Simultaneous Measurements of Radii and Wall Thickness of Microvessels in the Anesthetized Rat

Baez, Silvio

doi:10.1161/01.res.25.3.315

Cited by 70 publications

(44 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Reversal of blood-induced large vessel spasm has been reported in vivo, using alpha blockade. 9 ' 20 In vivo studies on the microcirculation have shown that alpha adrenergic stimulation with norepinephrine in higher doses than required to activate vessels elsewhere in the body 51 produced only a moderate vasoconstrictor effect in pial vessels. 38 -"• 48 These results, however, are not consistently reproducible.…”

Section: Discussionmentioning

confidence: 99%

Pial Microcirculation in Subarachnoid Hemorrhage

Herz

Baez

Shulman

1975

Stroke

View full text Add to dashboard Cite

Pial Microcirculalion in Subarachnoid Hemorrhage• Microsurgical and microscopic methods were employed in guinea pigs to expose, observe, and measure response characteristics of cerebral cortical pial microvessels and microcirculation to traumatic and nontraumatic experimental subarachnoid hemorrhage. Bleeding produced by vascular micropuncture was associated with a 44.3% arteriolar constriction. Topical application of homologous blood alone produced a 33.2% vasoconstriction. Observed microcirculatory flow characteristics subsequent to such microvascular changes were consistent with those known to be associated with cerebral cortical infarction. These changes could be prevented or reversed by topical application of the alpha adrenergic blocker, phenoxybenzamine. Topical pretreatment with the beta adrenergic blocker, propranolol, prevented blood-induced spasm, but did not reverse such spasm once it had been established. A chemo-mechanical mechanism is suggested as underlying the vasoconstriction associated with rupture of pial microvessels. It is thought that consideration of such microvascular characteristics, in conjunction with those known to be associated with larger intracranial vessels, adds to current knowledge of the pathophysiology of subarachnoid hemorrhage and may be extrapolated to bear future clinical import.Additional Key Words microvessels phenoxybenzamine propranolol image splitting vasospasm adrenergic blocker• It has been known for many years that rupture of intracranial aneurysms is associated with angiographically demonstrable cerebral vasospasm, 13 which can be confirmed visually at the operating table.2 Similar spasm has been noted in patients with traumatic subarachnoid hemorrhage, 46 and is seen less frequently with arteriovenous malformations and other disorders.2 It is clear, however, that blood experimentally introduced into the subarachnoid space by a variety of methods produces spasm of large intracranial arteries. "11 Vasospasm has been a deterrent to the surgical therapy of intracranial aneurysms, being associated with profound neurological deficits and death.1 ' 2t 12~17 Such a grave clinical problem has led to many laboratory investigations on the pathophysiology of blood-induced large vessel spasm.7 ' 9i "• 18~25 The regulation of blood supply to cerebral cortical tissue capillary beds is not exclusively a function of these large arteries, and is at least partially relegated to the precapillary resistance and distributing vessels of the pial microcirculation. systematically examine, by direct in vivo microscopy, pial microcirculatory changes in these states. MethodsForty-five young guinea pigs of both sexes, weighing 400 to 500 gm, were anesthetized with pentobarbital (40 mg per kilogram i.m.). The animals were usually not re-injected with pentobarbital after surgery, so that they were under light anesthesia at the time when their cerebral cortical vessels were studied. Using the Zeiss operating microscope a tracheostomy, right common carotid cannulation, and left pariet...

show abstract

Section: Discussionmentioning

confidence: 99%

Pial Microcirculation in Subarachnoid Hemorrhage

Herz

Baez

Shulman

1975

Stroke

View full text Add to dashboard Cite

show abstract

“…The leukocyte parameters were examined as previously described (2,20,43). Briefly, mice were anesthetized with an intraperitoneal injection of 40 mg of sodium pentobarbital kg Ϫ1 .…”

Section: Methodsmentioning

confidence: 99%

“…Images were recorded on a video recorder with a ϫ40 long-distance objective with a 0.65 numerical aperture. An image-splitting micrometer was adjusted to the phototube of the microscope as described by Baez (2). The image splitter sheared the optical image into two separate images and displaced one with respect to the other.…”

Section: Methodsmentioning

confidence: 99%

“…Macrophages obtained from iNOS Ϫ/Ϫ and wild-type mice were assayed for NO 2 Ϫ production and iNOS mRNA expression. It was observed that, unlike with macrophages obtained from wild-type mice, the macrophages obtained from iNOS Ϫ/Ϫ mice stimulated with LPS (200 ng ml Ϫ1 ) plus IFN-␥ (200 IU ml Ϫ1 ) were unable to produce NO 2 Ϫ (Fig.…”

Section: Absence Of No Production In Inosmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of Leukocyte Rolling by Nitric Oxide during Sepsis Leads to Reduced Migration of Active Microbicidal Neutrophils

et al. 2002

View full text Add to dashboard Cite

We developed two models of sepsis with different degrees of severity, sublethal and lethal sepsis, induced by cecal ligation and puncture. Lethal sepsis induced by cecal ligation and puncture (L-CLP) resulted in failure of neutrophil migration to the infection site and high mortality. Treatment of septic animals with aminoguanidine (AG), a nitric oxide (NO) synthase inhibitor, precluded the failure of neutrophil migration and protected the animals from death. However, cytokine-induced NO synthase (iNOS)-deficient (iNOS ؊/؊ ) mice subjected to L-CLP did not present neutrophil migration failure, but 100% lethality occurred. iNOS ؊/؊ mice subjected to sublethal sepsis induced by cecal ligation and puncture (SL-CLP) also suffered high mortality despite the occurrence of neutrophil migration. This apparent paradox could be explained by the lack of microbicidal activity in neutrophils of iNOS ؊/؊ mice present at the infection site due to their inability to produce NO. Notably, SL-and L-CLP iNOS ؊/؊ mice showed high bacterial numbers in exudates. The inhibition of neutrophil migration by NO is due to inhibition of a neutrophil/endothelium adhesion mechanism, since a reduction in leukocyte rolling, adhesion, and emigration was observed in L-CLP wild-type mice. These responses were prevented by AG treatment and were not observed in the iNOS ؊/؊ L-CLP group. There was no significant change in L-selectin expression in neutrophils from L-CLP mice. Thus, it seems that the decrease in leukocyte rolling is due to a defect in the expression of adhesion molecules on endothelial surfaces mediated by iNOS-derived NO. In conclusion, the results indicate that despite the importance of NO in neutrophil microbicidal activity, its generation in severe sepsis reduces neutrophil migration by inhibiting leukocyte rolling and their firm adhesion to the endothelium, in effect impairing the migration of leukocytes and consequently their fundamental role in host cell defense mechanisms.

show abstract

“…By rotating the image splitter in the phototube, the shearing was maintained at the right angles to the long axis of the vessel. The displacement of one image from the other permitted measurement of the vessel diameter (Baez, 1969). A terminal arteriole and the venule paired with it were selected for study, and any changes in vessel diameter were estimated after the topical application of histamine (2.7 nmol), bradykinin (30 pmol), PAF (39 pmol), sodium nitroprusside (38 nmol), and acetylcholine (17 nmol).…”

Section: Methodsmentioning

confidence: 99%

Minalrestat, an Aldose Reductase Inhibitor, Corrects the Impaired Microvascular Reactivity in Diabetes

Akamine¹,

Hohman²,

Nigro³

et al. 2002

J Pharmacol Exp Ther

View full text Add to dashboard Cite

We demonstrated that aldose reductase inhibition corrects the impaired microvascular responses to inflammatory mediators in diabetic rats. To study the mechanism involved in the restoring effect of aldose reductase inhibition, we examined the effects of minalrestat, another aldose reductase inhibitor, on the responses of mesenteric microvessels studied in vivo to permeability-increasing agents in diabetic and galactosemic rats. The diabetic group was treated from 3 days after the alloxan injection with minalrestat (10 mg/kg/day) for 30 days and the minalrestat treatment (10 mg/kg/day/7 days) of galactosemic rats started concomitantly with the induction of galactosemia. The mesenteric microvessel reactivity was studied using intravital microscopy and changes in vessel diameters were estimated after the topical application of vasoactive agents. The impaired responses to bradykinin, histamine, and platelet-activating factor of arterioles and venules observed in diabetic and galactosemic rats were completely prevented by minalrestat. Neither diabetes nor galactosemia affected responses to acetylcholine and sodium nitroprusside. Responses to these agents were not modified by aldose reductase inhibition. The restoring effect of minalrestat was reversed by inhibition of nitric oxide (NO) synthesis with N -nitro-L-arginine methyl ester, by blocking K ϩ channel with tetraethylammonium but not by cyclooxygenase inhibition with diclofenac. Therefore, we concluded that NO, membrane hyperpolarization, but not cyclooxygenase products are involved in the beneficial effect of minalrestat on the microvascular reactivity in diabetes. Together, these findings led us to suggest that aldose reductase inhibition might ameliorate diabetic complications through the correction of the altered microvascular reactivity by a mechanism that involves NO and membrane hyperpolarization.

show abstract

Simultaneous Measurements of Radii and Wall Thickness of Microvessels in the Anesthetized Rat

Cited by 70 publications

References 0 publications

Pial Microcirculation in Subarachnoid Hemorrhage

Pial Microcirculation in Subarachnoid Hemorrhage

Inhibition of Leukocyte Rolling by Nitric Oxide during Sepsis Leads to Reduced Migration of Active Microbicidal Neutrophils

Minalrestat, an Aldose Reductase Inhibitor, Corrects the Impaired Microvascular Reactivity in Diabetes

Contact Info

Product

Resources

About