Early atherosclerotic lesions in infancy: role of parental cigarette smoking

Cigarette smoking is associated with an increased incidence of atherosclerotic diseases. The aim of this study was to examine the progression of the preatherosclerotic lesions previously observed by us in coronary arteries of fetuses of smoker mothers and in infants with smoker parents. We examined the coronary arteries of 34 infants, aged 1–36 months, and the histological and biological [c-fos, proliferating cell nuclear antigen (PCNA), and apoptosis] features of the early atherosclerotic lesions. In 17 infants (50%), at least one parent smoked, generally more than five cigarettes a day. In 18 cases (53%), we observed variable thickening of the coronary walls from preatherosclerotic lesions to juvenile atherosclerotic plaques, related to parental smoking habit. This morphological progression of the lesions was accompanied by a sequence of biological changes in the smooth muscle cells of the tunica media. We suggest that the oxidants present in the gas phase of the parental cigarette smoke pass through the endothelium and induce at first the c-fos gene activation and subsequently the PCNA positivity, that is, a proliferative process.     

A nonlinear model of the arterial vessels within a limb segment

The relationship between the arterial blood pressure and the volume of the arteries within a segment of an extremity is nonlinear. The present paper shows how the flow and volume pulsations of the arteries within a limb segment can be simulated taking this property into account. An electrical model was constructed comprising one resistor and two voltage dependent ‘capacitors’, the latter corresponding to the pressure dependent elasticity, or compliance, of the arteries. Adequate simulations were obtained over a wide pressure range, which is impossible with linear models. The nonlinear, i.e. pressure dependent, relationship between the volume and pressure of arteries, observed under static conditions, must also be taken into consideration when studying pulsatile events with models whether mathematical or physical.     

颞骨岩部结构的定位解剖及临床意义

目的:为颅底手术中耳蜗的定位、岩尖的磨除范围提供解剖学方法。方法:在12个成人头颅标本上利用颅中窝入路暴露岩内面神经、耳蜗、颈内动脉等结构。观测岩内膝状神经节、颈内动脉(internalcarotidartery,ICA)的膝部、内耳道内侧缘、棘孔与耳蜗之间的解剖关系。结果:耳蜗位于面神经膝状神经节的前下方和岩内ICA膝部的后上方,耳蜗覆盖到ICA膝部的上方。ICA水平段与ICA膝部和内耳道内侧缘连线的夹角为67.1°±4.3°。结论:以棘孔和膝状神经节连线的中点、膝状神经节、内耳道内侧缘形成的三角定位耳蜗。在耳前—颞下窝斜坡手术入路中,在中颅底,过ICA膝部做与ICA水平段成67.1°±4.3°的夹角,在这个夹角内磨除岩尖骨质,不会损伤耳蜗、内耳道及其内容物。耳蜗基底圈至ICA膝部的距离为(0.302±0.016)cm。从前向后磨除岩尖骨质时,ICA膝部后方的骨质磨除不要超过(0.302±0.016)cm,否则会损伤耳蜗。     

NMDA受体在正常大鼠颈动脉体的表达

应用免疫组织化学方法观察了离子型谷氨酸受体——NMDA受体的NR1及NR2A亚单位在正常成年雄性SD和Wistar大鼠颈动脉体的表达,并对阳性产物的表达强度进行了灰度分析及统计学处理。结果表明:正常成年SD大鼠及Wistar大鼠的颈动脉体内均存在NMDA NR1免疫反应阳性细胞,从阳性细胞的形态和分布特点判断这些阳性细胞为主细胞,两种大鼠之间无明显差异(P>0.05);而两种大鼠的颈动脉体内几乎不存在NMDA NR2A免疫反应阳性细胞。本实验的结果提示:在正常成年大鼠颈动脉体的主细胞上有NMDA受体的分布,并且该受体的二聚体构成不同于经典受体,这可能与谷氨酸在颈动脉体发挥的特殊功能有关。     

Influence of pH and pCO2 on Alpha-Receptor Mediated Contraction in Brain Vessels

The response of isolated brain vessels to various pH levels or carbon dioxide tensions was analyzed. Reduction of the pH induced a slight relaxation of the vessel, whereas an increase in the pH produced a slight contraction. These effects were markedly exaggerated when the alpha-adrenergic receptors in the vascular wall were activated by noradrenaline. During these conditions the contractile response to noradrenaline was reduced by about 40 per cent at a pH of 7.01, while, on the other hand, the response was enhanced 3-fold at a pH of 7.80. Variations in carbon dioxide tension of the buffer solution between 16 mmHg and 64 mmHg produced no consistent change, provided the pH remained constant. The results indicate that an interaction between the perivascular pH and the adrenergic alpha-receptor mediated contraction in brain vessels may occur.     

Calcitonin gene-related peptide is present in mammalian cerebrovascular nerve fibres and dilates pial and peripheral arteries

Calcitonin gene-related peptide (CGRP) is a novel 37-amino acid peptide occurring in neurones within sensory ganglia, in brain stem, as well as in the walls of blood vessels of peripheral organs. Pial arteries of cat showed a well-developed supply of CGRP-positive nerve fibres. The peptide was found to be a potent dilator of both pial and peripheral vessels of rabbit and cat, and of pial vessels from man. The dilatory effect was independent of the vascular endothelium and was not mediated through adrenergic, cholinergic or histaminergic smooth muscle receptors. The neurogenic vasoconstriction induced by electrical field stimulation was temporarily inhibited by CGRP, as studied in central ear arteries from rabbits. The results suggest that CGRP is a transmitter or modulator playing a role in the regulation of vascular tone.     

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.