硬化性炎症的实际观察

E. Boult
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The intention to be fulfilled by expansion of the chest through raising the ribs and depressing the diaphragm, is to cause the air to rush into the cells of the lungs: now, if the tubes all expanded at the same time as the thorax, say, for the sake of argument, to thesame extent to which the capacity of the chest had been increaed by its expansion, it is obvious that no air whatever would penetrate into the cells, as all that was drawn into the chest would be required to fill the tubes. Or, if the parietes expanded mucT, and the tubes comparatively little, the real vacuum in the air-cells would be only the difference between the increasedcapacity of the chest, and the increased space occupied within itby the expanded tubes. But on the other hand, if instead of expanding, the tubes contract at the moment that the chest expands, thus occupying a less space in its interior just when its capacity is greatest, it is obvious that a much increased vacuum will be formed, and that it will take place in the air cells where alone it is required; and thus, whatever air enters the chest goes directly to its destination, instead of lingering in the tubes. Taking this view, the operation of expiration as well as of inspiration, will be more intelligible, for it will be seen that if the tubes expand at the same moment that the chest contracts, the air cells will be submitted to direct pressure between the expauding tubes and the contracting thoracic parietes ; and while the air that has ceased to be serviceable to the animal economy is thus more effectually expelled from them, the way is at the same time more widely opened for its exit. It will be seen from the above, that inspiration is principally due to msc6ular action in the thoracic muscles, the diaphragm and the circular fibres of the bronchial tubes, whereas expiration depends more on cartilaginous elaticity, bringing down the ribs and expanding the tubes. If additional argument be wanting for the belief that the lungs must in themselves possess considerable power of inspiration and expiration, while within the unopened chest, independent of the expansion and contraction of the thoracic parietes, we would point to the apparently very -mall amount of abdominea respiration in a case of fractured rib, bandaged ecundum artem, and to certain states of syncope, etc., that will suggest themselves to each of us, in which respiration is maintained without any apparent thoracic or diaphragmatic motion. It appears, then, that contraction and expansion of the bronchial tubes is the only satisfactory mode of accounting for the well established fact, that the sound made by the inhaled breath rushing through the tubes towards the aircells is considerably more protracted than that made by the same air returming in expiration; for there does not appear sufficient difference in the forces exerted in drawing in and expelling the breath, to account for the difference of time occupied in its entrance and its exit, if the calibre of the tube remained the same. No sooner, however, do we admit that the air-tubes contract during inspiration, and expand during expiration, than the full value of a slight prolongation of the expiratory murmur becomes apparent as a consequence, and therefore as a certain symptom, of the deposit of tubercle in the parenchyma of the lung: for what change should we a priori infer to have taken place in the condition of the bronchi, if we found the expiratory murmur becoming as long, or nearly so, as that of mspiration, but that something had occurred to impede their elastic expansion, and that the tubes remained nearly of the same calibre in expiration as during inspiration? Now the part in which the earliest deposit of tubercle is found in the structure of the lung is known to be the cellular tissue immediately surroundingthe minute bronchi; and the natural effect of this would be to impair their elastic expansibility, and cause the difference of calibre of the tube in its utmost degree of contraction and expansion to be less than in health, and consequently the duration of the murmur of expiration to approach that of inspiration. I do not know that it is ever so protracted as to equal the latter sound; nor should we expect that the deposit of tubercle, although plainly calculated to interfere with the elasticity of the bronchi, should do away with the contractile power of their muscular fibres. What gives peculiar value to prolonged expiratory murmur as a reliable Symptom of phthisis is, that so far as I know, there is no other condition of the lung capable of producing it; cancer of the lung is the only disease that appears to me likely to do so, but whether it does or not, I have had no opportunity lately of ascertaining. The importance of possessing any symptom on which we can implicitly rely, independently of concomitant evidence, cannot be too highly appreciated in this disease, because it enables us to begin and follow up earnestly a course of treatment at a stage of the malady so early as almost to insure success; and a firm conviction that this symptom is truly diagnostic has this farther advantage, that, by the concentration of our attention upon it the ear soon becomes educated to a much finer discrimination of the presence or non-existence of tubercle than at first could have been thought possible, and in some cases a diagnosis may be made from this alone with a degree of certainty, that a stethoscopist without faith in it could hardly venture to found on the aggregate of all the other evidence derivable from auscultation and percussion. But it is not only in their bearing on the early discovery of tubercle in the lungs that the above considerations will be found interesting; for there are nervous affections of respiration, in which it is important to consider the action of the bronchial tubes, such for example as the anomalous sounds heard in some curious forms of hysterical spasm of the chest and throat, but more especially in spasmodic asthma, in which it is often most painful to the ear to listen to the effects of continued muscular contraction of the tubes during expiration. To the consideration of these very interesting subjects, and that of the early treatment of phthisis, I_hope soon to return in a future paper.","PeriodicalId":88830,"journal":{"name":"Association medical journal","volume":"19 1","pages":"1015 - 1018"},"PeriodicalIF":0.0000,"publicationDate":"1856-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"PRACTICAL OBSERVATIONS OF INFLAMMATION OF THE SCLEROTIC\",\"authors\":\"E. Boult\",\"doi\":\"10.1136/bmj.s3-4.204.1015\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"pulmonary tubere. Many years ago, whenasisting at the vivisection of a stunnd rsbbit, in which the trachea and larger bronchi were fully exposed, I was surprised to observe their muscular fibres contract, dimshing the diameter of their tubes, at each movement of inspiration. It is not the general belief that the tubes are contracted during inspiration, and expanded in expiration; but if we consider the anatomical structure of the lungs and the physical effects which the whole apparatus of respiration is intended to produce, it will be obvious that, had the bronchial tubesbeen made to contract during expiration, and expand during inspiration, as they are generally imagined to do, this would have defeated the object of bestowing on them any contractility or power of elastic expansion. The intention to be fulfilled by expansion of the chest through raising the ribs and depressing the diaphragm, is to cause the air to rush into the cells of the lungs: now, if the tubes all expanded at the same time as the thorax, say, for the sake of argument, to thesame extent to which the capacity of the chest had been increaed by its expansion, it is obvious that no air whatever would penetrate into the cells, as all that was drawn into the chest would be required to fill the tubes. Or, if the parietes expanded mucT, and the tubes comparatively little, the real vacuum in the air-cells would be only the difference between the increasedcapacity of the chest, and the increased space occupied within itby the expanded tubes. But on the other hand, if instead of expanding, the tubes contract at the moment that the chest expands, thus occupying a less space in its interior just when its capacity is greatest, it is obvious that a much increased vacuum will be formed, and that it will take place in the air cells where alone it is required; and thus, whatever air enters the chest goes directly to its destination, instead of lingering in the tubes. Taking this view, the operation of expiration as well as of inspiration, will be more intelligible, for it will be seen that if the tubes expand at the same moment that the chest contracts, the air cells will be submitted to direct pressure between the expauding tubes and the contracting thoracic parietes ; and while the air that has ceased to be serviceable to the animal economy is thus more effectually expelled from them, the way is at the same time more widely opened for its exit. It will be seen from the above, that inspiration is principally due to msc6ular action in the thoracic muscles, the diaphragm and the circular fibres of the bronchial tubes, whereas expiration depends more on cartilaginous elaticity, bringing down the ribs and expanding the tubes. If additional argument be wanting for the belief that the lungs must in themselves possess considerable power of inspiration and expiration, while within the unopened chest, independent of the expansion and contraction of the thoracic parietes, we would point to the apparently very -mall amount of abdominea respiration in a case of fractured rib, bandaged ecundum artem, and to certain states of syncope, etc., that will suggest themselves to each of us, in which respiration is maintained without any apparent thoracic or diaphragmatic motion. It appears, then, that contraction and expansion of the bronchial tubes is the only satisfactory mode of accounting for the well established fact, that the sound made by the inhaled breath rushing through the tubes towards the aircells is considerably more protracted than that made by the same air returming in expiration; for there does not appear sufficient difference in the forces exerted in drawing in and expelling the breath, to account for the difference of time occupied in its entrance and its exit, if the calibre of the tube remained the same. No sooner, however, do we admit that the air-tubes contract during inspiration, and expand during expiration, than the full value of a slight prolongation of the expiratory murmur becomes apparent as a consequence, and therefore as a certain symptom, of the deposit of tubercle in the parenchyma of the lung: for what change should we a priori infer to have taken place in the condition of the bronchi, if we found the expiratory murmur becoming as long, or nearly so, as that of mspiration, but that something had occurred to impede their elastic expansion, and that the tubes remained nearly of the same calibre in expiration as during inspiration? Now the part in which the earliest deposit of tubercle is found in the structure of the lung is known to be the cellular tissue immediately surroundingthe minute bronchi; and the natural effect of this would be to impair their elastic expansibility, and cause the difference of calibre of the tube in its utmost degree of contraction and expansion to be less than in health, and consequently the duration of the murmur of expiration to approach that of inspiration. I do not know that it is ever so protracted as to equal the latter sound; nor should we expect that the deposit of tubercle, although plainly calculated to interfere with the elasticity of the bronchi, should do away with the contractile power of their muscular fibres. What gives peculiar value to prolonged expiratory murmur as a reliable Symptom of phthisis is, that so far as I know, there is no other condition of the lung capable of producing it; cancer of the lung is the only disease that appears to me likely to do so, but whether it does or not, I have had no opportunity lately of ascertaining. The importance of possessing any symptom on which we can implicitly rely, independently of concomitant evidence, cannot be too highly appreciated in this disease, because it enables us to begin and follow up earnestly a course of treatment at a stage of the malady so early as almost to insure success; and a firm conviction that this symptom is truly diagnostic has this farther advantage, that, by the concentration of our attention upon it the ear soon becomes educated to a much finer discrimination of the presence or non-existence of tubercle than at first could have been thought possible, and in some cases a diagnosis may be made from this alone with a degree of certainty, that a stethoscopist without faith in it could hardly venture to found on the aggregate of all the other evidence derivable from auscultation and percussion. 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引用次数: 0

摘要

肺tubere。许多年前,当我协助对一只受惊的兔子进行活体解剖时,我惊讶地发现,每次吸气时,它们的肌肉纤维都会收缩,气管和较大的支气管都会变细。一般人并不认为气管在吸气时收缩,呼气时扩张;但是,如果我们考虑到肺的解剖结构和整个呼吸装置所要产生的物理效果,很明显,如果支气管在呼气时收缩,在吸气时扩张,就像它们通常想象的那样,这将使它们失去任何收缩性或弹性扩张能力的目的。胸部的意图来实现扩张通过提高肋骨和令人沮丧的隔膜,是导致空气涌入肺细胞:现在,如果管胸腔扩大的同时,说,为了论证,程度以及对胸部的容量提高了其扩张,很明显,没有空气无论渗透细胞,因为所有卷入的胸部需要填补管。或者,如果肺泡壁膨胀得很大,而肺泡管膨胀得相对较小,那么肺泡里真正的真空就只是胸腔容量的增加与膨胀的肺泡管所占空间的增加之差。但另一方面,如果在胸腔扩张的同时,肺管不扩张,而是收缩,这样,在胸腔容量最大的时候,肺管在胸腔内部所占的空间就更小了,很明显,就会形成大得多的真空,而这种真空只会发生在需要真空的空气室里;因此,任何进入胸腔的空气都会直接到达目的地,而不是停留在管道中。从这个观点出发,呼气和吸气的操作就更容易理解了,因为可以看出,如果在胸部收缩的同时,气管也在扩张,那么在扩张的气管和收缩的胸壁之间,空气细胞就会受到直接的压力;当不再对动物经济有用的空气被更有效地从它们身上驱逐出去的同时,它的出路也更广泛地打开了。从上面可以看出,吸气主要是由于胸肌、膈肌和支气管的圆形纤维的肌肉活动,而呼气则更多地取决于软骨弹性,使肋骨下降并使管道扩张。如果没有更多的论据来证明肺本身一定具有相当大的吸气和呼气的能力,而在未打开的胸腔内,不受胸壁的扩张和收缩的影响,我们可以指出,在肋骨断裂的情况下,在包扎腋下硬膜的情况下,在某些晕厥状态下,等等,这是我们每个人都会想到的。呼吸维持,没有明显的胸廓或膈肌运动。因此,看来支气管的收缩和扩张是唯一能令人满意地解释这一公认事实的模式,即吸入的空气通过气管冲向空气细胞所发出的声音比同样的空气在呼气时返回所发出的声音要持久得多;因为,如果管子的口径保持不变,吸入和呼出空气时所施加的力似乎没有足够的差别来说明吸入和呼出空气所花费的时间的差别。然而,一旦我们承认气管在吸气时收缩,呼气时扩张,呼气杂音轻微延长的全部价值就会变得明显,这是肺实质中结节沉积的结果,因此也是某种症状。如果我们发现呼气杂音变得和吸气杂音一样长,或者几乎和吸气杂音一样长,但是发生了什么事情阻碍了它们的弹性扩张,并且气管在呼气时和吸气时几乎保持相同的口径,那么我们应该先验地推断支气管的状况发生了什么变化呢?现在,已知在肺结构中最早发现结核沉积的部分是紧挨着小支气管的细胞组织;这样做的自然结果是损害了它们的弹性膨胀性,导致气管在最大程度的收缩和扩张时的口径差异小于健康时,因此呼气时杂音的持续时间接近吸气时的持续时间。 我不知道它是否会拖得那么久,以至于和后一种声音一样长;我们也不应该期望结核的沉积,虽然显然会干扰支气管的弹性,但会消除肌肉纤维的收缩能力。延长的呼气杂音作为肺结核的可靠症状的特殊价值在于,据我所知,肺部没有其他条件能够产生这种杂音;在我看来,肺癌是唯一可能导致这种情况的疾病,但究竟是不是这样,我最近一直没有机会去查明。在这种疾病中,拥有任何我们可以隐含地依赖的症状的重要性,而不依赖于伴随的证据,这一点再怎么强调也不为过,因为它使我们能够在疾病的早期阶段开始并认真地跟踪一个疗程,几乎可以确保成功;坚信这种症状确实是诊断的,还有一个更大的好处,那就是,通过我们对它的集中注意力,耳朵很快就能比最初想象的更准确地分辨出是否存在结核病,在某些情况下,仅凭这一点就可以作出一定程度的诊断,一个听诊师如果不相信这一点,就很难在听诊和打击的所有其他证据的总和上发现这一点。但是,上述考虑的有趣之处不仅在于它们与早期发现肺部结核的关系;因为有呼吸的神经反应,在这种情况下,重要的是要考虑支气管的作用,例如,在一些奇怪的形式的歇斯底里的胸部和喉咙痉挛中听到的异常声音,但更特别的是在痉挛性哮喘中,在呼气时听到管的持续肌肉收缩的影响,耳朵往往是最痛苦的。考虑到这些非常有趣的主题,以及肺结核的早期治疗,我希望在未来的一篇论文中很快回来。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
PRACTICAL OBSERVATIONS OF INFLAMMATION OF THE SCLEROTIC
pulmonary tubere. Many years ago, whenasisting at the vivisection of a stunnd rsbbit, in which the trachea and larger bronchi were fully exposed, I was surprised to observe their muscular fibres contract, dimshing the diameter of their tubes, at each movement of inspiration. It is not the general belief that the tubes are contracted during inspiration, and expanded in expiration; but if we consider the anatomical structure of the lungs and the physical effects which the whole apparatus of respiration is intended to produce, it will be obvious that, had the bronchial tubesbeen made to contract during expiration, and expand during inspiration, as they are generally imagined to do, this would have defeated the object of bestowing on them any contractility or power of elastic expansion. The intention to be fulfilled by expansion of the chest through raising the ribs and depressing the diaphragm, is to cause the air to rush into the cells of the lungs: now, if the tubes all expanded at the same time as the thorax, say, for the sake of argument, to thesame extent to which the capacity of the chest had been increaed by its expansion, it is obvious that no air whatever would penetrate into the cells, as all that was drawn into the chest would be required to fill the tubes. Or, if the parietes expanded mucT, and the tubes comparatively little, the real vacuum in the air-cells would be only the difference between the increasedcapacity of the chest, and the increased space occupied within itby the expanded tubes. But on the other hand, if instead of expanding, the tubes contract at the moment that the chest expands, thus occupying a less space in its interior just when its capacity is greatest, it is obvious that a much increased vacuum will be formed, and that it will take place in the air cells where alone it is required; and thus, whatever air enters the chest goes directly to its destination, instead of lingering in the tubes. Taking this view, the operation of expiration as well as of inspiration, will be more intelligible, for it will be seen that if the tubes expand at the same moment that the chest contracts, the air cells will be submitted to direct pressure between the expauding tubes and the contracting thoracic parietes ; and while the air that has ceased to be serviceable to the animal economy is thus more effectually expelled from them, the way is at the same time more widely opened for its exit. It will be seen from the above, that inspiration is principally due to msc6ular action in the thoracic muscles, the diaphragm and the circular fibres of the bronchial tubes, whereas expiration depends more on cartilaginous elaticity, bringing down the ribs and expanding the tubes. If additional argument be wanting for the belief that the lungs must in themselves possess considerable power of inspiration and expiration, while within the unopened chest, independent of the expansion and contraction of the thoracic parietes, we would point to the apparently very -mall amount of abdominea respiration in a case of fractured rib, bandaged ecundum artem, and to certain states of syncope, etc., that will suggest themselves to each of us, in which respiration is maintained without any apparent thoracic or diaphragmatic motion. It appears, then, that contraction and expansion of the bronchial tubes is the only satisfactory mode of accounting for the well established fact, that the sound made by the inhaled breath rushing through the tubes towards the aircells is considerably more protracted than that made by the same air returming in expiration; for there does not appear sufficient difference in the forces exerted in drawing in and expelling the breath, to account for the difference of time occupied in its entrance and its exit, if the calibre of the tube remained the same. No sooner, however, do we admit that the air-tubes contract during inspiration, and expand during expiration, than the full value of a slight prolongation of the expiratory murmur becomes apparent as a consequence, and therefore as a certain symptom, of the deposit of tubercle in the parenchyma of the lung: for what change should we a priori infer to have taken place in the condition of the bronchi, if we found the expiratory murmur becoming as long, or nearly so, as that of mspiration, but that something had occurred to impede their elastic expansion, and that the tubes remained nearly of the same calibre in expiration as during inspiration? Now the part in which the earliest deposit of tubercle is found in the structure of the lung is known to be the cellular tissue immediately surroundingthe minute bronchi; and the natural effect of this would be to impair their elastic expansibility, and cause the difference of calibre of the tube in its utmost degree of contraction and expansion to be less than in health, and consequently the duration of the murmur of expiration to approach that of inspiration. I do not know that it is ever so protracted as to equal the latter sound; nor should we expect that the deposit of tubercle, although plainly calculated to interfere with the elasticity of the bronchi, should do away with the contractile power of their muscular fibres. What gives peculiar value to prolonged expiratory murmur as a reliable Symptom of phthisis is, that so far as I know, there is no other condition of the lung capable of producing it; cancer of the lung is the only disease that appears to me likely to do so, but whether it does or not, I have had no opportunity lately of ascertaining. The importance of possessing any symptom on which we can implicitly rely, independently of concomitant evidence, cannot be too highly appreciated in this disease, because it enables us to begin and follow up earnestly a course of treatment at a stage of the malady so early as almost to insure success; and a firm conviction that this symptom is truly diagnostic has this farther advantage, that, by the concentration of our attention upon it the ear soon becomes educated to a much finer discrimination of the presence or non-existence of tubercle than at first could have been thought possible, and in some cases a diagnosis may be made from this alone with a degree of certainty, that a stethoscopist without faith in it could hardly venture to found on the aggregate of all the other evidence derivable from auscultation and percussion. But it is not only in their bearing on the early discovery of tubercle in the lungs that the above considerations will be found interesting; for there are nervous affections of respiration, in which it is important to consider the action of the bronchial tubes, such for example as the anomalous sounds heard in some curious forms of hysterical spasm of the chest and throat, but more especially in spasmodic asthma, in which it is often most painful to the ear to listen to the effects of continued muscular contraction of the tubes during expiration. To the consideration of these very interesting subjects, and that of the early treatment of phthisis, I_hope soon to return in a future paper.
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