The ultrastructural changes, proximal to a constriction, in unmyelinated postganglionic sympathetic axons have been studied in the cat splenic and hypogastric nerves. They were con stricted with a fine ligature, which was left in situ , and examined at intervals up to 24h after operation. Immediately after tying the ligature there were definite changes in the morphology and organelle content of the axons adjacent to the constriction. These were due to the mechanical trauma produced by tying the ligature. From 10 min onwards there was a rapid accumulation of organelles in axons, which became progressively more swollen. Eventually the plasma membranes of both axons and Schwann cells broke down and later the Sclrwann cell basement membrane ruptured , allowing axonal organelles to escape into the interstitial spaces. The accumulating organelles included vesicles with an electron dense core, mitochondria, large vacuoles and myelin figures. Filamentous structures and both fine and wide tubules were more prominent and more numerous after operation. These were accompanied by a marked increase in the number of agranular vesicles. Tubular structures, morphologically similar to both the agranular vesicles and the vacuoles, were also very numerous. This similarity in appearance and the fact that many of these agranular vesicles, vacuoles and tubules were found joined together by either filaments or fine tubules suggests that they are part of the same system . At all times the greatest accumulation of organelles and the most marked axonal swelling was found in the first 0.5 to 1 mm segment of nerve immediately adjacent to the constriction. Less marked changes, affecting principally the agranular vesicles and finer tubules to gether with focal accumulations of mitochondria were seen at more proximal levels from 4h onwards. It is suggested that the axonal swelling is due to the accumulation of axoplasm and organelles. Two possible interpretations are discussed: (1) that this represents the effects of obstructing the normal flow of axoplasm from the cell body to the periphery, and (2) that some features, in particular the increase in the size and number of the various tubules may be indicative of an active reaction to the effects of axonal injury. These two phenomena probably take place simultaneously and are accompanied by degenerative changes.
. The accumulation of granular vesicles proximal to a constriction applied to hypogastric nerves has been investigated with the electron microscope in cats treated with reserpine and/or iproniazid. . The ultrastructural changes have been correlated with the accumulation of noradrenaline at the same site in similarly treated animals. . The findings give further support to the view that granular vesicles constitute a major storage site for intraneuronal noradrenaline.
Evidence suggests that pulmonary vascular resistance is reduced at high lung inflation in the normal individual [1]. The volume of vessels exposed to alveolar pressure is reduced, but that of larger "extra-alveolar" vessels is increased. It is thought that the latter are expanded by radial forces and increasing negative perivascular pressure, whereas the small "alveolar" vessels are compressed or narrowed by increased tension in the alveolar walls; the result is an overall increased lung vascular volume and decreased pulmonary vascular resistance (PVR) [1]. The anatomical identity of the two types of vessels is not defined. However, in normal animals and humans, most of the vessels within the acinus are nonmuscular, whereas in chronic hypoxia, many of them become muscularized [2,3]. We showed conspicuous changes in reactivity and haemodynamic properties of the pulmonary circulation in chronically hypoxic (CH), compared with normal (C) rats [4][5][6]. Lung arterioles are also muscularized in hypoxic chronic bronchitis and emphysema, although there are additional features that are found neither in experimental animals nor, with minor exceptions, in high altitude residents [7].In 1966, HARRIS et al. [8, 9] showed that patients with chronic bronchitis have an abnormal pressure/flow (P/Q'), relation on exercise. Unlike in normal subjects, the "exercise" line is displaced from that measured at rest; in normal subjects, a similar displacement is caused when they breathe against an expiratory resistance. They suggested that, in the patients, airways obstruction might lead to a raised alveolar pressure (Palv) that could lead to a rise in pulmonary artery pressure (Ppa). With this work in mind, we looked at the consequences, in CH rats, of raising Palv. We found that during vasoconstriction caused by hypoxia or almitrine, a rise in Palv caused a larger displacement of the P/Q' line than in C rats [5,10]. We attributed this to the remodelling of the chronically hypoxic pulmonary vessels. Our hypothesis was that in chronic hypoxia, lung inflation compresses newly muscularized "alveolar" vessels but fails to expand the stiffer "extra-alveolar" vessels and also that hypoxia constricts more peripheral muscular vessels than in normal rats. However, one feature of this work did not fit the hypothesis quantitatively. We measured the relation between Ppa and Palv while we rapidly deflated the lung. In normoxia below an "inflection point" at about Palv 0.27-0.40 kPa (2-3 mmHg) in both C and CH rats, Ppa ceased to fall and remained constant or increased. According to the work of PERMUTT et al. [11], the inflection point reflects the intervention of "extraalveolar" vessels whose upstream critical closing pressure prevents the transmission of Palv to Ppa. Thus, if C rats exhibit hypoxic pulmonary vasoconstriction (HPV) in "extra-alveolar" vessels, the inflection point should rise to a higher Palv during hypoxia: there was a rise, but smaller than expected.Further work showed that during vasoconstriction caused by either hypoxia or al...
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