Dynamic focal retinal arteriolar vasospasm in migraine.

A 48-year-old man presented following an episode of sudden onset simultaneous inferior altitudinal visual loss in his left eye and visual obscuration with shimmering in the inferonasal quadrant of the right eye. Clinical examination demonstrated left superior hemiretinal artery occlusion and an area of focal dynamic spasm along the right superior temporal branch retinal artery, the arteriolar spastic cycle was about 2 sec in duration. Hematological (including complete blood count, thrombophilia screen, vasculitic screen and serum magnesium), carotid, and cardiac investigations were normal. He was given acetazolamide 500 mg orally, timolol maleate 0.5% eye drops once daily and sublingual amyl-nitrate 0.8 mg, and maintained on felodipine 10 mg/day and aspirin 100 mg/day. The area of focal arteriolar spasm in the right eye resolved over two months. To our knowledge there are no prior reports of photographically documented dynamic focal retinal vascular spasm on a MEDLINE and PUBMED search.

Sildenafil preserves diastolic relaxation after reduction by L-NAME and increases phosphodiesterase-5 in the intercalated discs of cardiac myocytes and arterioles

OBJECTIVES: We investigated the influence of sildenafil on cardiac contractility and diastolic relaxation and examined the distribution of phosphodiesterase-5 in the hearts of hypertensive rats that were treated with by NG-nitro-L-arginine methyl ester (L-NAME). METHODS: Male Wistar rats were treated with L-NAME and/or sildenafil for eight weeks. The Langendorff method was used to examine the effects of sildenafil on cardiac contractility and diastolic relaxation. The presence and location of phosphodiesterase-5 and phosphodiesterase-3 were assessed by immunohistochemistry, and cGMP plasma levels were measured by ELISA. RESULTS: In isolated hearts, sildenafil prevented the reduction of diastolic relaxation (dP/dt) that was induced by L-NAME. In addition, phosphodiesterase-5 immunoreactivity was localized in the intercalated discs between the myocardial cells. The staining intensity was reduced by L-NAME, and sildenafil treatment abolished this reduction. Consistent with these results, the plasma levels of cGMP were decreased in the L-NAME-treated rats but not in rats that were treated with L-NAME + sildenafil. CONCLUSION: The sildenafil-induced attenuation of the deleterious hemodynamic and cardiac morphological effects of L-NAME in cardiac myocytes is mediated (at least in part) by the inhibition of phosphodiesterase-5.

Vimentin and laminin are altered on cheek pouch microvessels of streptozotocin-induced diabetic hamsters

OBJECTIVE: Normal endothelial cells respond to shear stress by elongating and aligning in the direction of fluid flow. Hyperglycemia impairs this response and contributes to microvascular complications, which result in deleterious effects to the endothelium. This work aimed to evaluate cheek pouch microvessel morphological characteristics, reactivity, permeability, and expression of cytoskeleton and extracellular matrix components in hamsters after the induction of diabetes with streptozotocin. METHODS: Syrian golden hamsters (90-130 g) were injected with streptozotocin (50 mg/kg, i.p.) or vehicle either 6 (the diabetes mellitus 6 group) or 15 (the diabetes mellitus 15 group) days before the experiment. Vascular dimensions and density per area of vessels were determined by morphometric and stereological measurements. Changes in blood flow were measured in response to acetylcholine, and plasma extravasation was measured by the number of leakage sites. Actin, talin, α-smooth muscle actin, vimentin, type IV collagen, and laminin were detected by immunohistochemistry and assessed through a semiquantitative scoring system. RESULTS: There were no major alterations in the lumen, wall diameters, or densities of the examined vessels. Likewise, vascular reactivity and permeability were not altered by diabetes. The arterioles demonstrated increased immunoreactivity to vimentin and laminin in the diabetes mellitus 6 and diabetes mellitus 15 groups. DISCUSSION: Antibodies against laminin and vimentin inhibit branching morphogenesis in vitro. Therefore, laminin and vimentin participating in the structure of the focal adhesion may play a role in angiogenesis. CONCLUSIONS: Our results indicated the existence of changes related to cell-matrix interactions, which may contribute to the pathological remodeling that was already underway one week after induction of experimental diabetes.

Cardiopatia isquêmica com artérias coronárias epicárdicas pérvias: provável espasmo das artérias coronárias; relato de caso / Ischemic cardiopathy with pervious coronary epicardial coronary arteries: probable apasm of the coronary arteries; a case report

Os autores relatam o caso de uma paciente de 33 anos de idade, que apresentou um quadro de dor precordial em repouso, com remissäo espontânea. A cinecoronariografia realizada na ocasiäo revelou vasos absolutamente normais, assim como a movimentaçäo do ventrículo esquerdo. Sessenta e três dias após o sintoma inicial, a doente voltou a referir dor precordial, agora persistente, e que evoluiu para o infarto do miocárdio. A coronariografia demonstrou obstruçäo total da artéria descendente anterior e area discinética em regiäo anterior do ventrículo esquerdo. Os autores interpretam o quadro como decorrente de espasmo coronariano, salientando que o fenômeno espático pode ser persistente, acometer segmentos relativamente extensos dos vasos e atingir tal magnitude que suplante a açäo de drogas coronariodilatadoras, representando um potencial mecanismo de isquemia miocárdica

Effects of hypertonic NaCl solution on the hamster cheek pouch microcirculation in normo- and hypovolemia

The aim of this study was evaluate the effects of a single, 10 min, intravenous infusion of a hyperonic NaCl solution [2.400 mOsm/l; infused volume 0.35 ñ 0.03 ml (SEM) on the hamster cheek pouch microcirculation during normovolemia and after acute bleeding to a hypotension level of about 40 mmHg. Upon bleeding, the arterial pressure dropped to 39 µ 1 mmHg, arterioles > 40 -m constricted 12 ñ 3% (from their control value), arterioles < 40 µm dilated 6 ñ 2%, venules stayed largely unchanged, while RBC velocity and volume flow decreased 57 ñ 7% in all vessels. Durign the subsequent hypertonic NaCl infusion, the arterial pressure increased rapidly to a new steady state level of 66 ñ 3 mmHg. After the infusion, the large arterioles stayed constricted 11 ñ 1% and the small arterioles dilated 7 ñ 1% for a 1-h observation period. The venules constricted iniatially by 6 ñ 2% and returned to control diameter in 30-40 min. RBC velocity and calculated volume flow returned to the pre-hemorrhage cotrol values in about 10 min for the arterioles and in 40 min for the venules. An identical hypertonic infusion given to normovolemic hamsters caused no significant alterations of the measured variables

Extracellular and membranal bound calcium on the contraction of mesenteric arteries of the rat

Después de perfundir la arteria mesentérica anterior de la rata y sus ramas con una solución de Tyrode sin Ca, que agora el Ca extracelular, es posible provocar contracciones mediante la inyección "en bolo" de Noradrenalina (NA), Adrenalina (AD), Serotonina (ST) y Vasopresina (VP). La infusión continua de NA produce un efecto vasoconstrictor sostenido cuando el líquido intersticial contiene Ca, pero declina cuando ést falta. Todos a la solución perfusora privada de Ca. Estos no se recuperan, perfundiendo una solución sin Ca, pero rápidamente si ésta lo contiene. Tanto el La3+ como el EDTA no ingresan a la célular muscular, sino que desplazan al Ca fijado al plasmalema, que pone en marcha el mecanismo contráctil. Cuando éste falta, los agonistas carecen del Ca que lleva su mensaje al interior de la célula y son, por lo tanto, inefectivos. Este Ca mensajero membranal es reemplazado por el Ca iónico extracelular, pero no por el Ca intracelular. Esta interpretación permite explicar el "efecto dual" de la NA, que postula que los efectos breves o fásicos se deberían a la liberación de Ca intracelular, mientras que los sostenidos o tónicos al ingreso de Ca extracelular. Cuando el medio no contiene Ca, los agonistas son capaces de provocar vasoconstricción a partir de Ca fijado a la membrana celular. Como éste no es repuesto, si el medio carece de Ca, las respuestas vasoconstrictoras delcina y acaban agotándose

Cardiopatia isquêmica com artérias coronárias epicárdicas pérvias: a vasomotricidade das arteríolas do coraçäo / Ischemic heart disease with patent epicardial coronary arteries: the vasomotricity of the heart arterioles

Foi estudada, em animal de experimentaçäo (cäo), a vasomotricidade das arteríolas intramiocárdicas, após a administraçäo de ergotrate (maleato de ergometrina). Foi avaliada a resposta vasomotora da rede arterial coronária, através de moldes plásticos e pelo exame histológico e mesoscópico, de cortes corados pela hematoxilina-eosina, tricrômico de Masson, Weighert-Moure e azo-carmin. Verificou-se uma intensa constriçäo arteriolar, nos coraçöes previamente injetados com ergotrate, caracterizada pelo desaparecimento da "penugem", que representa os pequenos vasos nos moldes plásticos e pela reduçäo do lume vascular e espessamento da parede arteriolar, nos exames histológicos. Concluiu-se que a vasoconstriçäo arteriolar, expressa nos diferentes procedimentos de estudo, pode traduzir a potencialidade dos pequenos vasos intramiocárdicos, de produzir espasmo vascular em condiçöes patológicas específicas, e representarem mecanismo eventual de isquemia miocárdica

Efeitos do diazóxido sobre a pressäo intracraniana e o diâmetro dos vasos piais: estudo experimental em cäes / Effects of the diazoxide in intracranial pressure and the diameter of pial vessels: experimental study in dogs

Várias drogas têm sido utilizadas em neurocirurgia para evitar o aumento da pressäo intracraniana e o espasmo de vasos cerebrais. O diazóxido, um agente hipotensor de açäo direta sobre a musculatura lisa dos vasos ainda näo foi estudado. Dessa maneira resolvemos pesquisar os efeitos dessa droga, administrada por via venosa (3 mg.kg-1) sobre a pressäo intracraniana e o diâmetro dos vasos piais em 16 cäes. Os animais foram divididos em dois grupos de 8. No grupo 1 foi estudado o efeito do diazóxido sobre a pressäo intracraniana, medida através de uma agulha colocada na cisterna magna, ligada a um transdutor e a um fisiógrafo. Ao mesmo tempo se registrava a pressäo arterial e se media o pH, PaO2 e PaCO2, nos tempos 1 (antes) 2,3 e 4 (1,15 e 30 min) após a injeçäo da droga. No grupo 2, media-se o diâmetro de arteríolas e vênulas piais através de uma perfuraçäo na regiäo craniana parieto-temporal e fotografia dos vasos piais nos mesmos tempos empregados no grupo anterior. Eram realizadas também medidas da pressäo arterial e dos gases sangüíneos. Observou-se que o diazóxido determina hipotensäo arterial logo após a sua injeçäo venosa, que persiste por 30 minutos. Ao mesmo tempo induz aumento significante do diâmetro das arteríolas piais. Näo há variaçäo significante da pressäo intracraniana e das vênulas piais. Esses resultados sugerem a possibilidade do uso dessa droga na profilaxia e no tratamento de espasmos vasculares cerebrais