Constriction of Pial Arterioles Produced by Prostaglandin F
            <sub>2α</sub>

Rosenblum, William I.

doi:10.1161/01.str.6.3.293

Cited by 38 publications

(20 citation statements)

References 21 publications

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“…29 - 31 The body temperature was maintained at 37° C. The cerebral surface was continuously suffused at 1 ml/min with artificial cerebrospinal fluid 32 at pH 7.34 ±0.01 (mean + SEM). 30 An arteriole (diameter, 30-40 fim) was arbitrarily selected for observation through a Leitz microscope (Rockleigh, New Jersey). The microscopic field was illuminated from the side by a halogen lamp and fiber-optic guide.…”

Section: Methodsmentioning

confidence: 99%

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Endothelium-dependent constriction demonstrated in vivo in mouse cerebral arterioles.

Rosenblum

Nelson

1988

Circulation Research

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Endothelium-dependent constriction in mouse pial arterioles was demonstrated by testing contractile responses before and after endothelial injury. All responses were monitored at the same site as the injury. Injury was produced in vivo by exposing an arteriole on the brain surface to the beam of a 6-mW helium-neon laser after first sensitizing the micro vascular bed to the laser energy by injecting Evans blue intravenously. The contractile response to serotonin creatinine sulfate (20 /tg/ml) and to sodium arachidonate (30 /ig/ml) was monitored in vivo with an Image splitter and TV microscope. The responses before laser injury were always constriction; the responses after laser injury were always relaxation. After laser injury, acetykholine chloride (80 /ig/ml) constricted every vessel tested at the injured site. Thus, the injured segment had not lost the capacity to constrict even though neither serotonin nor arachidonate remained able to induce a constriction. The endothelium-dependent constrictions to serotonin or arachidonate were also blocked by pretreatment of the mouse with cyclooxygenase inhibitors, acetylsaUcylic acid (100 mg/kg i.p.) or indomethacin (5 mg/kg). The data suggests that endothelium-dependent constriction to serotonin is mediated by release of arachidonate from the endothelial cell and conversion of that arachidonate by cyclooxygenase to some constricting prostanoid. (Circulation Research 1988;63:837-843) T he study of vascular physiology has been greatly altered by the relatively recent discovery that endothelial cell products mediate dilation by many agonists. '-3 The agonists involved differ somewhat depending on animal species and on the particular vascular bed within a species. '-5 The number and nature of the endothelium-derived relaxing factors that actually control the dilations in question have not yet been resolved.6 -' 2 The existence of endotheliumdependent constriction has also been reported but in relatively few investigations. n~22The evidence for both endothelium-dependent constriction and dilation was originally based on in vitro studies of large vessels. A major method used to establish the existence of these phenomena has been to destroy a portion of the endothelial cells and to demonstrate altered relaxation or constriction to selected agonists while the effects of other

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Section: Methodsmentioning

confidence: 99%

“…Prostaglandin F 2o is a likely candidate because this prostaglandin constricts pial arterioles in our preparation. 30 However, without additional studies, other mediators such as thromboxane cannot be ruled out. Thromboxane has been implicated as the endothelialderived mediator of arachidonate-stimulated constriction of canine basilar artery.…”

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confidence: 99%

Endothelium-dependent constriction demonstrated in vivo in mouse cerebral arterioles.

Rosenblum

Nelson

1988

Circulation Research

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“…The preparation has been described in great detail. 13 " 15 Briefly, a tracheostomy and craniotomy were performed in mice anesthetized with urethane. The dura was stripped and the pial vessels exposed and kept moist with a suffusate of artificial CSF, 15 -16 flowing at 2 ml per minute at 37°C, and pH of 7.35.…”

Section: Methodsmentioning

confidence: 99%

Endothelial dependent relaxation demonstrated in vivo in cerebral arterioles.

Rosenblum¹

1986

Stroke

132

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Wei EP, Kontos HA, Said SI: Mechanism of action of vasoactive intestinal polypeptide on cerebral arteries. Amer J Physiol 239: H765-768, 1980 Wilson DA, O'Neill JT, Said SUMMARY The endothelium of mouse pial arterioles was injured in situ with a light/dye technique. The response of the arterioles to acetylcholine or to bradykinin was compared before and after the injury. All vessels failed to dilate after injury. In fact the predominant response now became constriction. The injured vessels were still capable of dilating to papaverine. Uninjured vessels continued to dilate to acetylcholine or bradykinin. The data show that relaxation of pial arterioles to acetylcholine or bradykinin is dependent on a normal endothelium. This is in keeping with demonstrations by others that an endothelial dependent relaxing factor or factors is(are) the mediator of the dilation to either acetylcholine or bradykinin. The present demonstration of such endothelial dependence is important because in contrast with the bulk of the literature it deals with in vivo, rather than in vitro data, and with microcirculation rather than large vessels. It is also important because it concerns brain circulation. The data suggests that endothelial injury, known to occur in a wide variety of pathologic states, could enhance vasospastic potential by eliminating dilating influences and/or converting them to constricting forces.

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“…[3][4][5][6][7][8] Briefly, male mice (ICR strain, Harlan Sprague Dawley, Inc., Indianapolis, Ind.) were anesthetized with urethane.…”

Section: See Editorial Comment Page 270mentioning

confidence: 99%

Interaction of endothelium with dilation produced by inhibitors of cyclic nucleotide diesterases in mouse brain arterioles in vivo.

Rosenblum

Shimizu

Nelson

1993

Stroke

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Constriction of Pial Arterioles Produced by Prostaglandin F _2α

Abstract: Abstract

Cited by 38 publications

References 21 publications

Endothelium-dependent constriction demonstrated in vivo in mouse cerebral arterioles.

Endothelium-dependent constriction demonstrated in vivo in mouse cerebral arterioles.

Endothelial dependent relaxation demonstrated in vivo in cerebral arterioles.

Interaction of endothelium with dilation produced by inhibitors of cyclic nucleotide diesterases in mouse brain arterioles in vivo.

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Constriction of Pial Arterioles Produced by Prostaglandin F 2α

Abstract: Abstract

Cited by 38 publications

References 21 publications

Endothelium-dependent constriction demonstrated in vivo in mouse cerebral arterioles.

Endothelium-dependent constriction demonstrated in vivo in mouse cerebral arterioles.

Endothelial dependent relaxation demonstrated in vivo in cerebral arterioles.

Interaction of endothelium with dilation produced by inhibitors of cyclic nucleotide diesterases in mouse brain arterioles in vivo.

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Product

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Constriction of Pial Arterioles Produced by Prostaglandin F _2α