnormalities in the reactivity of retinal arterioles in diabetes. 相似文献
66.
Lisa M. Harrison-Bernard Pamela K. Carmines 《Clinical and experimental pharmacology & physiology》1995,22(10):732-738
1. Experiments were designed to evaluate the hypothesis that cyclo-oxygenase products modulate the influence of angiotensin II (AII) on the renal juxtamedullary microvasculature of enalaprilat-treated rats. 2. The in vitro blood-perfused juxtamedullary nephron technique was utilized to provide access to afferent arterioles, efferent arterioles and descending vasa recta located in the outer stripe of the outer medulla. 3. Baseline afferent arteriolar diameter was 20.8 ± 1.9 μm in kidneys subjected to cyclo-oxygenase blockade (1μmol/L piroxicam), a value significantly lower than that observed in untreated kidneys (26.1 ± 1.0 μm). Baseline diameters of efferent arterioles and outer medullary descending vasa recta did not differ between untreated and piroxicam-treated groups. 4. Topical application of 1 nmol/L AII reduced blood flow through outer medullary descending vasa recta by 22 ± 6% in untreated kidneys and by 24 ± 7% in piroxicam-treated kidneys. 5. In untreated kidneys, AII (0.01–100nmol/L) produced concentration-dependent afferent and efferent arteriolar constrictor responses of similar magnitudes. Neither afferent nor efferent arteriolar AII responsiveness was significantly altered in piroxicam-treated kidneys, although afferent responses exceeded efferent responses at AII concentrations ≥ 10 nmol/L. 6. We conclude that endogenous cyclo-oxygenase products exert a vasodilator influence on juxtamedullary afferent arterioles under baseline conditions. Although cyclo-oxygenase inhibition had little effect on juxtamedullary microvascular responses to AII, the response to high AII concentrations may be modulated by cyclo-oxygenase products in a manner which delicately alters the relative influence of the peptide on pre- vs postglomerular resistances. 相似文献
67.
A. G. Zakharov L. S. Ivanov E. V. Khmelevskii V. K. Bozhenko A. M. Shishkin 《Bulletin of experimental biology and medicine》1994,117(3):277-280
The duration and amplitude of pressor reactions of AP to intravenous injection of norepinephrine remain unchanged 1, 3 and
5–6 days after irradiation. The duration of norepinephrine-induced changes in the diameter of arterioles of the thumb extensor
muscle proper and the linear blood flow rate in them is decreased in irradiated animals.
Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 117, N
o
3, pp. 274–277, March, 1994 相似文献
68.
J. H. Vial A. C. Yong G. W. Boyd 《Clinical and experimental pharmacology & physiology》1983,10(3):335-339
Structural changes in resistance vessels were studied by (a) hindquarter perfusion; and (b) planimetry of cross-sections of renal arterioles in uninephrectomized rats treated for 10 weeks with saline and either DOCA (deoxycorticosterone acetate), DOCA plus hydrallazine, vehicle plus hydrallazine or vehicle only. DOCA-treated rats developed hypertension and structural change. Addition of hydrallazine prevented both hypertension and the development of structural change. Structural arteriolar change in DOCA/salt hypertension is related to the high blood pressure or a closely associated factor rather than some other effect of DOCA. 相似文献
69.
Integrins and regulation of the microcirculation: from arterioles to molecular studies using atomic force microscopy 总被引:3,自引:0,他引:3
Martinez-Lemus LA Sun Z Trache A Trzciakowski JP Meininger GA 《Microcirculation (New York, N.Y. : 1994)》2005,12(1):99-112
Integrins are an important class of receptors for extracellular matrix proteins that can mediate both force transmission, by virtue of their connections with the cell matrix and cytoskeleton; and signal transduction, resulting from the assemblages of signaling proteins that associate with focal contacts. Consequently, integrins have been proposed to be the mechanosensor in vascular smooth muscle and endothelial cells and to play a central role in mechanotransduction. In this regard, mechanical force is an important stimulus for many vascular functions, including contractile and relaxation processes,proliferation, migration, attachment, and cell phenotype determination. Collectively, these functions define physiological properties of the vasculature such as control of blood flow, capillary pressure,permeability, and peripheral vascular resistance, and play a role in pathophysiological processes like hypertension, diabetes, and arteriosclerosis. Our knowledge concerning how integrins sense and transduce physical forces into cellular signals and which integrins are involved is incomplete. Compared to other cell surface receptors, integrins have a relatively low affinity for their binding sites on the extracellular matrix and their affinity can be regulated. These characteristics of integrin-ligand interaction may facilitate dynamic processes such as cell migration, cell remodeling, and contractile activation in response to external forces. Important questions remain concerning the nature and origin of integrin-mediated signaling in the vascular wall. 相似文献
70.
This paper presents a mathematical model of cerebrovascular regulation, in which emphasis is given to the role of tissue hypoxia on cerebral blood flow (CBF). In the model, three different mechanisms are assumed to work on smooth muscle tension at the level of large and small pial arteries: CO2reactivity, tissue hypoxia, and a third mechanism necessary to provide good reproduction of autoregulation to cerebral perfusion pressure (CPP) changes. Using a single set of parameters for the mechanism gains, assigned via a best fitting procedure, the model is able to reproduce the pattern of pial artery caliber and CBF under a large variety of physiological stimuli, either acting separately (hypoxia, CPP changes, CO2 pressure changes) or in combination (hypercapnia+hypoxia; hypercapnia+hypotension). Furthermore, the model can explain the increase in CBF and the vasoconstriction of small pial arteries observed experimentally during hemodilution, ascribing it to the decrease in blood viscosity and to the antagonistic action of the flow-dependent mechanism (responsible for vasoconstriction) and of hypoxia (responsible for vasodilation). Finally, the interaction between hypoxia and intracranial pressure (ICP) has been analyzed. This interaction turns out quite complex, leading to different ICP time patterns depending on the status of the cerebrospinal fluid outflow pathways and of intracranial compliance. © 2001 Biomedical Engineering Society.
PAC01: 8719Uv, 8719Tt, 8719Ff, 8380Lz 相似文献