A study of rat intracerebral arterioles: methods, morphology, and reactivity

Summary:We compared the effect of the acute applica tion of ethanol, methanol, I-propanol, I-butanol, urea, and mannitol (1-100 mM) on the basal tone of isolated cannulated rat intracerebral arterioles to determine if the response of these arterioles to ethanol could be attributed to alteration of membrane fluidity or changes in osmolal ity. These arterioles spontaneously developed tone to 62.0 ± 8.4% of passive diameter (44.2 ± 11.9 vs. 70.9 ± 14.7 fJ-m). Ethanol caused a dose-dependent reduction in arteriolar diameter starting at 3 mM (p = 0.03), reaching a diameter of 81.4 ± 3.0% of basal tone at 100 mM. In comparison, all other agents tested caused the arterioles to dilate, with the exception of I-propanol, which pro duced inconsistent vessel responses. At 100 mM concen tration, methanol, I-butanol, urea, and mannitol dilated

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Differential Effects of Alcohols on Intracerebral Arterioles. Ethanol Alone Causes Vasoconstriction

et al. 1995

“…Studies in vitro have been performed in the cat and human by Hardebo and Edvinnson (1979), in the dog by Muramatsu et al (1980) and To da et al (1982), and in the rat by Dacey and Duling (1982). In all reports both in vivo and in vitro, aden osine was found to dilate cerebral arteries and ar terioles.…”

Section: Methodologic Consideration Of the Cranial Window Technique Imentioning

confidence: 97%

Reactivity of Rat Pial Arterioles and Venules to Adenosine and Carbon Dioxide: With Detailed Description of the Closed Cranial Window Technique in Rats

Morii

1986

192

This study describes a closed cranial window technique that allows the observation and measurement of rat pial arterioles and venules in situ. The resolving power of this system is 1–2 μm. Using this sensitive technique, we characterized the responses to 7% carbon dioxide inhalation and adenosine in arterioles (10–70 μm) and venules (15–100 μm). During carbon dioxide inhalation, larger arterioles (>40μm) dilated more than smaller arterioles (<20 μm). There was limited vasoreac-tivity of pial venules during CO2 inhalation. Dilation of arterioles was initially observed with an adenosine concentration of 10−8 M. Almost a twofold increase in diameter was noted at 10−3 M. In contrast to the effect of CO2 inhalation, the degree of dilation with topical application of adenosine was not size dependent. Pial venules did not respond to adenosine. The technique for observation of pial vessels using the closed cranial window and for measurement of vessel diameter by video camera system microscopy is a powerful tool for studying in vivo the cerebral circulation in the rat.

“…Penetrating intacerebral arterioles were isolated and cannulated in an organ bath, and changes in vessel diameter in response to the extraluminal administration of agents were measured, as described in detail pre viously (Duling et aI., 1981;Dacey and Duling, 1982). Briefly, penetrating arterioles, 30-70 f.Lm in diameter, were surgically isolated from the first (M -1) portion of the middle cerebral artery from the brains of pentobarbital anesthetized Sprague-Dawley rats weighing 300-400 g. The vessel segments were transferred to a temperature controlled chamber on the stage of a Nikon inverted mi croscope and were cannulated using glass pipettes.…”

Section: Isolation and Cannulation Of Vesselsmentioning

confidence: 99%

Vasomotor Responses of Rat Intracerebral Arterioles to Vasoactive Intestinal Peptide, Substance P, Neuropeptide Y, and Bradykinin

Dacey

Bassett

Takayasu

1988

Summary:The effect of vasoactive peptides on vascular smooth muscle in the cerebral microcirculation was ex amined using an isolated intracerebral arteriole prepara tion. Extraluminally applied vasoactive intestinal peptide (VIP) dilated the spontaneous tone of intracerebral arte rioles to 118.9 ± 3.1% of control diameter at pH 7.30, with an EC50 of 7.27 x 10-8 M. Similar degrees of dila tion to VIP were seen in vessels preconstricted by changing bath solution to pH 7.60. Substance P had no effect on vessel diameter at pH 7.30. However, in vessels precontracted by pH 7.60, significant dose-dependent di lation was observed with an EC50 of 2.55 x 10-1 0 M.Local chemical, neural, and humoral mecha nisms affect cerebral vascular resistance. Neural regulation of cerebral blood flow is mediated by ad renergic, cholinergic, and peptidergic mechanisms. These systems, acting either alone or in combina tion, change vessel caliber and thus change resis tance to blood flow. Adrenergic and cholinergic control of cerebral resistance vessels occurs mainly by the release of a vasoactive substance from nerve endings near the wall of the vessel. Innervation of cerebral vessels has been demonstrated both ana tomically, by histochemical methods, and physio logically by studies of vascular smooth muscle in vitro and studies of CBF regulation in vivo.Some neural responses of the cerebral circula tion, however, are not controlled by the classical 254Neuropeptide Y constricted intracerebral arterioles to 8l.22 ± 2.7% of control diameter, with an EC50 of 6.23 x 10-1 0 M. Bradykinin dilated intracerebral arterioles at pH 7.30 and pH 7.60 to 130 ± 3.0% of control diameter. VIP and bradykinin are potent vasodilators of intracerebral arterioles. Neuropeptide Y is a vasoconstrictor. The ef fect of substance P appeared to be either pH-dependent or dependent on some degree of precontraction by an other agonist, but no effect on vessel diameter was seen at pH 7.30.