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PubMed1991

Development of inner ear vessels. A scanning electron microscopic study.

The development of the inner ear vessels of guinea pigs were studied by SEM. Employing 32- to 55-gestational-day-old guinea pig embryos, corrosion casts of inner ear blood vessels were prepared using Mercox resin and then observed by scanning electron microscopy. Between the 35th and 40th gestational days, the vascular structure of the vestibule was sufficiently developed, but the capillary network in the wall of the cochlea remained immature. Thus, in the guinea pig, the development of the vestibular structure precedes the development of the cochlear vessels. Moreover, at both sites, the density of the embryonic blood vessels was high, and the vessels were believed to transport a large blood flow. From about the 40th day of gestation, the coiled vessels and the capillary network in the lateral wall of the cochlea underwent rapid development, and the vascular structure in both the vestibule and cochlea was nearly complete by the time of birth.

Animals↗
PubMed1991

Comparison of lectin reactivity in the vessel beds of the rat eye.

The capillary beds of the eye are lined by two types of endothelia, fenestrated in the choriocapillaris and ciliary body, and continuous in the retina and iris. In this study, we wished to find a marker for each of these types of vessel beds using lectin histochemistry. Sections of glutaraldehyde fixed rat eyes embedded in epoxy resin were extracted with sodium ethoxide and rehydrated. Binding of 15 different lectins was visualized using the avidin-biotin peroxidase technique. We found WGA, WGA-s, LFA and PHA-E to strongly bind retinal vessels. In addition to the above lectins, iris vessels bound GSL-I. Choriocapillaris reacted variably only with WGA and not at all with other lectins tested. Vessels of ciliary body processes did not react with any lectin studied. The less fenestrated vessels of the base of the ciliary process bound lectins similar to the retina. We speculate that the differential lectin staining of the various vessel beds of the eye may reflect the degree of fenestration of the endothelium. This reactivity may be influenced by variations in the surrounding milieu including cells and extracellular matrix.

Animals↗
PubMed1984

Norepinephrine turnover in the heart and blood vessels of rats subjected to bilateral renal infarction.

The total norepinephrine (NE) content, the uptake of [3H]NE, the turnover rate and the synthesis rate of the neurotransmitter at the heart and blood vessels have been studied during the development of hypertension in rats subjected to bilateral renal infarction. Normal and sham-operated rats were used as controls. Fifty percent of the rats with renal infarction became hypertensive. The weight of the hearts and blood vessels of the experimental animals was significantly increased 15 days after renal infarction. Changes were greater in hypertensive animals. NE concentration in the heart was slightly decreased without achieving statistical significance, while total NE content was unchanged. In the artery wall NE concentration was significantly decreased in normotensive and hypertensive operated rats. [3H]NE uptake in the heart and blood vessels was similar in experimental and control animals. In relation to NE turnover, in both the heart and blood vessels, normal and sham-operated animals behaved as one population while normotensive and hypertensive rats behaved as another population. The rate constant of NE turnover was increased in both tissues of operated experimental animals without achieving statistical significance in the case of the heart. NE synthesis rate was unchanged in the cardiac muscle but was significantly increased in the blood vessels of operated animals. Present data indicate that results describing NE dynamics in the heart cannot be extrapolated for the blood vessels level; on the other hand changes in the neurotransmitter do not seem to be related to the development of high blood pressure after renal infarction in the rat.

Animals↗
PubMed1989

Axon regeneration through blood vessel allografts after cyclosporine treatment.

The present study describes the usefulness of blood vessel allografts to repair gaps in rat peripheral nerve after immunosuppression with cyclosporine. Isogeneic strains of rats with known histoincompatibility were used for this study. A 10-mm gap was created in the peroneal nerve of host Fischer rats. The gap was bridged by a 12-mm section of internal carotid artery removed from a Buffalo strain of rat. The host rats were divided into two groups. One group received no immunosuppression, whereas the other group was treated with cyclosporine. Untreated control rats immunologically rejected the allografted vessels and were unable to support host axonal regeneration through them. On the other hand, in cyclosporine-treated rats the allografted vessels survived. The regenerating host axons reorganized to form a functional nerve within the vessel conduit. The regenerated axons persisted even after rejection of the allografted vessel caused by cessation of immunotherapy. These results show that blood vessel allografts can serve as an effective conduit for reorganization of regenerated nerves and can bridge gaps in peripheral nerves.

Animals↗
PubMed1998

Hemodynamic effects of the geometric dimensions of graft vessels in coronary artery bypass graft models.

The objectives of this investigation are to evaluate the rheologic properties in atherosclerotic disease treated with the various coronary artery bypass graft (CABG) models by numerical analysis, we used four different CABG models for the assessment of spatial fluctuation in wall shear stress, pressure variation and mass flow rate with Carreau model and Navier-Stokes equation. Wall shear stress was higher in a naturally tapered model (model 1) and a constant (non-tapered) diameter of the graft vessel the same as the distal LAD (model 4) than in others. Pressure variation along the native coronary artery and graft vessels was higher in a model 4, model 1 than in a reverse tapering model (model 2) and a constant diameter of the graft vessel the same as the proximal LAD (model 3). The mass flow rate of the distal part (kg/sec,.m(o)) was the highest in model 3. This study suggests that in vitro spatial simulation following CABG revealed that small caliber or tapered graft vessels have adverse hemodynamic effects on the native and graft vessels. By this technique it is possible to simulate the optimal distribution of local hemodynamic variables in patients treated with CABG, also to minimize the degeneration of graft vessel.

Computer Simulation↗
PubMed1989

[Correlation of vessel invasion and bone metastasis in prostatic adenocarcinoma. A clinico-pathological and immunohistochemical study of 33 cases of total prostatectomy].

Thirty three cases of prostatic adenocarcinoma treated by total perineal prostatectomy were studied clinicopathologically and immunohistochemically. There were 17 patients with clinical stage B, 12 with stage C and 8 with stage D. Interrelationship of tumor grade, surgical local tumor extent, vessel invasion, perineural invasion and bone metastasis was examined. For the identification of the vessel invasion, Ulex europaeus agglutinin 1 was adopted immunohistochemically. Tumor grade and local tumor extent were respectively correlated with bone metastasis. Vessel invasion was correlated with local tumor extent. Eight of 18 cases (44%) with vessel invasion and none of 15 cases without vessel invasion had bone metastasis. Although correlated with grade, perineural invasion had no significant effect on bone metastasis. The investigation of tumor staining used by monoclonal antibody for prostatic acid phosphatase (PSAP) disclosed that negative stained cases were associated with lower grade tumors and that one of 14 positive stained cases (7%) and 7 of 19 negative stained cases (36%) had bone metastasis. We concluded that vessel invasion may be a new prognostic pathological parameter and that monoclonal PSAP staining is also a useful method to predict malignant potential of prostatic cancer.

Acid Phosphatase↗
PubMed2002

[Effect of sharpening filter on vessel diameter measured by quantitative coronary arteriography].

At cardiac catheterization, analog images obtained using cinefilm are translated into digital images, and images appearing on the CRT are filtered by a sharpen filter. We investigated the effect of the sharpening filter on vessel diameter as measured by quantitative coronary arteriography. We acquired images of a vessel phantom filled with contrast material using an X-ray image intensifier. Vessel diameters measured by quantitative coronary arteriography were 1 mm, 1.5 mm, 2 mm, 3 mm, 4 mm, and 6 mm. Results showed that vessel diameters were decreased when the sharpening filter was used and that more intense filtering decreased the measured diameter further. When the diameter of the vessel phantom was less than 4 mm, the diameter was smaller and the ratio of decrease was larger. Vessel diameters of 2 mm, 3 mm, 4 mm, and 6 mm measured a maximum of 2.9 smaller, while those of 1 mm and 1.5 mm measured a maximum of 9.2 smaller.

Coronary Angiography↗
PubMed1999

Angiotensin II-induced constrictions are masked by bovine retinal vessels.

PURPOSE: To unmask the vasoconstricting effect of angiotensin II (Ang II) on retinal smooth muscle by studying its interaction with endothelium-derived paracrine substances. This study focused specifically on determining the changes in vascular diameter and the release of endothelial-derived vasodilators, nitric oxide (NO) and prostaglandin (PG) I2, from isolated retinal microvessels. METHODS: Bovine retinal central artery and vein were cannulated, and arterioles and venules were perfused with oxygenated/heparinized physiological salt solution at 37 degrees C. This ex vivo perfused retinal microcirculation model was used to observe the contractile effects of Ang II on arterioles and venules of different diameters. The NO and PGI2 synthase inhibitors, 1-NOARG and flurbiprofen, respectively, were used to unmask Ang II vasoconstriction; the changes in vascular diameters were then measured. Enzyme immunoassays were used to measure the release of cGMP (an index of NO release) and 6-keto-PG-F1alpha (a stable metabolite of PGI2) from isolated bovine retinal vessels. RESULTS: Topically applied Ang II (10(-10) M to 10(-4) M) caused significant (P < 0.05) arteriolar and venular constrictions in a dose-dependent manner, with the smallest retinal arterioles (7+/-0.2 microm luminal diameter) and venules (12+/-2 microm luminal diameter) significantly more sensitive than larger vessels. After the inhibition of endogenous NO and PGI2 synthesis by 1-NOARG and flurbiprofen, respectively, the vasoconstriction effects of Ang II became more pronounced. Again, the smallest vessels tested were significantly more sensitive, and synthesis of endothelial-derived relaxing factor (EDRF), therefore, may be most important in these vessels. Vasoactive doses of Ang II (10(-10) M to 10(-4) M) caused a dose-dependent increase in the release of NO and PGI2 from isolated bovine retinal vessels, indicating that the increase in EDRF may nullify direct Ang II-induced vasoconstriction. Interestingly, intraluminal administration of Ang II caused only vasodilation. CONCLUSIONS: This study demonstrates that the retinal vascular endothelium acts as a buffer against the vasoconstricting agent Ang II via release of vasodilators NO and PGI2, and the vasoconstriction effects due to Ang II are most prominent in the smallest diameter vessels.

6-Ketoprostaglandin F1 alpha↗
PubMed1976

Comparative effects of prostaglandins E1, E2, A1, F1 alpha and F2 alpha on the resistance of coronary vessels during intracoronary administration.

The effects of prostaglandins E1, E2, A1, F1 alpha, and F2 alpha on the coronary vascular resistance during intracoronary administration were studied in anaesthetized, open-chest dogs. PGE1 in doses of 0.1 - 3-10 mug/kg in single intracoronary administration produced a potent and comparatively long-lasting direct decrease of the resistance of the coronary vessels and a decrease in the systemic arterial pressure. The PGE2 and PGA1 actions on the coronary vessels were less potent. At variance with PGE1 and PGE2, the hypotensive effect of PGA1 is more expressed than its action on the resistivity of coronary vessels. PGE1 alpah and PGF2 alpha do not show any significant influence on the resistivity of the coronary vessels. The results of the investigations also permit to establish a correlation between the chemical structure and action of prostaglandins on the coronary vessels and to conclude that one of the most important functional groups that determines the prostaglandin action on the coronary vessels most decisively is the keto-group at C-9 of cyclopentane ring. As coronary dilatator agents in anaesthetized dogs, the activity of the prostaglandins ranged in the order E1 greater than E2 greater than A1 greater than F1 alpha greater than F2 alpha.

Animals↗
PubMed1999

Taxane-induced apoptosis decompresses blood vessels and lowers interstitial fluid pressure in solid tumors: clinical implications.

Elevated tumor interstitial fluid pressure (IFP) is partly responsible for the poor penetration and distribution of therapeutic agents in solid tumors. The etiology of tumor interstitial hypertension is poorly understood. We have postulated that the solid stress generated by tumor cells growing in a confined space compresses blood vessels and increases tumor microvascular pressure and IFP. To test the hypothesis that neoplastic cell loss would decompress blood vessels and lower IFP, we induced apoptosis in tumors with paclitaxel and docetaxel. Taxanes inhibited the growth of the murine mammary carcinoma (MCa-IV) and of the human soft tissue sarcoma (HSTS-26T). Taxanes induced apoptosis and reduced the density of intact neoplastic cells in both MCa-IV and HSTS-26T. To determine whether neoplastic cell loss decompressed blood vessels, we measured the diameter of tumor vessels in HSTS-26T tumors implanted in transparent dorsal skin fold chambers. At 48 and 96 h after paclitaxel, the diameter of tumor vessels was significantly increased. The increase in vascular diameters was associated with reductions in microvascular pressure and IFP. The changes in neoplastic cell density and IFP were also correlated. In the human glioblastoma U87, which is resistant to paclitaxel, the IFP and cellular density were not modified by paclitaxel treatment. Collectively, these results support the hypothesis that solid stress generated by neoplastic cell proliferation increases vascular resistance and IFP. The increase in vessel diameter induced by paclitaxel and docetaxel suggests that taxanes could improve tumor response by increasing the vascular surface area for delivery of therapeutic agents.

Animals↗
PubMed1975

Vascularization of normal and neoplastic tissues grafted to the chick chorioallantois. Role of host and preexisting graft blood vessels.

Adult, embryonic, and tumor tissues were grafted to the chorioallantoic membrane of the chick embryo to determine whether blood vessels originally within implants were reused in the establishment of a new blood supply. Grafts were examined daily by in vivo stereomicroscopy and in histologic sections. Colloidal carbon injections into the host vasculature served to confirm the precise onset of graft circulation; Preexisting tumor blood vessels disintegrated by 24 hours after implantation and revascularization occurred at 3 days by penetration of proliferating host vessels into the tumor tissue. Adult tissues did not revascularize, and the original graft vasculature progressively disintegrated during the 9 days of observation, Most embryonic tissues revascularized in 1 or 2 days by reperfusion of the existing graft vasculature. Anastomosis of host and graft blood vessels seemed to result from connections between newly formed vascular sprouts arising from both vasculatures. This study indicates that only tumor grafts acquire their blood supply solely by formation of new blood vessels from the host microvasculature. By contrast revascularization of normal tissues, when it does occur, is predominately the result of perfusion of the preexisting graft blood vessels.

Allantois↗
PubMed2000

Astrocytes and blood vessels define the foveal rim during primate retinal development.

PURPOSE: To investigate the relationship between development of the perifoveal blood vessels and formation of the foveal depression. METHODS: Retinal sections and flatmounts from monkeys aged between fetal day (Fd)80 and 2 years of age were double labeled using antisera to CD31 or von Willebrand factor to detect vascular endothelial cells and antiserum to glial fibrillary acidic protein to detect astrocytes. Sections were studied by fluorescence or confocal microscopy. RESULTS: From Fd88 to 115, vessels on the horizontal meridian were found only at the level of the ganglion cell layer (GCL)-inner plexiform layer (IPL) border where they form the ganglion cell layer plexus (GCP). Stellate astrocytes accompany GCP vessels and extend closer to the fovea than vessels. The foveal avascular zone was present within the GCP at Fd101, and at Fd105 a shallow foveal depression encircled by the GCP was present. The GCP foveal margin had the same dimensions as the adult foveal pit. Both blood vessels and astrocytes were excluded from the emerging fovea throughout development. After Fd140, capillary plexuses in the outer retina anastomosed with the GCP on the foveal slope to form a perifoveal plexus, but this plexus did not mature until a month or more after birth. After Fd142, astrocytes rapidly disappeared from the GCP and most of central retina. CONCLUSIONS: An avascular area is outlined by the GCP before the foveal pit begins to form, suggesting that molecular factors in this region exclude both vessels and astrocytes. These factors may also guide neuronal migration to form the pit. Because the perifoveal plexus is formed during late gestation, both capillary growth and foveal development may be affected adversely by prematurity.

Animals↗
PubMed2000

[Abdominal trauma with injuries of the major vessels].

Treatment results in 87 patients (mean age 30.1 years) with traumatic injuries of major abdominal vessels were analyzed. 73 patients had stab-incised wounds, 9--blunt trauma, 5--gunshot wounds. Hemodynamics of the majority of hospitalized patients (66 from 87) was unstable. Inferior cava vein injury was revealed in 29 patients, aorta injury--in 21, iliac vessels injury--in 22, visceral vessels injury--in 15. One vascular wall was injured in 58 cases, two walls--in 27 cases, complete transection or separation of vessel was revealed in 6 cases. Major vessel injuries were associated with abdominal visceral trauma in 97% cases. Vascular operations (side suture--in 49 patients, circular suture--in 11, vein ligation--in 5, prosthesis--in 3) were performed in 17 (25%) patients by general surgeons, in the rest (75%)--by vascular surgeons. General mortality (including hospitalized but non-operated patients, and patients who died during the operation and in postoperative period) was 46%. It is necessary to teach vascular surgery to general surgeons for high-quality and timely care in patients with abdominal trauma complicated by major vessels injuries.

Abdomen↗
PubMed1975

Patient selection and improved technical factors in small-vessel bypass procedures of the lower extremity.

Thirty-two small-vessel bypasses were constructed as limb-salvage procedures. The one month patency rate was 72 percent and the one year cumulative patency rate was 55 percent. Preoperative, intraoperative, and postoperative angiography was performed in most cases and the results correlated with the ultimate fate of the graft. Preoperative angiography is critical in determining the location of a suitable small vessel, including the peroneal artery, and the quality of the runoff. Intraoperative angiography is required to delineate correctable intraoperative defects usually appearing at the distal anastomotic area. Additionally, failure to demonstrate runoff or a pedal arch can help support a decision not to re-explore a graft should early closure occur. Postoperative angiography is essential to validate clinical success with graft patency and function. It also serves to discover potential graft defects that might otherwise lead to closure and potential limb loss. Selected cases of failed small-vessel bypass grafts may be salvaged by thrombectomy with or without graft revision. Small-vessel bypass is generally contraindicated if there is extensive tissue necrosis and infection extending into the proximal foot. In cases where the necrotizing infection is localized, particularly to the forefoot, then open drainage, debridement, or amputation should be performed together with small-vessel bypass. Finally, the risks indigenous to small-vessel bypass procedures demand optimal patient selection and exquisite operative technique.

Amputation, Surgical↗
PubMed1975

[Effect of potassium ions on the reactions of resistive and capacitive vessels in the skeletal muscles and intestines].

L. a. administration of 4.2% KCl was followed by contractile responses of the resistance intestinal vessels, whereas contractile-dilatatory responses were observed in the skeletal muscles. The intestinal capacitance vessels responded with insignificant increase of the venous outflow, while the contractile-dilatatory responses of the resistance vessel were not followed by any increase of the venous outflow in skeletal muscles. After papaverin administration, contractile responses of the resistance intestinal vessels were insignificant, while the contractile-dilatatory responses of the skeletal muscles resistance vessels became contractile only. After noradrenaline injections only contractile responses were observed in the resistance intestinal vessels.

Animals↗
PubMed1975

[The effect of acidic metabolic products on the capacitance and resistance vessels of the skeletal muscles and intestines].

Under conditions of the resistography of the skeletal muscle and intestinal vessels intraarterial injections of the acetic and lactic acid solutions in 75% cases evoked significant dilatation of the resistance vessels. Simultaneously enhancement of the venous outflou takes place, which is determined mainly by venous constriction and partly by the transfer of liquid from tissues into the blood. The rise of the venous outflow was lasted for 45 sec. and for 90 sec. in several experiments. This was not observed by the intraarterial injection of hypertonic solutions of NaCl Glucose, MgSO4 and others. The reactions of capacitance vessels was not dependent on the reactions of resistance vessels since the rise of the venous outflow took place also when only constriction of the resistance vessels (8 experiments) or when constrictor-dilatator reactions of the resistance vessels were observed.

Acetates↗
PubMed1975

[K+, H+ and Ca++ concentrations in the perivascular fluid as a factor in the regulation of the lumina of the vessels of the pia mater].

The author separed the vascular vessels of pia mater with a size of 20-150 microns in cats under penthobarbital narcosis. The perivascular area of the vessels was perfused by an artificial fluid with varying concentrations of potassium, hydrogen and calcium. The local contraction of the smooth vascular musculature was induced by stimulation with rectangular impulses by means of electrodes introduced by micromanipulators in immediate vicinity of a vessel. The changes were recorded by means of microphotographic images of the vessels. It was established that the contraction of the vessels was observed when there was a lack of potassium or at concentration of 100 meq/l. There was no change at 2,5-3,0 and at 50-60 meq/l of potassium. Vasodilatation was found at 10-20 meq/l. Electrical stimulation caused stronger contraction of the vessel, when there was a lack of potassium in comparison with the norm (2,7 meq/l). The increase of potassium caused a reduction of the dimensions of the effect due to electrical stimulation. The vascular dilatation, induced by 10-20 meq/l of potassium was not affected by the increase of the calcium concentration (6-9 meq/l) in artificial fluid. The vasodilatation, induced by an increase of hydrogen, was abolished by raising the concentration of calcium in the artificial fluid. The obtained results were discussed.

Animals↗
PubMedDate not supplied

[A simple model of a vessel with a wall sensitive to mechanical stimuli].

Smooth muscles in the walls of small blood vessels under normal conditions are always moderately active, so that there is a certain reserve for blood flow adaptation to changed conditions by either narrowing or expanding of the vessel lumen. The previous studies of small vessel hydrodynamics have shown that the activity can cause specific instability of vessel steady states. In order to trace qualitatively the influence of numerous factors on the active state of the vessel, a simplified model of the vessel was proposed, which is reduced to a nonlinear ordinary equation of the first order with delayed argument.

Algorithms↗