Extravasation Of Blood Research Articles

Effects of insulin-induced hypoglycemia on cerebrovascular permeability to horseradish peroxidase.

The effects of hypoglycemia on cerebrovascular permeability to a protein, horseradish peroxidase (HRP), were studied in mice given 3 or 8 units of crytalline zinc insulin intraperitoneally. HRP (10 mg in 0.1 ml saline) was injected intravenously 15 to 20 minutes prior to sacrifice. Both mildly and severely hypoglycemic groups of mice showed a drastic reduction in the normal transit of HRP across cerebral arterioles. The number of normally-stained vessel segments and of HRP-filled endothelial vesicles decreased in insulin-treated mice. In the brains of severely hypoglycemic mice, however, increased parenchymal HRP accumulation occurred. A ruptured blood vessel was found in the center of one-fourth of the focal exudates examined. Electron microscopic examination revealed thrombin, sometimes extending through the vessel wall, and hemorrhage, yet inter-endothelial tight junctions remained intact. Seizures were associated with severe hypoglycemia in 6 out of 10 mice with serum glucose levels below 40 mg/100 ml following 8 units of insulin, but the number of focal exudates per brain was similar in all 10 mice. We conclude that insulin-induced hypoglycemia is associated with decreased HRP transit across cerebral arterioles, and that severe insulin shock is also accompanied by actual rupture of vessel walls and extravasation of blood and HRP into the parenchyma of the brain.

Morphology of haemostasis in menstrual endometrium.

Light microscopy, electron microscopy and immunofluorescence were used to study the endometrium from nine uteri removed during the first 72 hours of normal menstruation. During premenstrual spotting, stromal disintegration and vessel lesions without any haemostatic reaction were seen. Up to 20 hours after the onset of menstrual bleeding, blood extravasation was prominent in the functional endometrium. The vessels in this layer were partly or totally sealed by intravascular thrombi functioning as haemostatic plugs. The thrombi contained various amounts of platelets and fibrin and were shed with the tissue. New plugs formed up-stream in the same vessels. Twenty hours after the onset of menstruation, most of the functional endometrium had been desquamated. From 20 to 72 hours after the start of menstrual bleeding no or few thrombi were seen. Haemostasis may then be caused by adherence of vessel lips.

Effects of intracortical injection of blood and blood components on the electrocorticogram.

Long term effects of the intracortical implantation of blood and blood products on the electrocorticogram were studied in cats and guinea pigs. Focal epileptiform paroxysmal discharges developed after implantation of whole blood, hemolyzed erythrocytes, methemoglobin, ferritin, ferrous chloride, ferric chloride, fibrinogen, hemin, and cottonoid. In each group recurrent paroxysmal discharges became more prominent and more frequent after several months, suggesting a physiological change caused by a breakdown product of blood. The lesions were characterized by varying degrees of cell loss, iron deposition and glial proliferation. It is thought that posttraumatic epilepsy, which is frequently accompanied by extravasation of blood into the brain, might share a similar physiopathogenesis.

A Scanning Electron Microscopic Study on Vascular Changes in the Endometrium at the Pre-Implantation Stage in the Rabbit

The changes of vascular architecture in the endometrium on the 5th day after coitus were studied in the rabbit by means of scanning electron microscopy of the resin casts, in relation to implantation. The changes of the endometrial vascualr bed in the placental fold were remarkable. Vessels in the cores of the placental fold became voluminous and elongated. The subepithelial plexus surrounding uterine glands was found well developed. There was neither evidence for extravasation of blood nor for local vascular differences indicating implantation sites in the endometrial vascular bed.

A CASE OF HEREDITARY HEMORRHAGIC TENDENCY (HEMOPHILIA) REPORTED IN 1832 BY A PHYSICIAN PRACTICING IN SIMPSONVILLE, KENTUCKY

Credit is usually given to Dr. J. C. Otto (1774-1844) of Philadelphia for offering, in 1803, the first clear description of a bleeding disease affecting males and sparing females.1 Twenty-nine years later, Dr. James N. Hughes of Simpsonville, Kentucky, apparently unaware of Otto's report, published this succinct clinical report of a case of hemophilia, including the hereditary aspects of this disease.2 On visiting the house of a respectable farmer of this neighbourhood, my attention was directed to the case of a youth ten or twelve years old, which appeared to be rheumatic, and which was so pronounced. The correctness of my opinion was called in question by an old lady present, who was herself a member of the family, and intimately acquainted with the history of the case. On further inquiry I ascertained it to be one of hereditary origin, the rheumatism being only the sequel of another affection to which the boy had been subjected from infancy, viz. haemorrhage. Learning that this disease was common in every branch of the N. family, of which that of my friend Mr. P. was one, I enquired particularly concerning it, when the following facts were communicated: 1st. That spitting, vomiting and purging of blood; bloody urine; bleeding at the nose; extravasations of blood among the muscles and integuments of the body generally, especially of the extremities, producing dark discolorations and swelling, attended frequently, after a few days, continuance, with obtuse pain and stiffness, and copious and obstinate haemorrhage from very inconsiderable incisions, on whatever part of the body they are made, have been exceedingly common among the male members of the connection.

Acute cardiomyopathy induced by the vasodilating antihypertensive agent minoxidil

Minoxidil, a vasodilating antihypertensive drug, was given orally in doses of 0.5, 1.0, or 3.0 mg/kg to adult Beagle dogs on 2 consecutive days. Within 2 hr of administration, each of these doses produced hypotension and a marked tachycardia which persisted for as long as 24 hr after the second dose of minoxidil. Necropsies performed 24 hr after the second dose revealed focal, superficial areas of epicardial or endocardial hemorrhage in dogs given each of the three dose levels. Hemorrhage was associated with a mild inflammatory reaction and was not limited to the right atrium. Focal arteritis, characterized by extravasation of blood and by focal accumulation of erythrocytes and fibrin-like material in the walls of small coronary arteries, occurred in three hearts from the 3-mg/kg dose group. Myocardial necrosis was noted in one of eight dogs given the minimal pharmacologic dose of 0.5 mg/kg, and in five of eight dogs in each of the groups given 1 or 3 mg/kg. Necrosis was most frequent in the left ventricular papillary muscles, particularly the posterior one. An ischemic origin of the necrosis is suggested by the localization of the lesions and by the pharmacologic effects of minoxidil.

Hyperemia, stasis, and increase in vascular permeability: new methods for their quantitation.

Of the four cardinal signs and symptoms of inflammation, redness (rubor), swelling (tumor), heat (calor), and pain (dolor), redness is due primarily to hyperemia, i.e., enhanced flow through dilated vessels of the microcirculation. However, redness of an inflammatory lesion may also be caused by extravasation of blood into the tissues or microhemorrhages or by standstill of the blood in dilated vessels (stasis). In an experimental inflammatory lesion the redness due to hyperemia will disappear with death and cessation of blood flow, but the redness due to hemorrhage or stasis will persist. The swelling of inflammation is due to exudation of plasma into the tissues resulting from hyperpermeability of vessels of the microcirculation.

Extravasation of contrast-enhanced blood into the subarachnoid space during computed tomography

Four cases are described in which there was extravasation of contrast medium into the subarachnoid space at the time of enhanced CT. Three were being investigated for a previous subarachnoid haemorrhage which was due to an aneurysm in two and an angioma in one. The other patient had suffered a severe head injury.

Computed tomography in spontaneous intracerebral haematomas.

The typical computed tomographic (CT) features of a recent intracerebral haematoma are a homogenous region of increased attenuation surrounded by a well demarcated relatively narrow low attenuation ring (LAR). The pathology of the LAR is controversial, but it corresponds well with a zone of ischaemic necrosis which is observed around most intracerebral haematomas exmined at autopsy. Observations are made on spontaneous intracerebral haematomas and on blood samples which confirm that extravasated blood clot undergoes a variable degree of retraction which is completed within six hours. This suggests that the LAR in recent haematoma is due to damage caused by the greater volume of the precontracted haemorrhage on the surrounding brain. CT abnormalities in intracerebral haematomas were studied; features which were useful in distinguishing spontaneous haematomas and those which affected prognosis are discussed.

Peroperative Endoscopic Diagnosis of Small Intestinal Bleeding

Two patients with recurrent bleeding from vascular anomalies in the small intestine are described. In both patients intestinal angiography had shown either pathological vessels or extravasation of blood into the proximal part of jejunum, but during explorative laparotomy the source of bleeding had not been found. The diagnosis was made by performing peroperative endoscopy. After resection of the involved small bowel segment one patient with cavernous hemangioma has remained asymptomatic. In the other patient, who suffered from a combination of multiple arteriovenous malformations and a congenital platelet defect, limited surgical resection did not influence the need of blood transfusions. This investigational approach should become the method of choice in patients suspected of bleeding from the small intestine.

Erythrophagocytosis by epithelial cells of a breast carcinoma

Erytrophagocytosis by epithelial tumor cells has been observed in metastases of ductal carcinoma of the female breast. Some malignant cells of this tumor seem to be capable of phagocytizing and digesting extravasated red blood cells with for formation of residual hemosiderin probably from their hemoglobin content. Erythrophagocytosis has been observed only in hemorrhagic areas of the tumor. Erythrophagocytosis has been observed only in hemorrhagic areas of the tumor. Although the nature of this phenomenon is unknown, it is postulated that acquired hematological disturbancess during the natural course of the malignant disease affect the surface of the red blood cells making them vulnerable to phagocytosis by the malignant cells. This case seems to represent the second time such a phenomenon has been reported in an epithelial neoplasm in man. However, it has been more frequently observed in reticulo-endothelial malignancies. The possible occurence of this phenomenon should alert pathologists to search for it in primary and metastatic epithelial tumors and in living patients to correlate pertinent hematological studies in an attempt to elucidate its possible significance.

A Theory of the Mechanism of Cerebral Vasospasm and Its Reversal, the Role of Calcium and Cyclic AMP

It is proposed that the basic mechanism of vasospasm which sometimes follows subarachnoid hemorrhage is dependent on increased free intracellular calcium ion produced by spasmogens from closely applied extravasated blood. Relaxation of this spasm occurs when the intracellular cyclic AMP levels are raised, resulting in sequestration of calcium ion by the vascular smooth muscle cell sarcoplasmic reticulum.

Histopathologic correlates of otoneurologic manifestations following head trauma.

The clinical course of patients dying of head trauma and the physiologic evaluation of audition in guinea pigs subjected to several forms of head trauma are correlated with the histopathologic findings in the brains and temporal bones. In the patients there was wide spread hemorrhage, edema, disorganization and disruption of neural tissue. Loss of Purkinje cells and other neural elements was prominent. The temporal bone findings in the patients included laceration of and hemorrhage into the VIIIth nerve as well as bleeding into the scala tympani. The membranous labyrinths demonstrated no specific changes secondary to the trauma. The guinea pigs developed a central form of hearing loss with elevated thresholds for evoked responses from the inferior colliculus and normal AC cochlear potentials. In the animals hemorrhage in the substance of the brain, necrosis of neural tissue, edema, disorganization and disruption were prominent. Although there was extravasation of blood in the tympanic and vestibular scalae, the membranous structures of the inner ears were well preserved.

Tributary vein obstruction: pathogenesis and treatment of sequelae.

An acute branch retinal vein obstruction or occlusion is followed by a series of haemodynamic events designed to overcome the obstruction and restore equilibrium within the retinal vasculature. Experimental studies would indicate that the immediate post-obstructive retinal oedema is probably the result of capillary and venular distension due to the sudden increase in intraluminar hydrostatic pressure. The widespread extravasation of blood which occurs some time later is probably the result of degenerative changes in the capillary walls secondary to prolonged stasis and hypoxia. In many tributary vein obstructions, readjustments within the involved retinal microvasculature are effective in overcoming the effects of the obstruction. The involved retinal capillaries gradually return to normal or nearly normal, with preservation of their physiological functions. Good vision is often maintained and no therapy is required. In other cases, often where associated arterial insufficiency exists, significant venous stasis persists and the retinal capillaries remain incompetent with the formation of intraretinal oedema. Evidence available at this time would indicate that selective photocoagulation is of some benefit in preventing the chronic accumulation of macular fluid in certain cases and avoiding the unwanted sequelae of cystic macular degenerative changes and pigmentation abnormalities at the fovea. Photocoagulation appears to be less justified in cases of long-established macular oedema with degenerative changes already in evidence. In certain varieties of tributary vein occlusion characterized by marked arterial insufficiency, the involved capillary bed fails to perfuse fully. Neovascularization is frequently associated with extensive areas of non-perfused retina. Neovascularization, although it may appear 3 – 6 months following the acute obstructive episode, rarely demands treatment within the year. The neovascularization associated with a branch vein occlusion is generally subtle, slow-growing, and responds well to photocoagulation. Papillary neovascularization indicates widespread ischaemia, and often suggests implication of further quadrants of the retina in the ischaemic process. Papillary neovascularization can be indirectly influenced by extensive photocoagulation of the ischaemic retina resulting from the vein occlusion.

The embryogenesis of trypan-blue induced spina bifida aperta and short tail in the rat.

The study of litters from 140 Wistar-derived rats injected with trypan blue during gestation leads to conclusion that a myelocele can result from faulty closure of the neural plate and that this is accompanied in many cases by blebs in the paraxial mesoderm. Haematomata usually underlie the open neural plate at an early stage and they form by extravasation of blood from the dorsal aortae into the blebs. Local ventral deflection of the notochord beneath a myelocele probably results from delayed separation of the notochord from the hindgut. Complete failure of separation and abnormality induced in the tail-bud could result in sacral agenesis and/or a short tail. All these malformations may result from varying severity of the action of the trypan blue at different developmental stages.

Endotoxin-induced liver necrosis and intravascular coagulation in rats enhanced by portacaval collateral circulation.

The effects of intravenously administered endotoxin on the hepatic and systemic circulation as well as on the coagulation system were evaluated in normal rats (n = 26), in rats with experimental portal hypertension (n = 15), and in rats with portacaval anastomosis (n = 22). Endotoxin (1-5 mg/kg) in the normal rat leads to a prompt increase of transaminase activity and to a hyperdynamic circulation with a consequent increase in the total hepatic blood flow. In a later phase (6 h postoperatively) the hepatic artery dilated with a consequent hepatic arterial hyperperfusion. The coagulation system was affected with signs of consumption coagulopathy. In the rats with portal hypertension and portacaval collaterals as well as in those with portacaval anastomosis, the endotoxin injection resulted in acute liver necrosis within 12 to 15 hours. The hepatic artery became overdilated with a cardiac output fraction of 25% (normal 5-5%). Blood extravasates and thrombi, rich in fibrin, were detected in the liver. It is suggested that this exaggeration of the endotoxin effect was due to an impaired clearance function of the reticuloendothelial system, probably as consequence of portacaval collateral circulation. It is concluded that endotoxins (1) damage the liver even in a normal organism; (2) are potent to induce acute liver necrosis, if the reticuloendothelial system is altered; (3) have to be taken into consideration as contribution to the pathogenesis of acute as well as chronic liver diseases.

Spontaneous spinal epidural haemorrhage: good results after early treatment.

Extravasation of blood in the spinal epidural space is an uncommon but often disastrous problem. Severe trauma, anticoagulants, bleeding diatheses, and intraspinal vascular malformations have been associated with such haemorrhage, but occasionally it occurs without apparent cause. It may then be confused with transverse myelopathy or vascular occlusion. Early diagnosis by myelography and treatment by surgery can result in good recovery, as illustrated by two cases.

Gastric Ulceration in the Pig Subjected to Haemorrhagic Shock

Kivilaakso, E., Kalima, T. V. & Lempinen, M. Gastric ulceration in the pig subjected to haemorrhagic shock. Scand. J. Gastroent. 1974, 9, 685–690.The evolvement of gastric ulcers as well as the morphology of mature lesions were studied in 17 piglets subjected to haemorrhagic shock (mean arterial pressure 40 mm Hg) of 3 hours’ duration. Five animals were discarded because of early death. In all but one of the surviving animals mucosal lesions developed. The first findings, as recorded by endoscopy during exsanguination, involved inhibition, and later, complete cessation of gastric motility, followed by a copious reflux of bile and duodenal contents into the stomach. The first mucosal changes, seen soon after establishment of the shock, comprised a network of ischaemic and hyperaemic areas with extravasation of blood. Towards the end of the shock period small mucosal haematomas developed within these areas. After transfusion these areas became intensely red-coloured with transient focal haemorrhages and, later, small superficial erosions could be seen at these sites. More extensive lesions, confined almost exclusively to the body of the stomach, were seen 24 hours after the shock, including ‘punched-out’ ulcers, superficial ulcerations, and areas of haemorrhagic gastritis.

Some effects of Naja nigricollis envenomation on developing fetal tissue

The effects of maternal envenomation with N. nigricollis venom on developing fetal tissue were studied in mice. The venom passed the placental barrier and injured the kidney nephrons. In the liver, it produced disorganization of lobules with cellular degeneration and congestion of the liver sinusoids. The hepatic erythropoietic tissue seemed not affected. In the heart, subendocardial hemorrhages together with fragmentation of the myocardium were observed. Edematous changes were noticed in the wall of the aorta and the large blood vessels. The endothelial lining of some of the vessels ruptured and extravasated blood was noticed in the lumen of the gut and respiratory passages.

Ultrastructure of the placenta of Antarctic seals during the first third of pregnancy.

AbstractThe chorioallantoic placenta from six crabeater seals (Lobodon carcinophagus) with fetuses from 15–180 mm crown rump length (CRL), and two leopard seals (Hydrurga leptonyx) with fetuses 76 and 86 mm CRL was lobulated, zonary, labyrinthine and endotheliochorial. The fine structure of the placenta was essentially similar in both species. Maternal capillaries of the labyrinth had attenuated endothelial cells unlike the fissiped carnivores. They were surrounded by an outer syncytiotrophoblast, incomplete inner cytotrophoblast, and a core of mesenchymal tissue containing fetal vessels. In general, the cytotrophoblastic cells were less electron‐opaque than the syncytium; the former possessed abundant free ribosomes, while the latter had many nuclei, mitochondria, and numerous strands of rough endoplasmic reticulum. Mitotic figures were observed only in the cytotrophoblast. Plasma membranes between the trophoblastic layers had interdigitating processes which showed many desmosomes along the intercellular spaces, whereas membranes surrounding the maternal capillaries were usually smooth. In the limb‐bud stage embryo, the syncytiotrophoblast had thick and thin areas which became progressively attenuated in older fetuses. Instances of intratrophoblastic fetal capillaries were observed in seals with fetuses of 40 mm CRL and older, with consequent greatly thinned placental barriers. By Perl's reactions, Turnbull's method, and electron microscopy, rows of granular bodies positive for iron were demonstrated along the basement membrane of the trophoblastic cells and in the mesenchymal cells of the crabeater seals, but not the leopard seals. Furthermore, it is suggested that the deposits of granular bodies show the sites of iron storage in the placentas. In the limb‐bud stage embryo the hematome borders and isolated pouches of the central hematome were observed. The central hematome was antimesometrial. The hematomes were lined by columnar cytotrophoblastic cells which phagocytized extravasated maternal blood and absorbed histiotrophic material.