Terminal Arterioles Research Articles

MODELING COUPLED DIAMETER AND HEMODYNAMIC OSCILLATIONS IN ARTERIOLAR NETWORKS

Regulation of convective O2 supply to capillary beds in organs is accomplished by coordinated changes in upstream arteriolar diameter. To study this regulation system, in vivo experiments have been performed using a gas exchange chamber to sinusoidally oscillate the O2 environment at the surface of a rat skeletal muscle. Capillary hematocrit (H) changes were delayed by several seconds relative to changes in red cell velocity (V) and the delay varied with the animal suggesting geometry dependence. To assess how alterations in diameters led to observed hemodynamics, a computational model was developed that couples variations in network blood flow to conducted diameter changes. The model uses an arteriolar tree that was constructed based on measured data in rat skeletal muscle and a two‐phase (red cells and plasma) time‐dependent model of microvascular blood flow. The initial response to imposed surface O2 oscillations was simulated by applying diameter oscillations at the distal ends of selected terminal arterioles. The model was used to calculate hemodynamic oscillations in the network and, in particular, examine how the transit time for red cells in the network could lead to the observed delay in changes in H relative to those in V. Initial results show similarities to experimental observations, including decreases in hemodynamic response amplitude with increases in forcing frequency and a delay in H relative to V.

BKCa and KV channels modify remote Ca2+ responses to local depolarization in rat mesenteric arterioles

Conducted vasoconstriction plays an important role in determining microvascular resistance. The spread of depolarization along an arteriole occurs through cell‐cell coupling via gap junctions. The decay of conducted depolarization is characterized by the length constant λ, and depends on the membrane (rm) and junctional resistances (rj) as follows: λ=v(rm/rj). We hypothesized that this decay can be diminished by increasing rm through inhibition of K+ channels. We investigated this hypothesis in rat mesenteric terminal arterioles (<40 µm) by monitoring local and remote Ca2+ responses to localized delivery of 155 mM KCl. Ca2+ responses were recorded simultaneously at 6 positions along a short arteriolar segment and λ was estimated by non‐linear curve‐fitting. The KV channel blocker 4‐AP (1 mM) augmented the remote Ca2+ responses (λ increased from 296 ± 30 to 417 ± 64 µm; P=0.05, n=5). The BKCa channel blocker IbTx (100 nM) increased λ from 254 ± 37 to 343 ± 54 µm (P<0.01, n=6). Preconstriction of arterioles (norepinephrine + neuropeptide Y) increased λ from 289 ± 37 to 336 ± 40 µm (P<0.05; n=6), and subsequent addition of IbTx further increased λ to 425 ± 59 µm (P<0.01; n=6). BKCa, KV1.5, and KV2.1 channels were immuno‐localized to VSMC. These data are consistent with the idea that BKCa and KV channel expression modulates conduction of depolarization through an effect on smooth muscle rm in mesenteric arterioles.

Erratum

The Journal of PhysiologyVolume 587, Issue 6 p. 1367-1367 Free Access Erratum This article corrects the following: Multiple regulation by external ATP of nifedipine-insensitive, high voltage-activated Ca2+ current in guinea-pig mesenteric terminal arteriole Hiromitsu Morita, Thapaliya Sharada, Tadashi Takewaki, Yushi Ito, Ryuji Inoue, Volume 539Issue 3The Journal of Physiology pages: 805-816 First Published online: March 1, 2002 First published: 13 March 2009 https://doi.org/10.1113/jphysiol.2009.169714AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat The paper by Morita et al. (2002) contained an error in Fig. 5A. The figure should have appeared as follows. Reference Morita H, Sharada T, Takewaki T, Ito Y & Inoue R (2002). Multiple regulation by external ATP of nifedipine-insensitive, high voltage-activated Ca2+ current in guinea-pig mesenteric terminal arteriole. J Physiol 539, 805– 816. Volume587, Issue6March 2009Pages 1367-1367 ReferencesRelatedInformation

Is there a role for T-type Ca2+ channels in regulation of vasomotor tone in mesenteric arterioles?This article is part of a Special Issue on Information Transfer in the Microcirculation.

The largest peripheral blood pressure drop occurs in terminal arterioles (<40 microm lumen diameter). L-type voltage-dependent Ca2+ channels (VDCCs) are considered the primary pathway for Ca2+ influx during physiologic activation of vascular smooth muscle cells (VSMC). Recent evidence suggests that T-type VDCCs are expressed in renal afferent and efferent arterioles, mesenteric arterioles, and skeletal muscle arterioles. T-type channels are small-conductance, low voltage-activated, fast-inactivating channels. Thus, their role in supplying Ca2+ for contraction of VSMC has been disputed. However, T-type channels display non-inactivating window currents, which may play a role in sustained Ca2+ entry. Here, we review the possible role of T-type channels in vasomotor tone regulation in rat mesenteric terminal arterioles. The CaV3.1 channel was immunolocalized in VSMC, whereas the CaV3.2 channel was predominantly expressed in endothelial cells. Voltage-dependent Ca2+ entry was inhibited by the new specific T-type blockers R(-)-efonidipine and NNC 55-0396. The effect of NNC 55-0396 persisted in depolarized arterioles, suggesting an unusually high activation threshold of mesenteric T-type channels. T-type channels were not necessary for conduction of vasoconstriction, but appear to be important for local electromechanical coupling in VSMC. The first direct demonstration of endothelial T-type channels warrants new investigations of their role in vascular biology.

Thrombotic microangiopathy in pregnancy

Following the initial reports by Moschowitz in 1925 [ 1 Moschcowitz E An acute febrile pleiochromic anemia with hyaline thrombosis of the terminal arterioles and capillaries. Arch Int Med. 1925; 36: 89-98 Crossref Scopus (362) Google Scholar ] and by Baehr et al. in 1936 [ 2 Baehr G Klemperer P Schifrin A An acute febrile anemia and thrombocytopenic purpura with diffuse platelet thrombosis of capillaries and arterioles. Trans Assoc Am Phys. 1936; 51: 43-49 Google Scholar ], Singer [ 3 Singer K, Bornstein FP, Wile SA: Thrombotic thrombocytopenic purpura. Hemorrhagic diathesis with generalized platelet thromboses. Blood 1047;2:542–7. Google Scholar ] and Gasser [ 4 Gasser C Gautier C Steck A Siebenmann RE Oechslin R Hemolytic–uremic syndrome: bilateral necrosis of the renal cortex in acute acquired haemolytic anemia. Schweiz Med Wochenschchr. 1955; 85: 905-909 PubMed Google Scholar ] suggested the terms of “thrombotic thrombocytopenic purpura, TTP” and of “hemolytic uremic syndrome, HUS” to describe related disorders consisting of Coombs' negative hemolytic anemia, thrombocytopenia, and renal failure. TTP and HUS, commonly referred to as thrombotic microangiopathies (TMA), share features of microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and microvascular thrombotic lesions, and their clinical and pathologic features often overlap. However, TTP and HUS are to be considered different entities, which may both complicate the course of pregnancy and imitate more frequently occurring syndromes, like pre-eclampsia, acute fatty liver, HELLP and SLE in association with antiphospholipid antibodies [ 5 Sibai BM Imitators of severe preeclampsia. Obstet Gynecol. 2007; 109: 956-966 Crossref PubMed Scopus (116) Google Scholar ].

The subpleural pulmonary microvasculature in newborn yak (Bos grunniens)

Yak is a unique domestic animal of Qinghai-Tibetan Plateau. Its unique adaptability to the high altitude environment has been hypothesized due to special pulmonary microvasculature. However, the anatomical evidence is still less. The present study characterized the subpleural pulmonary microvascular architecture of newborn yak by vascular corrosion cast and the scanning electron microscopy. The results showed the dense vascular network occurred in subpleural area in newborn yak. Subpleural vascular network was found in most of observed areas, while the sparse vascular network crept onto the subpleural network in some fields of view. The subpleural microvessels and their branches made up of the subpleural microvascular network. According to the branching sequence of vessels, the subpleural arterioles could be divided into four grades: the arteriole, terminal arteriole, precapillary arteriole and capillary. The subpleural capillary network in the local area could be classified into three different forms, including sheetlike vascular network, wrinkled vascular network and weblike vascular network. It was the specific characteristics on the cast surface of the microvessels that was the adaptable peculiarities. Anastomoses were found between the pleural microvessels and the interlobular capillaries, or between the pleural microvessels and the subpleural capillaries, or between the interlobular capillaries and the subpleural capillaries. Therefore, there was significant difference on the subpleural pulmonary microvasculature between newborn yak and other adult mammals.

The Role of L- and T-Type Calcium Channels in Local and Remote Calcium Responses in Rat Mesenteric Terminal Arterioles

Background/Aims: The roles of intercellular communication and T-type versus L-type voltage-dependent Ca²⁺ channels (VDCCs) in conducted vasoconstriction to local KCl-induced depolarization were investigated in mesenteric arterioles. Methods: Ratiometric Ca²⁺ imaging (R) using Fura-PE3 with micro-ejection of depolarizing KCl solution and VDCC blockers, and immunohistochemical and RT-PCR techniques were applied to isolated rat mesenteric terminal arterioles (n = 71 from 47 rats; intraluminal diameter: 24 ± 1 μm; length: 550–700 μm). Results: Local application of KCl (at 0 μm) led to local (ΔR = 0.54) and remote (ΔR = 0.17 at 500 μm) increases in intracellular Ca²⁺. Remote Ca²⁺ responses were inhibited by the gap junction uncouplers carbenoxolone and palmitoleic acid. Ca_V1.2, Ca_V3.1 and Ca_V3.2 channels were immunolocalized in vascular smooth muscle cells and Ca_V3.2 in adjacent endothelial cells. Local and remote Ca²⁺ responses were inhibited by bath application of L- and T-type blockers [nifedipine, NNC 55-0396 and R(–)-efonidipine]. Remote Ca²⁺ responses (500 μm) were not affected by abolishing Ca²⁺ entry at an intermediate position on the arterioles (at 200–300 μm) using micro-application of VDCC blockers. Conclusion: Both L- and T-type channels mediate Ca²⁺ entry during conducted vasoconstriction to local KCl in mesenteric arterioles. However, these channels do not participate in the conduction process per se.

Liver Anatomy: Microcirculation of the Liver

Comprehension of the structural and functional characteristics of the hepatic microcirculation can help improve the design, planning, and practice of imaging-guided treatment for hepatic tumors and for portal vein embolization (PVE). The hepatic microcirculation derives dual blood supply from the portal vein and the hepatic artery. The terminal portal venules directly connect to the hepatic sinusoids, but the terminal hepatic arterioles connect to arterioportal communications before entering the sinusoids: the peribiliary plexus, the terminal arteriosinus twigs, the vasa vasorum on the portal vein, and the direct arterioportal anastomosis. These communications play important roles in the balance of blood perfusion to the liver parenchyma and in controlling the blood supply to hepatic tumors and the anticipated remnant liver (in cases of PVE). At the microcirculatory level, various embolic agents present different distribution patterns. To further our understanding, iodized oil has been found to pass into the portal vein after hepatic arterial administration through the peribiliary plexus and subsequently traverses the sinusoids to enter the lungs and then the systemic circulation. Ultimately, a thorough knowledge of the host environment at the microcirculatory level is essential in developing strategies for both tumor treatment and for inducing liver regeneration.

Autoimmune destruction of pericytes as the cause of diabetic retinopathy.

In diabetic retinopathy, collapse of the retinal vasculature is associated with loss of the pericytes. These are contractile cells that together with endothelial cells form the terminal arterioles of the retina. The cause of the loss of pericytes is not known. Recently, it has been discovered that type 1 diabetes is caused by forbidden clones of cytotoxic T lymphocytes, which destroy the insulin-making cells with exquisite specificity. In the light of this, I postulate that an antigenically-related forbidden clone of cytotoxic T lymphocytes selectively destroys the pericytes and that this is the cause of the vascular collapse of diabetic retinopathy. If this is so, the therapeutic implications are immense, involving a switch from ineffectual tight glycemic control to immunotherapy. This is already used as immunosuppression to prevent organ transplant rejection, and as the immune ablation and autologous bone marrow cell reconstitution that has saved the lives of patients with lethally-severe scleroderma. Once the pericyte surface auto-antigen for the T lymphocytes has been isolated, selective destruction of the pathogenic T lymphocytes would be possible by manufacture and use of cytotoxic auto-antigen complexes, which arrests progression of the retinopathy.

Severe Coagulopathy after 90Y Microsphere Administration: Resemblance to the Kasabach-Merritt Syndrome

bthe rehe le to . nw a the y, ARTERIAL administration of Yttrium 90 (Y) microspheres is increasingl being used for the treatment of p mary and metastatic hepatic mali nancies. This strategy takes advantag of the fact that tumors derive most their blood supply from the hepa arterial circulation. Both glass an resin microspheres have been used deliver large intrahepatic doses of Y. The microspheres have diameters 20–40 m and thus lodge in precap lary terminal arterioles, predom nantly at the periphery of tumor n ules (1). A typical microsphere activi vial consists of 1.2– 8 10 glass microspheres or 40 – 80 10 resin spheres. Y emits pure high-energ beta energy with a maximum range penetration of 11 m. Ninety-four p cent of the radiation is given within days (1,2). A complication with radioembol zation that is not uncommonly se

Expression of Inducible Nitric Oxide Synthase in Lungs of Broiler Chickens Following Intravenous Cellulose Microparticle Injection

Intravenous microparticle (MP) injection is a patented method used to select broilers with a robust pulmonary capacity and improved resistance to pulmonary hypertension syndrome (PHS, ascites). Injected MP become entrapped in the terminal pulmonary arterioles where they elicit an increase in pulmonary arterial pressure attributable to vascular occlusion and focal thrombocyte aggregation. Within 2 to 48 h postinjection perivascular mononuclear cell aggregates begin to form around MP-occluded vessels. Nitric oxide (NO) has been shown to modulate the pulmonary arterial pressure response to MP entrapment, but a role of NO during the more chronic (2 to 48 h) focal inflammatory response has not been evaluated. In this study we determined the time-course of inducible nitric oxide synthase (iNOS) expression in the lungs of MP-injected broilers from PHS-resistant (RES) and PHS-susceptible (SUS) lines. Four-week-old broilers (10 broilers/line per time point) were injected i.v. with a minimally lethal dose of MP, and the right lung was collected at 0 h (no MP) and 2, 24, and 48 h postinjection. Immunohistochemistry revealed that macrophage infiltration increased over time in both lines and was higher in the RES line than the SUS line (P<0.0001) at all time points. Nicotinamide adenine dinucleotide phosphate diaphorase staining showed nitric oxide synthase activity around MP-occluded vessels and in the perivascular mononuclear cell aggregates. Relative iNOS expression in lung tissue was examined by 2-step reverse transcription PCR. Lines differed in relative iNOS mRNA expression only at 24 h (P<0.001; RES > SUS line). For the RES line iNOS mRNA expression increased consistently from 0 to 48 h, but for the SUS line iNOS mRNA expression increased at 2 h, decreased to baseline at 24 h, and increased again by 48 h. The decline in iNOS expression in the SUS line between 2 and 24 h coincides with the interval when most of the MP-induced mortality occurs, which suggests that NO synthesized by iNOS may contribute to lower MP-induced mortality in the RES line when compared with the SUS line.

Modeling the hemodynamic response due to vasodilatory signals conducted upstream along the arteriolar tree

To study local regulation of convective O2 delivery, in vivo experiments were conducted using a gas chamber to oscillate the O2 environment at one surface of rat skeletal muscle. Intravital video microscopy enabled quantification of the hemodynamic (RBC velocity, V, and hematocrit, H) and O2 saturation responses in capillaries. To assess how changes in arteriolar diameters lead to the observed blood flow response, a model of the lower three levels of the arteriolar tree was constructed based on published data. Sinusoidal changes in vessel diameter were imposed at the distal end of one terminal arteriole, and the upstream conduction of these diameter changes was simulated. A quasi‐steady model of two‐phase (RBCs and plasma) blood flow was used to calculate time‐dependent hemodynamics in the network. For a range of forcing frequencies, conduction velocities (Vcond), and attenuation lengths, the ability of the system to control RBC supply in a terminal arteriole was studied. Attenuation lengths within the physiological range (2mm to 2cm) did not affect the flow response. Decreases in frequency and increases in Vcond increased the amplitude of the flow response. For a frequency of 0.025 Hz, varying Vcond from 10 μm/sec to 50 μm/sec increased the RBC supply response by 35%. Predicted changes in H and V showed qualitative agreement with experimental results. Supported by NIH HL‐089125, CIHR to CGE and DG, and NSERC to SJMM.

Last Word on Point:Counterpoint: There is/is not capillary recruitment in active skeletal muscle during exercise

TO THE EDITOR: The vigorous commentary on this debate underscores the importance of understanding muscle microvascular perfusion and its control.

A Highly Efficient Method to Differentiate Smooth Muscle Cells From Human Embryonic Stem Cells

To the Editor: The molecular mechanisms and the control of smooth muscle cell (SMC) differentiation have been extensively investigated because of its therapeutic potential.1 To date, different cell types have been used to study SMC differentiation, including a variety of mouse embryonic stem cells,2 adult stem cells,3,4 and others.5 Because several fundamental differences exist between mouse and human embryonic development,6 lack of a good model system to study human SMC differentiation has hampered the progress of translating SMC knowledge to novel clinical therapies. Human embryonic stem (hES) cells provide a valuable source of cells for studying human cell differentiation and developing therapeutic potentials in regenerative medicine. Since the initial report describing the derivation of hES cells,7 a variety of studies have established in vitro differentiation strategies to several lineages. Recently, it has been demonstrated that vascular progenitors derived from hES cells could be differentiated into endothelial cells and SMCs by endothelial …

Structural changes of microvessels in the extensor digitorum longus muscle of the aged rat

We examined the structural changes of microvessels (arterioles, capillaries, and venules) in the extensor digitorum longus muscle of the aged (27 months) rat. Muscle bundles in the aged muscle almost consisted of medium-sized muscle fibers which were peculiar in the aged EDL muscle. However, microvessels in and around these muscle bundles varied in shape. Degenerating capillaries and scaffolds of basal laminae remaining after necrosis of preexisting capillaries were frequently observed around these medium-sized muscle fibers. In addition, the vascular lumen was often very narrow or irregular slit-like. In terminal and precapillary arterioles, the endothelium and smooth muscle cells showed a constricted appearance and their vascular lumen was often irregular slit-like, probably playing an important role in intercepting the blood flow into the disrupted capillaries. Moreover, some venules had the slit-like vascular lumen, sawtooth-like endothelium and thick or multilayered basal laminae, and occasional erythrocytes were found outside the endothelium, probably indicating that these venules are in the course of regeneration. These findings suggest that in addition to the frequent destruction of capillaries, the structural changes of arterioles and venules may be involved in remodeling the microvasculature of the muscle bundles after maturation of regenerating muscle fibers.

Expression and functional role of L‐type and T‐type calcium channels in conducted calcium responses to local KCl application in rat mesenteric terminal arterioles

Expression and functional role of L‐type and T‐type calcium channels in conducted calcium responses to local KCl application in rat mesenteric terminal arterioles

Quantitative assessments of morphological and functional properties of biological trees based on their fractal nature

The branching systems in our body (vascular and bronchial trees) and those in the environment (plant trees and river systems) are characterized by a fractal nature: the self-similarity in the bifurcation pattern. They increase their branch density toward terminals according to a power function with the exponent called fractal dimension (D). From a stochastic model based-on this feature, we formulated the fractal-based integrals to calculate such morphological parameters as aggregated branch length, surface area, and content volume for any given range of radius (r). It was followed by the derivation of branch number and cross-sectional area, by virtue of the logarithmic sectioning of the r axis and of the branch radius-length relation also given by a power function of r with an exponent (alpha). These derivatives allowed us to quantify various hydrodynamic parameters of vascular and bronchial trees as fluid conduit systems, including the individual branch flow rate, mean flow velocity, wall shear rate and stress, internal pressure, and circumferential tension. The validity of these expressions was verified by comparing the outcomes with actual data measured in vivo in the vascular beds. From additional analyses of the terminal branch number, we found a simple equation relating the exponent (m) of the empirical power law (Murray's so-called cube law) to the other exponents as (m=D+alpha). Finally, allometric studies of mammalian vascular trees revealed uniform and scale-independent distributions of terminal arterioles in organs, which afforded an infarct index, reflecting the severity of tissue damage following arterial infarction.

Application of local heat induces capillary recruitment in the Pallid bat wing

Skin blood flow increases in response to local heat due to sensorineural and nitric oxide (NO)-mediated dilation. It has been previously demonstrated that arteriolar dilation is inhibited with NO synthase (NOS) blockade. Flow, nonetheless, increases with local heat. This implies that the previously unexamined nonarteriolar responses play a significant role in modulating flow. We thus hypothesized that local heating induces capillary recruitment. We heated a portion (3 cm2) of the Pallid bat wing from 25 degrees C to 37 degrees C for 20 min, and measured changes in terminal feed arteriole (approximately 25 microm) diameter and blood velocity to calculate blood flow (n = 8). Arteriolar dilation was reduced with NOS and sensorineural blockade using a 1% (wt/vol) NG-nitro-L-arginine methyl ester (L-NAME) and 2% (wt/vol) lidocaine solution (n = 8). We also measured changes in the number of perfused capillaries, and the time precapillary sphincters were open with (n = 8) and without (n = 8) NOS plus sensorineural blockade. With heat, the total number of perfused capillaries increased 92.7 +/- 17.9% (P = 0.011), and a similar increase occurred despite NOS plus sensorineural blockade 114.4 +/- 30.0% (P = 0.014). Blockade eliminated arteriolar dilation (-4.5 +/- 2.1%). With heat, the percent time precapillary sphincters remained open increased 32.3 +/- 6.0% (P = 0.0006), and this increase occurred despite NOS plus sensorineural blockade (34.1 +/- 5.8%, P = 0.0004). With heat, arteriolar blood flow increased (187.2 +/- 28.5%, P = 0.00003), which was significantly attenuated with NOS plus sensorineural blockade (88.6 +/- 37.2%, P = 0.04). Thus, capillary recruitment is a fundamental microvascular response to local heat, independent of arteriolar dilation and the well-documented sensorineural and NOS mechanisms mediating the response to local heat.

DISTRIBUTION OF CONNEXINS IN THE MICROCIRCULATION

Longitudinal intercellular communication along the arteriolar endothelium has been shown be a critical part of the regulation of microvascular function. Such communication is mediated in large part by gap junctions, which are composed of 3 connexin proteins (Cx) 37, 40, 43. To date, there has been no systematic exploration of the connexins expressed in the microvascular endothelium. We have used the Olympus confocal microscope to examine frozen sections and enface whole mounts from unperfused mouse cremaster muscles using antibodies directed toward these proteins. In unperfused arteriolar microvessels all three connexins are expressed at the endothelial cell junctions. Cx43 is also detectable in a perinuclear location. In the terminal arterioles Cx40 and 37 expression is reduced and in the capillaries expression of both becomes patchy and in many capillaries undetectable toward the venous end. Cx43 is robustly expressed throughout the capillaries. All of the 3 connexin proteins are sharply reduced in the venules. Where expressed, all three proteins may be present singly in individual plaques or co-localized with other connexins. Both Cx40 and Cx43 are positioned within the IEL at locations favorable for the formation of the myoendothelial junction. Supported by USPHS NIH Grant #53318

Artérite à cellules géantes révélée par des nodules cotonneux

Giant cell arteritis is the most common vasculitis in the elderly. Visual loss is established as the most dreaded and irreversible complication of the disease, which makes giant cell arteritis an ophthalmic emergency. It is important to recognize its various ocular manifestations; isolated cotton wool spots are one of them. We describe a patient with constitutional symptoms and mild visual loss who was found to have giant cell arteritis. The ophthalmic examination was significant for only isolated cotton-wool spots. A delay in arm-to-retina circulation time was demonstrated by fluorescein angiography. Prompt treatment with corticosteroids led to preservation of vision and uneventful resolution of the cotton-wool spots. Common ophthalmologic presentations include anterior ischemic optic neuropathy or choroidal ischemia when short posterior ciliary arteries are involved, and central retinal artery occlusion. Retinal ischemia has also been recognized as a possible manifestation. Because the disease concerns medium-size and larger arteries, it cannot involve terminal retinal arterioles to produce cotton-wool spots. These are probably caused by platelet microembolization from the partially thrombosed regional arteries. Isolated cotton-wool spots can be an early ophthalmoscopic finding in giant cell arteritis and precede severe irreversible visual loss. Their detection is essential because it allows the ophthalmologist to establish a prompt treatment and preserve vision.