Pathological Structural Changes Research Articles

Migration of porcine endothelial and smooth muscle cells in response to platelet-associated factors.

A NeuroProbe multiwell microchemotaxis assembly has been used to study the migration of porcine aortic endothelial and smooth muscle cells in vitro in response to serum factors. Whole pig serum was found to be chemokinetic for endothelial cells but not smooth muscle cells. Chemokinetic activity was higher in platelet-enriched, plasma-derived serum (PDS) than in platelet-free PDS. The supernatant from washed, lysed pig platelets also showed chemokinetic activity both for endothelial and smooth muscle cells. Chromatography on Sephadex G-200 showed that the lysate contained a number of activities that act independently on the two cell types. The chemokinetic activity that we have detected appears to be distinct from the chemotactic effect of platelet-derived growth factor and platelet factor 4 on the basis of insensitivity to protamine sulfate and molecular size. The role of these platelet factors in pathological changes in vascular structure is currently under study.

Morphological changes in ganglia of the celiac plexus following major abdominal operations

Experiments on 163 dogs were made to study the time course of histological and ultrastructural changes in celiac plexus nodes after resection of the two-thirds of the stomach as well as after some other large operations on the abdominal organs (economic gastric resection, cholecystectomy, resection of the small intestine). It has been demonstrated that since the first days after operation the gangliocytes and neuroglial cells of celiac plexus nodes manifested histological changes detectable at light and electron microscopy levels. These changes were largely reversible in nature despite destructive processes eventuating in the death of some gangliocytes, pericapsular gliocytes and neurolemmocytes. The most overt changes were observed towards the first week after operation, the number of neurons with reversible changes amounting to 42% and that having the signs of destruction to 9.9%. At the later stages the intensity of the histological changes was noticeably reduced. Analogous data were obtained during studies of the time course of the histological changes after other above-indicated operations. However, the intensity of the changes was substantially less than that seen after resection of the two-thirds of the stomach. The evidence obtained allows the conclusion that the pathological structural changes that develop in the celiac plexus after resection of the two-thirds of the stomach play one of the leading parts in the pathogenesis of the post-gastroresection syndrome.

A Psychophysiological Interpretation of Voodoo Illness and Voodoo Death

Voodoo illness is a form of psychosomatic illness. When sufficiently intense and prolonged, the extreme physiological arousal pattern to stimulation that comprises emotional behavior produces pathological changes in physiological functioning and anatomic structure, which are psychophysiological and psychosomatic disorders. New stimuli may become associated with established autonomic reaction patterns that are emotional behavior; also particular autonomic reactions may be strengthened through differential reinforcement. Thus, emotional stimuli and emotional response patterns may be learned. When the emotional reaction patterns are sufficiently frequent or prolonged and sufficiently intense in the person socially prepared to react and physically predisposed (i.e., vulnerable via genetically determined or later acquired biological weakness), changes of such magnitude may occur in physiological functioning or anatomical structure as to be incompatible with continued life. Voodoo death corresponds to that formulation of psychosomatic death.

Mitochondrial abnormalities in muscle from vitamin B 12-deficient sheep

Skeletal and cardiac muscles from vitamin B 12-deficient sheep were examined. Histochemical studies did not reveal any gross pathological changes in the muscle structure, but there was an abnormal distribution of the product of the NADH-diaphorase reaction. Electron microscopy revealed an abnormal distribution of mitochondria, changes in the number and arrangement of cristae within the mitochondria and the presence of inclusions. The possibility that alterations in mitochondrial morphology are early lesions attributable to metabolic changes in vitamin B 12 deficiency is discussed.

Teratogenic effects of hyperthermia in the bonnet monkey (Macaca radiata).

AbstractSeventeen timed‐mated bonnet monkeys (Macaca radiata) were exposed to hyperthermia in a forced‐draft incubator for a duration of one, three, four or eight days between 21 and 46 days of gestation. On each day of exposure the core temperature of the pregnant animal was elevated 2.4 to 5.4°C above the reference temperature recorded before heat exposure. Malformations occurred following a one‐hour daily elevation of the core temperature above the reference temperature under the following exposure conditions: 3.8°C, days 23 to 26; 3.9°C, days 24 to 27; 2.4°C, days 27, 28 and 30; and 4.1°C, day 26 of gestation. Five resorptions occurred following exposure for one, three or four days between days 24 and 29 of gestation after core temperature elevation of 3.7 to 4.4°C and three abortions occurred following exposure for four days between days 24 and 35 of gestation after core temperature elevation of 2.6 to 3.9°C. The results clearly indicate that the teratogenic sensitive period is from 23 to 30 days gestation following elevations of the core temperature from 2.4 to 4.1°C. No distinct pattern of malformations was observed although skeletal and umbilical cord malformations were the most common. Pathological changes in placental structure, expecially maternal surface infarctions and intervillous thrombi, were associated with three of the four abnormal fetuses, suggesting a relationship between pathological placental characteristics and fetal malformations in this study. The degree of core temperature elevation which resulted in malformations in the present study are similar to those applied to other mammalian species, and the specific anomalies observed in the bonnet monkey resemble those observed in other mammalian species, including man.

Two-dimensional echo-encephalography. 1. Acoustic properties of some tissues and the characteristics of echo patterns obtained using equipment especially adapted for detection of these tissues.

In this paper the results of measurements of ultrasound velocity in, and density of, a number of normal and pathological tissues are given. From the results it can be concluded that intracranial pathological regions will often be detectable with ultrasound techniques, but is is not possible with any degree of certainty to localise precisely the morphological boundaries of these abnormal regions. Because, in the large majority of cases, the echoes from intracranial pathological structural changes are of weak intensity, a simple electronic device is described which, in conjunction with standard echo equipment, has been shown to be of use for better detection of these weak signals.

Quantitative evaluation of myocardial ultrastructure following hypothermic anoxic arrest

Thirty-six anesthetized mongrel dogs were subjected to systemic hypothermia and anoxic cardiac arrest while on cardiopulmonary bypass. Myocardial fine structure in the left ventricle was evaluated by quantitative analysis in the subepicardial, mid-myocardial, and subendocardial layers. The specimens were obtained by a transmural myocardial biopsy method. Graded hypothermia was employed at 36 degrees, 30 degrees, 28 degrees, 25 degrees, and 22 degrees C. The aorta was cross-clamped for 30 minutes at 36 degrees, 30 degrees, 28 degrees, and 25 degrees C. or for 45 minutes at 25 degrees and 22 degrees C. Observations indicated that pathological changes of the myocardial fine structure were significant after anoxic arrest in the normothermic group. Lesions were most extensive in the subendocardial layer after normothermic anoxic arrest, whereas hypothermia below 30 degrees C. preserved the myocardium throughout all layers without difference in pathological changes in the fine structure among the layers. Mitochondria and glycogen granules in the mid-myocardial layer and the subendocardial layer were best preserved with hypothermia at 25 degrees and 22 degrees C. after 30 minutes or 45 minutes of anoxic arrest, and dogs in these groups had a survival rate of 100 percent. Quantitative analysis of ultrastructural changes induced in these experiments suggest that a safe duration of anoxic arrest at 22 degrees to 25 degrees C. is between 30 and 45 minutes.

Ventricular fibrillation during cardiopulmonary bypass.

Changes in ultrastructure after induced ventricular fibrillation were studied in the normothermic and nonhypertrophic canine heart using a transmural myocardial biopsy method. Comparisons were made between subendocardial and subepicardial layers by the quantitative evaluation of ultrastructural changes in mitochondria and glycogen granules. Slight abnormalities characterized by interstitial edema, mitochondrial derangement, contraction bands, swelling of capillary endothelium were demonstrated throughout the myocardium following ventricular fibrillation. The myocardium following ventricular fibrillation did not demonstrate differences in ultrastructure between the subendocardial and subepicardial layers. These pathologic fine structural changes were at least in part reversible. Quantification of ultrastructure showed that mitochondria and glycogen granules were well preserved. It was suggested that the myocardium following ventricular fibrillation may be less affected by the no-reflow phenomenon after restoring normal coronary circulation.

Plasmodium simium: Ultrastructure of erythrocytic phase

An electron microscopic study of Plasmodium simium infections in the squirrel monkey has supplied information on the ultrastructure of erythrocytic trophozoites, schizonts, merozoites, and gametocytes, in addition to an unusual form of host cell pathology. In general, the structural features, as well as certain specialized functions, e.g., hemoglobin ingestion and utilization, nuclear and cytoplasmic division, were found to be similar to those described for other malarial parasites. Some striking features were noted, however. A highly asynchronous mode of merozoite production was observed within single segmenting parasites in spite of the overall developmental synchrony displayed by the population as a whole. Secondly, during parasite segmentation, newly formed merozoites are connected to one another, as well as to the parasitophorous membrane, by periodic surface strands. It is speculated that these interparasite bridges serve as structural support to the segmenting parasite. When merozoites are matured fully, these interconnections break, leaving a uniform array of short surface bristles. In addition, a number of different pathological changes in host cell structure have been noted. Localized surface discontinuities appear in region of infected cells where apical regions of developing or fully mature merozoites are abutted against the plasma membrane. These profiles suggest that these specialized apical regions of the merozoite function in release as well as in host cell penetration. More generalized surface pathology occurs within parasitized erythrocytes in the form of surface blebs, surface clefts, and associated cytoplasmic microvesicles. The severity of this pathology increases as the intraerythrocytic parasite matures. Topographically these altered cells have a “berry-like” surface texture which makes them quite distinctive when viewed by scanning electron microscopy.

The microcirculatory hepatic unit

The hepatic microcirculation, the result of the total merging of hepatic arterial and portal stream in the sinusoidal delta, is organized in well-defined microcirculatory hepatic units. The unit consists of a terminal portal venule (TPV) and a glomus of sinusoids branching off from it. The associated hepatic arterioles form a periductular plexus wherefrom efferent arterial capillaries join the sinusoids close to TPV; other arterioles bypass the periductular plexus and empty directly into the sinusoids. The microcirculatory unit provides the vascular framework for the structural and functional hepatic unit, the liver acinus. Simple and complex acini are microscopic masses of parenchyma surrounding like berries their supplying terminal and preterminal vessels, respectively, along with the associated ductules, lymph vessels, and nerve fibres. The structure and dimensions of the hepatic microvasculature and their hemodynamic relevance is discussed. Hydrostatic pressure in the TPV is low. The impressive drop of pressure in the sinusoidal bed down to hepatic venular level is tentatively explained. In the sinusoids, the site of A-V shunting, the energy of arteriolar pressure is transformed into velocity; the fast flow of arterial blood exerts a symphoning effect on interconnected sinusoids. Intermittent flow in the microcirculatory units is regulated by the smooth muscles in the arteriolar wall and by precapillary sphincters responding to nervous stimuli, hormones, metabolites, bile salts, and vasoactive substances. Portal flow is controlled by the mesenteric and splenic microvessels. The definition of the microcirculatory unit within the acinus offers a hemodynamic approach to the understanding of pathologic circulatory and structural changes in the liver.

Ultrastructural changes in the midgut epithelium of an elaterid larva (Coleoptera) infected enterically with Pseudomonas aeruginosa.

Soil bacteria enter the digestive tract of wireworms at ecdysis through the dorsal exuvial split and ecdysial space. Pseudomonas aeruginosa, a potential pathogen of insects, multiplies in the enteron, but many are killed within it. The mucopeptide layer of the bacterial cell wall is affected early in the degenerative process.A surface epithelial mucoid layer provides a temporary protective barrier for the midgut epithelium against the bacteria. The bacteria affect the fine structure of the host midgut epithelium in three primary ways. (1) The cells take up and retain fluids in the cytoplasm and membrane-bound vacuoles to the point of apical rupture; the selective permeability of the membranes of the cell and vacuoles appears to be affected. (2) The surface mucoid covering is degraded, the exposed plasma membrane is disrupted, and a lytic erosion of the exposed cytoplasm occurs opposite bacterial colonies. Lesions thus form in the midgut epithelium, and could lead to perforation of the wall at these points. (3) Pathological changes occur in various cell organelles, the most striking of which are an increase in abundance of rough endoplasmic reticulum (RER) and cytoplasmic ribosomes, and a transposition of membrane material from mitochondria and Golgi complexes to RER. The functional implications of these pathological changes in fine structure are discussed.

CHICAGO LARYNGOLOGICAL AND OTOLOGICAL SOCIETY: Regular Meeting, Feb. 6, 1928

ALTERATION IN THEACTIVITY OF THEEIGHTHNERVEPRODUCED BYRAPIDCHANGES IN THEBLOODPRESSURE IN THENORMALHUMANBEING. ByDR. J.FRANKPEARCYandDR.DANIELB.HAYDEN. In clinical hypertension there is frequently a decrease in auditory acuity for the higher (but not the highest) tones. Such patients commonly complain of tinnitus aurium and vertigo. That these symptoms are caused by the high blood pressure per se is a gratuitous assumption. It is equally likely that the pathologic structural changes associated with the hypertension produce the symptoms. In some instances, hypotension has been associated with vertigo, tinnitus and a similar defect in hearing. These symptoms are found occasionally in severe cases of anemia. One is tempted to speculate on a common cause for the symptoms in the three cases. Such a cause might be an insufficient supply of oxygen to the internal ear. There is

THE RELATION OF PATHOLOGIC PHYSIOLOGY TO INTERNAL MEDICINE

For surgery, pathologic anatomy has furnished a basis for both diagnosis and treatment. The tumor or foreign body can be taken out, the inflamed part incised or removed, the obstructed passage dilated or the hollow viscus drained. For internal medicine, pathologic anatomy has been equally important as a fundamental basis in the diagnosis of disease; and it has furnished an exact demonstrable basis for many symptom-complexes. So far as treatment is concerned, however, its direct value is far less evident, for pathologic changes in structure are but rarely influenced by medicine. The clinician schooled in pathologic anatomy is therefore apt to be led into a position of therapeutic nihilism, placing his reliance chiefly on the curative forces of Nature which are to be assisted here and there by medical care and by nursing. This attitude, which was prominent in certain clinical schools during the last century, found its expression in