Enhancement of depolarization-induced contractions after endothelium denudation is not related to an impaired production of nitric oxide or prostacyclin in the rabbit basilar artery

Enhancement of the extracellular potassium ion (K⁺) concentration combined with endothelial injury have been suggested to occur during cerebral ischaemia-reperfusion and vasospasm after subarachnoid hemorrhage. The effect of potassium (K⁺) depolarization was therefore investigated in isolated segments of the rabbit basilar artery with and without an intact endothelial cell layer. Addition of potassium chloride to the organ bath induced a concentration-dependent contraction. Endothelial denudation of the artery resulted in an unstable baseline tension and a leftward shift of the K⁺ concentration-response curve. The K⁺ concentration eliciting half maximum contraction decreased from 26 mmol l^-1 in the presence to 12 mmol l“¹ in the absence of an intact endothelium. Nimodipine (3 × 10^-7 mol l^-1) or exposure to a calcium-free medium abolished the spontaneous as well as K⁺-induced contractions. A^-nitro-L-arginine (10^-4 mol l^-1), indomethacin (3 × 10^-6 mol l^-1) and glibenclamide (10^-5 mol I^-1) did not affect the contractile response to K⁺ in intact arteries. However, N_w-nitro-D-arginine increased the baseline tension, and this effect could not be reproduced with N_w-nitro-D-arginine. Pinacidil (10^-6mol l^-l) abolished the spontaneous contractile activity in endothelium-denuded arteries and reduce the K⁺ sensitivity to the same level as in intact arteries. Tetraethylammonium (3 mmol l^-1) and ouabain (10^-5 mol I^-l) increased the basal tension and shifted the K⁺ concentration-response curve to the left. Calcium-induced contractions in preparations exposed to a calcium-free, 124 mmol l^-l K.⁺ solution did not differ between endothelium-denuded and intact arteries. It is suggested that the endothelium of the rabbit basilar artery releases a hyperpolarizing factor, distinct from nitric oxide or a cyclooxygenase product, which attenuates the vasoconstrictor effect of K⁺ depolarization.     

Effects of angiotensin-converting enzyme inhibition on arterial,venous and capillary functions in cat skeletal muscle in vivo

The aim of the present study was to analyse quantitatively, on a cat gastrocnemius muscle preparation in vivo, the effects of local angiotensin-converting enzyme (ACE) inhibition by enalaprilat on total regional vascular resistance (tone) and its distribution to the large-bore arterial resistance vessels (>25 μm), the small arterioles (<25 μm) and the veins. Associated effects on capillary pressure and fluid exchange were also studied. Close-arterial infusion of enalaprilat (0.05–0.20 mg kg muscle tissue min^-1) elicited a moderate dilator response in all three consecutive sections of the muscle vascular bed, an increase in capillary pressure and transcapillary fluid filtration. This dilation could be abolished by the selective bradykinin B₂-receptor antagonist Hoe 140 (2 mg kg^-1 min^-1, i.a.), indicating that the dilator mechanism of ACE inhibition was an increased local concentration of bradykinin, and hardly at all a decreased concentration of angiotensin (AT) II. The generalized dilator response to ACE inhibition along the vascular bed suggested a relatively uniform distribution of ACE from artery to vein and this was further supported by the finding that a close-arterial infusion of AT I (0.04–0.32 μg kg^-1 min^-1), which was vasoactive only after conversion to AT II by local ACE, elicited a generalized constrictor response in all three vascular sections. In contrast, infused AT II (0.01–0.16 μg kg^-1 min^-1) constricted almost selectively the large-bore arterial vessels. The specific angiotensin AT₁-receptor antagonist losartan (2 mg kg^-1 min^-1, i.a.) abolished the constrictor response to AT II but did not affect vascular tone under control conditions, indicating that AT II is not involved in the initiation of basal vascular tone in muscle. These results, taken together, indicate that under basal conditions vascular ACE contributes to the local control of vascular tone in skeletal muscle by degrading the endogenous dilator bradykinin, and not by converting AT I into vasoconstrictor AT II.     

Histopathology of carotid body in heroin addiction. Possible chemosensitive impairment

AIMS: To perform a morphometric analysis of carotid bodies in opiate addicts. METHODS AND RESULTS: Carotid bodies were sampled at autopsy from 35 subjects who died of heroin intoxication (mean age 26 years), and from eight young (22 years) and eight older subjects (66.5 years) who died of trauma. Sections were stained with haematoxylin-eosin, azan-Mallory, and double-labelling immunohistochemistry with antineuronal specific enolase and anti-S100, to count type I and type II cells. Interlobular and intralobular connective tissue was increased both in the opiate cases (43.45 +/- 6.79%, P < 0.001, and 13.34 +/- 5.72%, P < 0.001, respectively) and older cases (46.67 +/- 1.65%, P < 0.001, and 9.62 +/- 2.11%, P < 0.05, respectively) compared with young cases (33.17 +/- 6.41% and 4.33 +/- 1.84%, respectively). The percentage of type II cells in the opiate cases (51.6 +/- 7.3%, P < 0.001) and in the older controls (49.0 +/- 7.2%, P < 0.01) was higher than in the young cases (37.9 +/- 3.0%). Among type I cells, the light cell percentage in the opiate cases (65.85 +/- 11%, P < 0.001) was reduced with respect to the two control groups (82.8 +/- 5.34%, young; 81.62 +/- 8.58%, older). CONCLUSIONS: The increases in connective tissue and type II cells are similar to findings in ageing and chronic pulmonary disease, and may be ascribed to glomic hypoxia. A direct action of opiates should be taken into account for the decrease in light cells in heroin addiction. The histopathological changes in the carotid body, by impairing chemosensivity, may play a role in the fatal cardiorespiratory derangement of heroin addicts.     

Immunohistochemical localization of apolipoproteins A-I and B in human carotid arteries

Decreased plasma levels of apolipoprotein A-I (apo A-I) and increased plasma levels of apolipoprotein B (apo B) have been shown to correlate with increased risk of atherosclerosis. While many studies have investigated the plasma levels of these apolipoproteins with regard to their value as predictors of cardiovascular disease, comparatively little is known about their precise tissue localization in atherosclerotic plaques. The purpose of this study was to determine the tissue localization of apo A-I and apo B in atherosclerotic segments of human carotid arteries through the use of immunohistochemical techniques. With tissue samples obtained from surgery and autopsy, apo A-I and apo B were found to be present in atherosclerotic plaques and absent in normal arterial tissue. In the plaques, both apo A-I and apo B were found extracellularly, primarily in the lipid core, but also in connective tissue. In addition, both apo A-I and apo B were found intracellularly in foam cells. This similar intracellular and extracellular distribution of apo A-I and apo B was unexpected, in view of their differing associations with atherosclerosis.     

Epoxy-resin injection of the cerebral arterial microvasculature: An evaluation of the limits of spatial resolution in 8 Tesla MRI

The purpose of this study was to quantify the spatial resolution of microscopic arteries on magnetic resonance images acquired at 8 Tesla (T). Techniques similar to those used for standard MRI of the human brain in vivo at 8 T were utilized to generate high-resolution gradient echo (GE) images of a whole postmortem human brain whose common carotid arterial system had been injected with an epoxy-resin. Single slice images, along with summed images of up to 5 contiguous slices, were then compared to color digital photographs detailing the distribution of the arterial system on the surface of the same injected brain. There was excellent MR visualization of the microscopic cerebral arteries down to a spatial resolution of 200 microm. Through the use of an 8 T whole-body MRI scanner and standard GE imaging sequences, microscopic arterial structures can be clearly resolved down to a dimension of 200 microm.     

脑动脉DSA形态分析及其意义

目的：探讨脑血管造影各主要动脉的投影规律及其分支的显示率，为脑血管疾病的影像诊断和介入治疗提供重要参考。方法：随机抽取140例全脑血管DSA系列图像，选择其中无脑血管疾病的51例进行观察。分别统计颈内动脉和椎动脉造影时正常脑血管各主要分支的显示率；归纳大脑前动脉A1段、大脑中动脉M1段及大脑后动脉P1段在平面上的投影规律并分析总结了脑动脉的正常解剖学特征及其变异。结果：①脑底动脉变异较大；②颈内动脉照影时OA、AChA、ACoA、PCoA、ACA和MCA的显示率分别为96.1％、92．2％、52．9％、69．6％、100％和100％；③椎动脉造影时PICA、AICA、BA、SCA、PCA和PCoA的显示率分别为66．7％、62．7％、100％、70．6％、80．4％和41．2％。结论：①尽管脑底血管实际解剖关系较为复杂，但造影时反映到平面上可简捷的用“水平、上升、下降”等来描述血管的形态和走行；②虽然是平面图像，通过调整投照体位仍可非常逼真的反映血流的动态变化。     

Characterization of the prostanoid receptors and of the contractile effects of prostaglandin F2a in human pial arteries

The contractile and relaxant effects of various prostanoids were studied on isolated human pial arteries. Contractions were elicited with the following order of potency: U46619?U44069>PGB₂>PGF_2a>PGE₂?PGD₂>PGF_1a≥TXB₂, indicating that prostanoid-induced contractions probably are mediated by a thromboxane-sensitive receptor. Relaxation of PGF_2a-contracted arteries was induced with the order of potency: PGE₂> PGE₁>PGD₂?PGD₁. Vessels contrated by K⁺ were relaxed only by PGE,. Since PGI₂ was previously found to be more potent than all the prostanoids tested in the present study, relaxant responses are probably mediated via a PGI₂-sensitive receptor. The roles of free extracellular and cellularly bound calcium for the contractile effects of PGF_2a and K⁺ were estimated by incubating the arteries for various times in calcium-free medium containing 10^-5 M EGTA. Incubation for 5–10 min abolished K⁺-induced contractions, whereas after 40 min of incubation PGF_2a still induced contractions that reached 70% of control. The PGF_2a-induced contraction was biphasic in 8 out of 10 preparations. The second phase could be eliminated by increasing the EGTA-concentration to 10^-4 M, as well as by nifedipine pretreatment. In calcium-free, high K⁺ medium calcium-induced contractions were elicited at lower concentrations in the presence of PGF_2a. The results suggest that PGF_2a-induced contractions in human pial arteries are relatively independent of free extracellular calcium. PGF_2a may promote trans-membrane influx of calcium, as well as release calcium from seemingly superficially located cellular stores.     

The human placental bed: histology, immunohistochemistry and pathology

There has been much interest recently on local intra-uterine materno-fetal interactions particularly in the placental bed where cellular relationships between mother and fetus are at their most intimate. While few histopathologists are expected to interpret formal placental bed biopsy specimens, confrontation with tissue from this site is common following abortion, post-partum haemorrhage or molar gestation. This review gives an account of recent advances in our knowledge of the histology, immunohistochemistry and pathology of the placental bed. It focuses particularly on extravillous trophoblast populations and their relationship to maternal cells and emphasizes the importance of vascular changes.     

“Cross-over” duplication of middle cerebral artery,agenesis of internal carotid artery and saccular aneurysms

Summary The authors describe a patient with anomalous branches of the left internal carotid artery, cross-over duplication of its middle cerebral artery and agenesis of the contra-lateral internal carotid artery associated with two aneurysms successfully clipped. Pertinent literature is reviewed.