Changes In Small Blood Vessels Research Articles

Anti-inflammatory and analgesic activities of Vatavidhvamsana rasa, An Ayurvedic herbo-mineral formulation

Background: Inflammation is a complex process mainly comprises of three phases namely acute, sub-acute and chronic. In acute inflammatory conditions fluid and granulocytic cells accumulate at the site of injury because of the changes in small blood vessels. This response often activates systemic response such as leucocytosis, protein catabolism, fever and synthesis of C-reactive protein, an acute-phase protein In Ayurvedic texts, several herbo-mineral preparations to fight against inflammation have been found; among them, Vatavidhvamsana Rasa (VVR) is one, which is said to be remarkable in inflammation condition. Aim and Objectives: To assess the anti-inflammatory and analgesic effects of VVR in pharmacologically validated models. Materials and methods: Wistar strain albino rats weighing 200 ± 20 of either sex were used in the study. VVR was administered at a dose of 22.5 mg/kg for the rat. Results: Vatavidhvamsana Rasa (VVR) showed a significant decrease in the carrageenan-induced paw oedema after 1-hour interval in comparison to the control group (P<0.05) and at 3 hours and 5 hours intervals it showed a non-significant decrease in carrageenan-induced paw oedema in albino rats. In the analgesic activity, VVR treated group showed a significant increase in radiant heat response at 30 min. interval (P<0.05) and non-significant increase at 60 mins in comparison to initial and control group. Conclusion: The results concluded that Vatavidhvamsana Rasa has anti-inflammatory and analgesic activity. Accordingly, it can be used in the management of pain and inflammatory conditions.

Anti‐C1q antibodies in scleroderma

Systemic sclerosis (SSc) is an autoimmune condition which means that the body's immune system, which usually fights off disease, wrongly targets healthy parts of the body, and SSc patients produce antibodies to their own tissues (‘autoantibodies’). Extensive thickening and scarring of tissues (fibrosis) is the main feature of the condition and is due to over‐production of collagen. Changes in small blood vessels also occur. When fibrosis occurs in the lungs (pulmonary fibrosis) it can lead to high blood pressure in the arteries going to the lungs, and this may be life‐threatening. The condition is commoner in women. SSc can be localised or disseminated (generalised), depending on the extent of skin involvement. Although the cause of SSc has not been fully worked out, many of the autoantibodies associated with the condition are believed to be involved in one way or another. Autoantibodies called ‘anti‐C1q’ are certainly found in another autoimmune condition called systemic lupus erythematosus, so the aim of this study from Greece and the USA was to see if they were also present in SSc. Anti‐C1q autoantibodies were found in 16.1% of the 124 SSc patients in the study, occurring as often as the third most frequently found autoantibody, known as anti‐RNA polymerase III. They were found particularly in men and in patients with disseminated SSc. Presence of anti‐C1q antibodies was associated with pulmonary fibrosis but not with any of the other features of SSc. The authors therefore suggest that anti‐C1q autoantibodies could be looked at as a marker for (sign of) pulmonary fibrosis in SSc patients.

Hematologic toxicity of immunosuppressive treatment

The administration of immunosuppressive agents may be associated with the occurrence of hematologic toxicity, such as anemia, due to bone marrow suppression or hemolysis, leukopenia, and thrombocytopenia. The administration of azathioprine and mycophenolate mofetil is more frequently associated with bone marrow suppression, while hemolytic-uremic syndrome may occur after administration of cyclosporine, tacrolimus, or muromonab (OKT3) and may be associated with the loss of the allograft. Moreover, microangiopathic hemolytic anemia and thrombocytopenia are rare, but potentially severe, complications of immunosuppressive treatment with tacrolimus and cyclosporine; they are characterized by intravascular hemolysis due to mechanical destruction of red cells as a result of pathological changes in small blood vessels. Viral infections (cytomegalovirus), administration of antiviral agents (gancyclovir), inhibitors of angiotensin-converting enzyme and angiotensin II receptor antagonists, antibacterial agents (sulfamethoxazole and trimethoprim), and allopurinol may aggravate bone marrow suppression, particularly when administered with agents that interfere with purine biosynthesis, including azathioprine and mycophenolate mofetil.

Primary Hypertrophic Osteoarthropathy: Clinical, Radiologic, and Scintigraphic Characteristics

Background Our aim was to establish clinical and imaging characteristics of primary hypertrophic osteoarthropathy (PHO). Methods A group of 76 patients (71 men and 5 women) with primary hypertrophic osteoarthropathy was examined. Extensive history and status of the locomotor system were determined in all patients. Radiologic and scintigraphic examinations of the bones, thermography, capillaroscopy, gastroscopy, and histologic analysis were also performed. Results Family history was positive in all 55 patients (100%) summoned for a check-up. Finger clubbing of the hands and feet as well as positive Schamroth test were found in all patients, while hyperhydrosis was found in 65 (85.5%), seborrhea in 39 (51%), and involvement of the joints in 52 (68.5%) patients. Histologic analysis in 18 (23.7%) patients predominantly showed periarticular edema and moderate cellular activity. Periostosis of the long bones was also found in all patients, while scintigraphy, performed in 44 patients, was positive in 18 (33.5%) patients in the active phase of the disease. Thermography, performed in 10 patients, ranged from hypothermia to thermal amputation of feet and hands. Capillaroscopy of hands and feet in 47 (61.8%) patients showed changes in small blood vessels. Gastroscopy indicated abnormalities (ulcer and hypertrophic gastritis) in 21 patients (27.6%). Conclusions PHO has special clinical and radiographic manifestations (finger clubbing and periostosis of the long bones) that are associated with some minor manifestations. Development of the disease is gradual (to 20 years) and requires a special diagnostic assessment.

Pathology of the heart and blood vessels in Hansen's disease

There are few reports on the cardiovascular changes accompanying Hansen's disease, and many aspects remain unclear. We performed macroscopic and histologic examinations on the cardiovascular system in autopsy (47 cases of L type, 2 cases of B type and 14 cases of T type) and biopsy cases of Hansen's disease. The changes in small blood vessels and capillaries were also observed using electron microscopy. Cardiac changes such as atrophy, hypertrophy, fibrosis and endocarditis, epicarditis and coronary sclerosis, were observed, and severe fibrosis was significantly more common in the T type cases. The heart weight tended to decrease with age in the T type cases, but such tendency was not observed in the L type cases, with some cases showing an increased heart weight. Marked atrophy, fibrosis, swelling and hyperplasia were observed in the peripheral nerves around the arteries in the epicardial adipose tissue and arterioles in the myocardium. These changes were caused by ageing of the vessels feeding the peripheral nerves, together with changes due to Hansen's disease, such as circulatory disturbance in vessels feeding the peripheral nerves, augmentation of vascular permeability and ischemic changes due to over-stratification of the basement membrane. Because these peripheral nerves were distributed around the arteries in the epicardial adipose tissue and they were probably vasomotor nerves. These results suggest that paralytic arterial changes may promote the ischemic cardiac disease or fibrosis.

Diffuse vacuolization (spongiosis) and arteriolosclerosis in the frontal white matter occurs in vascular dementia.

To examine quantitatively white-matter changes at different sites in patients with definite vascular dementia and Alzheimer's disease. Prospective clinical and neuropathological series. University Hospital clinics (Helsinki, Finland and London, Ontario). Twenty-two patients with a clinical and neuropathological diagnosis of vascular dementia and 20 patients with Alzheimer's disease. The frequencies of focal white-matter lesions, arteriolosclerosis, and cerebral amyloid angiopathy were assessed. Validated ratings and cell counts were done in the subcortical U-fiber, centrum semiovale, and periventricular areas of the frontal white matter. Degrees of abnormality (none, mild, moderate, severe) were rated for spongiosis (vacuolization of white matter), état criblé (widening of perivascular spaces), myelin loss, oligodendrocyte density, axonal loss, and overall. Densities of oligodendrocytes and astrocytes (cells per square millimeter) were determined. Patients with vascular dementia showed focal white-matter lesions and arteriolosclerosis more often than patients with Alzheimer's disease. The patients with vascular dementia also had significantly greater spongiosis (P<.001), état criblé (P=.004), myelin loss (P<.005) and overall white-matter abnormality (P<.001). Arteriolosclerosis was found in association with spongiosis but not with état criblé. Cerebral amyloid angiopathy did not appear to be related to any of the white-matter changes in patients with either vascular dementia or Alzheimer's disease. The U-fiber area showed fewer changes, and the periventricular area tended to be most affected. In addition to focal infarcts, patients with vascular dementia showed widespread diffuse changes, including spongiosis and arteriolosclerosis, along with état criblé and myelin loss. White-matter changes in patients with Alzheimer's disease could not be related to infarction. Pathologic changes in small blood vessels are associated with diffuse white-matter changes and may have a distinct role in the genesis of vascular dementia.

Pathological and pathogenetic changes in the central nervous system of guinea pigs given tunicamycin.

Guinea pigs were injected with tunicamycin and the sequential morphological alterations in the brain examined to investigate further the pathogenesis of cerebral lesions in this experimental model of annual ryegrass toxicity, a central nervous system disease of livestock caused by members of the tunicamycin group of antibiotics. Brain damage was most commonly observed in the cerebellum, and the important alterations in the development of degenerative parenchymal lesions appeared to be largely referrable to changes in small blood vessels. Endothelial damage, with increased vascular permeability, resulted in capillary obstruction leading to localised ischaemia and hypoxic neuronal damage. There was evidence for several possible mechanisms which may have contributed to vascular occlusion.

Morphological changes in the brains of female patients who died in connection with pregnancy or delivery.

The authors examined 23 brains of female patients who died during pregnancy or after delivery. Four clinical groups were distinguished: 1. sepsis, 2. gestosis, 3. patients with cardiac diseases, 4. other cases of death. General autopsy on all the dead patients was performed. Macroscopically the brain revealed the signs of oedema and herniationes. Microscopic findings showed in the sepsis and gestosis groups, distinct changes in small blood vessels. Their walls were often statified and impregnated with fibrin. In the cases with the DIC syndrome microthrombosis could be seen. Only in 2 patients cerebral arterial occlusion was noted. Neurons revealed the secondary changes described as anoxic encephalopathy.

Elevated plasma beta-thromboglobulin levels in systemic lupus erythematosis.

g-thromboglobulin (B-TG) is a specific constituent of plateleta-granules which is released upon stimulation of platelets with agents such as ADP, thrombin, or collagen (l-3). Its presence in carefully prepared plasma samples is felt to reflect the in vivo release of platelet granule constituents -subsequent to platelet activation or aggregation (4,5). Elevated plasma levels have been reported in a number of conditions associated with intravascular coagulation or microvascular injury, including thrombophlebitis (6,7), acute myocardial infarction (8), preeclampsia (9), and diabetes mellitus (10, 12). However, to our knowledge, no determination of plasma @-TG in conditions associated with inflammatory vasculitis is available. We report here the results of plasma 8-TG measurements in 29 patients with systemic lupus erythematosus (SLE), a disease characterized by widespread inflammatory changes in small blood vessels.

Changes in Small Blood Vessels During Cyclical Luteal Regression in Sheep

Changes in small blood vessels of corpora lutea (CL) undergoing cyclical regression were studied by light and electron microscopy and the progesterone content of some CL was assayed. Vascular changes were 1st identified at Day 14 of the estrous cycle were consistently present by Day 16 and were observed in all CL in which progesterone content was less than 10 mcg/gm luteal tissue. Vascular changes involved both the luminal contents and walls of capillaries and small venules. Many capillaries contained degenerating cellular fragments incorporating nuclear and cytoplasmic remnants together with blood cells. The walls of many vessels containing cellular fragments appeared normal. In others abnormalities observed included folding of the basal lamina increase in the size and number of gaps in the endothelium increased endothelial cell projection into the lumen the inclusion of hetero- and/or autophagic vacuoles in the cytoplasm of many endothelial cells and pericytes and endothelial cell degeneration leading to ultimate disintegration of affected vessels. By Day 1 of the following cycle the number of capillaries was much reduced. It is concluded that at a relatively early stage of luteolysis many luteal capillaries show changes involving obstruction of the lumina by large amounts of cellular debris at least a part of which is of endothelial origin. The relationship of these changes to other phenomena associated with luteolysis is discussed.(Authors modified)

ASPECTS OF THE MICROCIRCULATION

The microcirculation is an important but little understood part of the cardiovascular system. As new techniques have been developed, more accurate information has become available concerning the changes in the microcirculation in both health and disease. A review has been made of some of the more important facets of the microcirculation of particular interest to surgeons. Reference is made to basic physiology, especially the mechanisms controlling flow in the microcirculation. The significance of changes in small blood vessels in hypovolaemic, septic, and progressive shock is also discussed, and the role of platelet aggregation in shock states is explored.

Bone Marrow and Bone Tissue. Color Atlas of Clinical Histopathology.

row aspiration. The author believes that his system produces material for study superior to those obtained by marrow aspiration and the generally used methods for marrow section. This volume is his chef d'oeuvre for promoting his system and for guiding those who would use it. The technique involves removing a cylinder of bone and marrow about 4 \m=x\18 mm. After special embedding it is cut into serial sections of 1\g=m\to 3\g=m thickness with a microtome adapted to hard sections. These methods are adequately explained and illustrated. The preparation of slides for exami¬ nation takes about six days. The quality of photomicrographs chosen and their arrangement and re¬ production are superb. Magnification is appropriate; color balance is excel¬ lent; cellular details are clear. Struc¬ tural elements of the marrow that most of us have previously taken on faith are readily distinguished. Mar¬ row blood vessels, sinusoids, fibrous meshwork, bone cells, and matrix and various hematopoietic cells, as well as their relationships to one another, are clearly distinguishable. A plastic grid can be placed over the illustrations to find particular cells or structures mentioned in the legend. This is a most useful device. While the author at times uses no¬ menclature which is not widely ac¬ cepted, his meaning is generally clear. Too often he does not tell us which findings are nonspecific and of little importance, which are suggestive of a diagnosis, and which are pathognomonic. There are clinical arenas in which this method appears clearly superior. Such conditions include bone diseases, suspected granulomatous conditions, and diseases associated with changes in small blood vessels. During the past 30 years, however, marrow aspi¬ ration and smear, using Romanowsky stains, have proven highly satisfac¬ tory as an aid in the diagnosis of disorders of erythrocytes, leukocytes, and platelets. In most such cases Burkhardt's methods would add little or nothing to the clinical diagnosis. Aplastic anemia and myelofibrosis are the major exceptions, and in these disorders conventional methods of preparing marrow sections should suffice. It is an interesting method and the results are superbly illustrated; some centers in this country should be en¬ couraged to duplicate Burkhardt's work and add independent, firsthand evaluations.

Ultrastructural changes in chick cerebellum induced by vitamin E deficiency.

Focal lesions were induced in the cerebellum by feeding chickens a diet high in unsaturated fats and deficient in vitamin E. Ultrastructurally, the lesions consisted of central and peripheral zones. The central zone was characterized in the cortex and white matter by enlargement of the intercellular space, swelling of astrocytes, vacuolization of oligodendrocytes, ballooning of nerve fibers, degenerative changes in small blood vessels, and extravasation of plasma and blood cells. The peripheral zone was characterized by enlargement of the intercellular space in the white matter, swelling of astrocytes in the cortex, and the accumulation of dark bodies in the endothelium of small blood vessels. The results suggest that this nutritional encephalopathy is caused by alterations in the permeability of the vascular bed due to the dietary stress of unsaturated fatty acids in the absence of vitamin E.

Inflammatory changes in small blood vessels induced by kallikrein (kininogenase) in the blood of Macaca mulatta infected with Plasmodium knowlesi.

(1970). Inflammatory changes in small blood vessels induced by kallikrein (kininogenase) in the blood of Macaca mulatta, infected with Plasmodium knowlesi. Annals of Tropical Medicine & Parasitology: Vol. 64, No. 2, pp. 227-236.

CHAPTER I: BRIEF SURVEY OF THE LITERATURE ON MORPHOLOGICAL CHANGES IN SMALL BLOOD VESSELS IN PATIENTS WITH DIABETES MELLITUS

Acta Medica ScandinavicaVolume 183, Issue S480 p. 7-17 CHAPTER I: BRIEF SURVEY OF THE LITERATURE ON MORPHOLOGICAL CHANGES IN SMALL BLOOD VESSELS IN PATIENTS WITH DIABETES MELLITUS First published: January/December 1968 https://doi.org/10.1111/j.0954-6820.1968.tb05187.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume183, IssueS480January/December 1968Pages 7-17 RelatedInformation