Blood Sludging Research Articles

Hemoadhican, a Tissue Adhesion Hemostatic Material Independent of Blood Coagulation.

Uncontrolled hemorrhage is a leading cause of death, emphasizing the need for novel hemostatic agents. Here, a novel hemostatic polysaccharide hemoadhican (HD) is screened out by analyzing the rheological properties of screened material mixed blood sludges, which is prepared by mixing polysaccharide granules and whole blood to mimic the coagulation in vitro. HD is produced by a bacterial isolate Paenibacillus sp.1229, and the repeating units of HD are →)-α-L-Rhap-(1→3)-β-D-Glcp-(1→4)[4,6-ethylidene-α-D-Galp-(1→4)-α-D-Glcp-(1→3)]-α-D-Manp-(1→. Compared to chitosan and celox, HD achieves more effective hemostasis in animal models with mouse and rat femoral arteries, rat carotid arteries, and rabbit femoral arteries. Especially, HD maintains an excellent hemostatic capability in animals with heparin-induced hemorrhage diathesis. In vitro experiments show HD granules can quickly absorb a small amount of blood component to create a hemophobic blood sludge resistant to high pressure. The blood sludge firmly adheres to damaged tissue and efficiently repels blood. In vitro experiments show that HD does not actively trigger blood coagulation cascade and is independent of blood conditions including heparin treatment. In addition, HD moisturizes wounds and accelerates wound healing, exhibiting excellent biodegradability, and hemocompatibility. The results indicate that HD is a promising hemostatic material for treating traumatic hemorrhages and uncontrollable surgical bleeding.

Manual removal of a rare cystic calculus concurrent with recurrent hemorrhagic cystitis in an Arabian mare: A case report

A nine-year-old Arabian mare was presented with symptoms of frequent hematuria, dysuria, pollakiuria and urine dribbling. This report describes a manual removal procedure of a cystic urolith in an Arabian mare. A complete blood count showed a slight reduction in hemoglobin. Renal function tests showed high normal ranges in BUN. The urine sample was very cloudy and had a specific gravity of (1.019) with alkaline pH. The chemical examination showed high hemoglobin concentration with glucose traces. The microscopic examination showed a high number of pus cells and red blood cells with few numbers of rounded epithelial cells. Bacterial culture revealed Klebsiella spp and as a result of the sensitivity test, sensitivity to amoxicillin/ clavulanic acid, amikacin and gentamicin was determined. Cystoscopy revealed a large cystic urolith cranioventrally on the left wall of the urinary bladder. The apex vesicae was inflamed, with blood sludge. The definitive diagnosis was chronic hemorrhagic cystitis caused by a large cystic urolith. As a result, it was concluded that the removal of relatively large calculi through the urethra in the mare, while providing some protection to the bladder neck and urethral mucosa, has been effective with minimal complications.

Відтворення експериментальної моделі впливу на печінку гострого стресу шляхом фіксації щурів за шийну складку

Stress-related studies remain relevant notwithstanding its long-lasting history of research. Experimental studies are crucial in the study the impact of stress on a living organism. Currently, there is a great variety of simulation animal acute stress reaction models, in particular, cervical fold suspension of mice, which is cost effective and easy-to-use. However, there are insufficient data on using this technique to reproduce the acute stress response in rats, particularly, in studying the impact of immobilization stress on the liver. The purpose of the work was to study the impact of 6-hour-long cervical fold suspension simulation model of acute immobilization stress on the albino rats’ liver. Material and methods. Based on the international bioethical regulations, 20 male albino rats were involved into the study. The intact animals were assigned into group I (n=10) (control); the animals, exposed to 6-hour-long cervical fold suspension simulation model of acute immobilization stress were assigned to experimental group (n=10) (group II). After euthanasia, macro- and microscopic examination of the liver was performed. Micro-specimens were stained with hematoxylin and eosin. Results and discussion. The macroscopic examination of the liver did not reveal any visual differences in the rats of the experimental group compared to the control ones. Histological study of the liver specimens of group II rats showed that the experimental model of simulated acute immobilization stress in rats by atraumatic cervical fold suspension for 6 hours caused significant changes. They were especially pronounced in the bloodstream of the liver, manifested by the plethora and the phenomena of interlobular vein thrombosis. The central veins were also plethoric and a significant dilatation of the perisinusoidal spaces was noted. Changes in the hemomicrocirculation were characterized by manifestations of blood stasis and sludge in most sinusoidal capillaries. We detected the phenomena of tissue infiltration by the segmented neutrophils, as well as macrophages and lymphocytes perivascularly and in the portal tracts. Changes were also found in the liver cells, namely, the phenomena of karyopyknosis; subcapsular focal colliquational necrosis in the individual hepatocytes; hydropic dystrophy in hepatocytes located on the periphery of the liver lobuli. Conclusion. The implementation of experimental model of acute immobilization stress in rats by atraumatic cervical fold suspension caused significant histological changes in rat liver

Regional blood flow and microcirculation disorders

The lecture analyzes modern data on the types, etiology, key stages of pathogenesis, manifestations and consequences of typical forms of regional blood flow and microcirculation disorders. The lecturer dwells on typical forms of regional blood flow (in medium vessels): pathological arterial hyperemia, venous hyperemia, ischemia, and stasis. The variants of ischemia associated with increased arterial inflow to tissue or organ are considered as compared to medium-normal inflow. The lecture provides data on typical hemolymph microcirculation disorders, including intravascular, transmural, extravascular disorders, as well as capillary-trophic insufficiency as a final result of one or more microcirculatory disorders. The blood sludge phenomenon is characterized as a pathology of the blood aggregate state, which is either a cause or a consequence of a microhemocirculation disorder. The lecture is recommended for students, medical residents, post-graduate students, and trainees of the system of post-graduate professional education at medical universities.

Bulbar capillaroscopy and plethysmography for assessment of blood microcirculation and endothelium properties in type 1 diabetes

To evaluate the properties of the microvasculature of bulbar conjunctiva and to assess the function of endothelium of the main arteries in type 1 diabetes mellitus (T1DM). The study included 35 patients with T1DM and initial nonproliferative diabetic retinopathy (NPDR). The control group consisted of 30 subjects. In addition to standard ophthalmic examination, all participants underwent digital bulbar capillaroscopy (DBC), pulse wave velocity (PWV) test, and plethysmography for assessment of endothelium function. According to DBC, in comparison to the control group, diabetic patients with even initial NPDR had disturbances of blood microcirculation manifested as increased average venous vessel width (p=0.04), reduced arterial capillary blood flow (p=0.02), increased blood sludging (p=0.001), and increased duration of blood stasis (p=0.03). Evaluation of vessel endothelium in T1DM patients with NPDR showed increased PWV (p=0.03). Diabetic patients with NPDR showed marked changes of capillary blood flow alongside signs of endothelial dysfunction. The most significant change was increased venous vessel width.

On red blood cell (RBC) filterability, presented in 1958 by Robin Fåraeus, his controversy to Knisely’s ‘blood sludge’ and Copley’s concept on blood cellular clumping

On red blood cell (RBC) filterability, presented in 1958 by Robin Fåraeus, his controversy to Knisely’s ‘blood sludge’ and Copley’s concept on blood cellular clumping

ISOTT from the Beginning: A Tribute to Our Deceased Members (Icons).

ISOTT was founded by Drs. Duane F. Bruley and Haim I. Bicher in the state of South Carolina, USA in 1973. The symposium was jointly held at Clemson University (Clemson, SC, USA) and the Medical College of South Carolina (Charleston, SC, USA), which are geographically located 260 miles apart. This venue resulted from Dr. Bruley's (Clemson University) wish to have a meeting on Oxygen Transport to Tissue and with it to honor the research collaboration between the two universities and Dr. Melvin H. Knisely's accomplishments on studies regarding "blood sludging" in the microcirculation. Because of the unexpected large response to the symposium, Drs. Bruley and Bicher decided to found an international society at this meeting (ISOTT). The purpose of this paper is to summarize the formalization of ISOTT and to honor important contributors to the society who have since passed away. The authors did their best to include a brief overview of our past icons who have excelled in leadership as well as science/engineering, and apologize if someone has been mistakenly left out or if data is inaccurate or incomplete.

Cerebral Perfusion Patterns in Transgenic Murine Models of Sickle Cell Disease As Seen By MRI Is Reflective of Their Anemia Profile and Parallels the Human Disease

Background: Sickle cell disease is an anemia disorder of the red blood cell in which hemoglobin S (HbS) undergoes polymerization and sickling under low-oxygenation conditions, leading to vaso-occlusive events. Major frequent neurological complications of SCD include ischemia and stroke leading to cognitive deficits and morbidity. Clinical observations have done little to identify the causes of stroke in SCD. Animal models of SCD, and in particular transgenic models have been useful in understanding the microvascular phenomena leading to vasculopathy. Polymerization and consequent sickling of red blood cells (RBC) under oxygen stress conditions likely result in sludging of blood and consequent vasoocclusion, at least in peripheral post-capillary tissues. Most animal studies suggest that the primary site for interaction of RBC's carrying HbSreside in the venous vasculature, yet large arterial stroke remains a significant occurrence in clinical SCD, where suggested risk factors include elevated carotid blood velocity and turbulence, cerebral blood flow asymmetry, loss of cerebrovascular reactivity and cerebral hyperemia. In particular, human cerebral hyperemia appears to be a frequent and significant finding, presumably a compensatory response to the SCD anemia.We sought to determine how closely Tg animal models of SCD mimic the cerebral findings associated with human SCD. Several models have been developed, including the NY1DD model which does not exhibit anemia, but in which sickling only occurs following a period of hypoxia, the S+S Antilles (SSAnt) model which suffers mild anemia and sickling under normal conditions, and the Berkley (BERK) which exhibits severe anemia, sickling and early mortality. We used MRI to evaluate these SCD models and compared the findings to those of WT animals.Methods: NY1DD (n=11, 2.6± 0.8 mo, HCT=0.47± 0.04), SSAnt (n=11, 3.3 ± 1.2 mo, HCT=0.43± 0.04), BERK (n=11 at 3 mo, n=5 at 10 mo, HCT=0.33± 0.03) and WT (C57bl, n=5 at 10 mo, n=4) were studied in accord with PHS and AALAC guidelines. Anesthetized (isoflurane) animals were studied with a 9.4 T MRI (Agilent, Inc., CA). MRI included assessment of perfusion (FAIR-ASL), fMRI (BOLD response to a period of hyperoxia), Diffusion Tensor Imaging (DTI), and structural imaging.Results: No differences were observed in CBF, BRHO or MD between young and old animals. Cerebral blood flow increased with severity of anemia-with BERK CBF higher than WT, NY1DD or SSAnt CBF (P < 0.0001). NY1DD and SSAnt CBF were not different, but both were higher than WT CBF (p < 0.001). Bold Response to hyperoxia indicated that BERK animals suffered the greatest oxygen debt, while NY1DD and SSAnt were not significantly worse than WT under normoxia conditions. Mean tissue diffusivity (obtained from DTI), a marker for edema and inflammation, was elevated only in BERK mice compared to WT mice (p < 0.05), while fractional anisotropy was not different between groups.Conclusion: As the degree of anemia worsens, CBF increases presumably to compensate for lower hemoglobin and reduced oxygen carrying capacity. In BERK mice, this increase in CBF is inadequate to compensate for reduced oxygen delivery, and this is indicated by an increase in the BOLD response to hyperoxia (BRHO measure). SSAnt and NY1DD animals both exhibited elevated CBF, but their BRHO was not significantly different from WT animals. This suggests that their increase in CBF was adequate to compensate for sickle induced vasoocclusion and/or mild anemia under normal oxygenation conditions. Our findings suggest that the BERK mouse may be the best model for evaluating therapeutics directed at treating the chronic anemia associated with human SCD, and for evaluating therapeutics aimed at remedying hypoxia induced oxygen radical damage. However, NY1DD or SSAnt may be better models for studying experimentally induced sickle crisis (extended durations of hypoxia), as BERK mice are to fragile to survive such perturbations. [Display omitted] [Display omitted] DisclosuresNo relevant conflicts of interest to declare.

Anesthesia Dogmas and Shibboleths

Anesthesia Dogmas and Shibboleths

血管条血管の特徴―血管の透過性について―

When the cochleas of guinea pigs were fixed after decapitation, HRP leakage from the strial capillaries was observed with blood sludge. HRP was transported to the extracapillary space by many pinocytotic vesicles and marginal folds. However, when the cochleas were fixed before decapitation, blood sludge was not observed in the strial capillaries and leakage of HRP from the capillaries was not observed 10 minutes after HRP injection. Thereafter, the level of HRP leakage increased with time. It was noted that capillary permeability to HRP at the basal turn was lower than that of the upper three turns. HRP leakage was not observed in the capillaries of the spiral ligament even beyond one hour after injection.As a result of severe hemorrhagic shock in guinea pigs, blood sludge appeared in strial capillaries and capillary permeability to HRP increased. However, in moderate hemorrhagic shock, both blood sludge and accentuation of capillary permeability did not occur.After the inoculation of endotoxin in the middle ear, a large amount of HRP leaked out of the capillaries through the opened endothelial cell junctions.After vibration administered to auditory ossicle is by a drill, the permeability of the strial capillaries to HRP also increased. High permeability was thought to be caused by damage to the strial endothelial cells. HRP leakage initially took place through the tubules in the endothelial cytoplasm, and HRP leaked in to the extracapillary space when the cell membranes were damaged by vibration. Administration of the steroid inhibited HRP leakage from the strial capillaries.The stria vascularis became markedly edematous after the administration of furosemide, while capillary permeability to HRP was decreased.From the above, the route of HRP leakage is different depending on the type of stimulation, even if it occurs alongside increased capillary permeability.

Danshen: What every cardiologist should know about this Chinese herbal drug

1. Danshen ( ), with the structural formula C10H17 O6SNa, is the root of Salvia miltiorrhiza [2]. It has long been judged highly effective in ‘‘activating circulation and dispersing stasis or sludging of blood’’ [2]. Among the classical teachings of Chinese traditional medicine, it is stated that ‘‘when blockage is opened, pain is relieved’’ [2]. Because of its properties of improving microcirculation, causing coronary vasodilatation, suppressing the formation of thromboxane, inhibiting platelet adhesion and aggregation, and protecting against myocardial ischemia [2–4], it is widely used either alone or in combination with other herbal ingredients for patients with coronary artery disease, in both China and other countries including the United States. It is conspicuously advertised in the Chinese Journal of Cardiology, which is the official publication of the Chinese Society of Cardiology (Fig. 1). 2. Danshen not only possesses coronary vasodilating properties but also interacts with warfarin (Coumadin\) by potentiating its anticoagulant action [4–6]. Warfarin is a commonly used oral anticoagulant frequently prescribed for patients with atrial fibrillation, valvular heart disease, congestive heart failure, stroke, pulmonary embolism, peripheral vascular disease and deep venous thrombosis

Deterioration of Visual Function as Examined by Electroretinograms inToxoplasma gondii–Infected IFN-γ-Knockout Mice

To investigate by ERG the effects of Toxoplasma gondii infection on the visual function of interferon gamma knockout (GKO) mice, as a model of immunocompromised hosts. Susceptible wild-type (WT) C57BL/6 and GKO C57BL/6 mice were infected with five cysts of the avirulent T. gondii perorally. ERGs were recorded before and after the infection. The eyes of WT and GKO mice were enucleated and prepared for histologic studies 4 weeks and 12 days after infection, respectively. The a- and b-waves of ERGs did not change significantly up to 1 month after infection in WT mice, but those of GKO mice were significantly reduced 11 days after infection. Histopathology revealed focal retinitis and vasculitis in WT mice 4 weeks after infection. Mild inflammation and sludging of blood in the retina and choroid were found in GKO mice 12 days after infection, just before death. Cysts were found in the inner nuclear layer, with little disturbance of the surrounding retinal architecture in both WT and GKO mice. ERG clearly showed deterioration of visual function in GKO but not in WT mice after T. gondii infection. ERG is a sensitive and reliable method for observing activity in mice severely affected with experimental toxoplasmic retinochoroiditis.

Interleukin-13 in systemic sclerosis: relationship to nailfold capillaroscopy abnormalities.

The aim of this study was to investigate whether interleukin-13 (IL-13) serum levels correlate to different nailfold capillaroscopy (NC) findings in patients with systemic sclerosis (SSc). IL-13 serum levels were measured using an ELISA method. The following NC abnormalities were considered: the presence of giant loops, haemorrhages, loss of capillaries, disorganisation of the vascular array, ramified/bushy capillaries and sludging of blood. A semiquantitative rating scale was adopted to score these changes, as well as a rating system for avascular areas and three morphological NC patterns ('early', 'active' and 'late'). Mean capillary density was determined by counting the total number of capillaries in a 1 mm length, and the arterial and venous diameters of the capillary as well as the total loop diameter were measured. In SSc patients IL-13 serum levels were significantly higher than in controls ( P < 00.1), whereas in patients with ( n=8) and without ( n=24) abnormal IL-13 serum levels (>17 pg/ml) the comparison of the NC features showed significantly relevant differences concerning a more frequent 'active' NC pattern ( P < 0.02), the presence of haemorrhages ( P < 0.0037) and sludging of blood ( P < 0.038), as well as larger total loop ( P < 0.036) and arterial ( P < 0.03) diameters, in those patients with elevated IL-13 serum levels. The study confirmed that IL-13 serum levels are higher in the sera of patients with SSc, and shows for the first time the significant correlations between this serological finding and some of the main relevant SSc capillaroscopic features, leading us to believe that this cytokine not only seems to sustain the immunological and fibrotic process of SSc, but might have a role in determining the more severe microvascular lesions in this disease.

Priapism Secondary To Hypertriglyceridemia

Various etiologies of priapism have been described, including sickle-cell disease, cocaine abuse, hematological malignancies, penile metastases, trauma, intracavernous injection therapy for erectile dysfunction and oral medications. Nevertheless, many cases of priapism are classified as idiopathic. We report a case of priapism secondary to hypertriglyceridemia, and recommend screening patients with a serum lipid profile if an obvious etiology cannot be identified. CASE REPORT A 33-year-old black male with diet controlled diabetes mellitus presented with a painful erection 18 hours in duration. The patient had woken in the morning with an erection unrelated to sexual stimulation. He denied a history of sickle cell anemia, cocaine abuse or penile trauma, and he was not taking any medications. The patient reported occasional marijuana and heavy alcohol use. He described a previous episode of priapism approximately 3 months prior that had lasted 8 hours but resolved without intervention. Physical examination confirmed classic low flow priapism that was extremely tender to palpation. Laboratory evaluation revealed a serum white blood count of 10.8 10 9 /l., hematocrit 42.4% and platelet count 248 10 9 /l., all of which were within normal limits. A sickle cell screening panel was negative. Blood glucose level was 109 mg./dl. (normal 65 to 110) and serum creatinine 1.3 mg./dl. (0.7 to 1.4). Urine toxicology screen was positive only for cannabinoids. It is noteworthy that during the blood collection process the phlebotomist observed a thick white layer on top of the blood drawn in the chemistry tube. This finding prompted measurement of serum triglyceride, which was increased to 2,041 mg./dl. (normal 40 to 160). Liver function tests were within normal limits. Corporeal blood gas demonstrated a pH of 6.95, partial carbon dioxide pressure 93 mm. Hg and partial oxygen pressure 16 mm. Hg. The patient was treated with multiple intracavernous injections of 250 to 500 g. phenylephrine, cavernous aspiration and cavernous irrigation with saline. Aspiration of corporeal blood showed a fatty layering similar to that seen in the blood collection tube. Complete detumescence was achieved with these treatments. Endocrinology consultation for evaluation of hypertriglyceridemia was obtained, and treatment was started with gemfibrozil. Serum lipid profile was obtained the next day, and revealed total cholesterol 393 mg./dl. (normal 80 to 220), high density lipoprotein 41.6 mg./dl. (35.0 to 68.0) and repeat triglyceride level 856 mg./dl. (40 to 160). DISCUSSION Previous reports have described an association of priapism with total parenteral nutrition.1, 2 It is hypothesized that the lipid emulsion is the precipitating factor. To our knowledge this case of priapism secondary to hypertriglyceridemia unrelated to total parenteral nutrition represents the first such case reported in the English literature. Hypertriglyceridemia may cause sludging of blood, hypercoagulability and fat embolus leading to venous outlet obstruction of the corpora cavernosa. Investigators have demonstrated distortion of erythrocyte morphology, increased erythrocyte aggregation and adhesiveness, and decreased capillary flow associated with the intravenous infusion of fat.3 Our patient presented with a serum triglyceride level more than 12 times the upper limit of normal. It was postulated that the hypertriglyceridemia was related to pancreatic insufficiency secondary to alcohol abuse, although the patient might have had an undiagnosed familial disease. Urine toxicology screen confirmed the use of marijuana but we do not believe that marijuana use is an etiological factor in priapism. In addition, we are unaware of any case reports associating marijuana with priapism. Since many cases of priapism have an unidentifiable etiology, we believe a serum lipid profile screen is indicated in the diagnostic evaluation. REFERENCES

Microvascular abnormalities in sickle cell disease: a computer-assisted intravital microscopy study

The conjunctival microcirculation of 18 homozygous sickle cell disease (SCD) patients during steady-state, painful crisis, and postcrisis conditions was recorded on high-resolution videotapes using intravital microscopy. Selected videotape sequences were subsequently coded, frame-captured, studied, and blindly analyzed using computer-assisted image analysis protocols. At steady-state (baseline), all SCD patients exhibited some of the following morphometric abnormalities: abnormal vessel diameter, comma signs, blood sludging, boxcar blood flow phenomenon, distended vessels, damaged vessels, hemosiderin deposits, vessel tortuosity, and microaneurysms. There was a decrease in vascularity (diminished presence of conjunctival vessels) in SCD patients compared with non-SCD controls, giving the bulbar conjunctiva a "blanched" avascular appearance in most but not all SCD patients during steady-state. Averaged steady-state red cell velocity in SCD patients was slower than in non-SCD controls. During painful crisis, a further decrease in vascularity (caused by flow stoppage in small vessels) and a 36.7% +/- 5.2% decrease in large vessel (mostly venular) diameter resulted. In addition, the conjunctival red cell velocities either slowed significantly (6.6% +/- 13.1%; P <.01) or were reduced to a trickle (unmeasurable) during crisis. The microvascular changes observed during crisis were transient and reverted to steady-state baseline after resolution of crisis. When combined, intravital microscopy and computer-assisted image analysis (computer-assisted intravital microscopy) represent the availability of a noninvasive tool to quantify microvascular abnormalities in vascular diseases, including sickle cell disease. The ability to identify and relocate the same conjunctival vessels for longitudinal studies uniquely underscores the applicability of this quantitative real-time technology.

Horseradish peroxidase permeation from the capillaries of the stria vascularis after inoculation of endotoxin into the middle ear.

Escherichia coli-derived endotoxin was inoculated in the middle ear of guinea pigs 24 hours after being injected intraperitoneally. Twenty-four hours after the middle ear inoculation, horseradish peroxidase (HRP) was injected via the femoral vein and the permeability of HRP through the capillaries of the stria vascularis and the destination of the leaked HRP were examined. A large amount of HRP leaked out of the capillary through he opened endothelial cell junctions and penetrated the enlarged intercellular spaces. Leaked HRP entered the pinocytotic vesicles of the intermediate cells. Even slightly degenerated intermediate cells retained this function. The HRP penetrated the spongelike structure of the marginal cells leading to the intercellular space. This structure was not observed without endotoxin. The HRP could not pass the cochlear duct through the tight junctions between marginal cells. Blood sludging was observed in the strial capillaries. It appeared more frequently in the upper three turns than in the basal turn. The HRP leakage out of the capillaries was observed not only in the upper three turns but also in the basal turn.

Cochlear morphological changes over time after the introduction of bacterial endotoxin into the middle ear

Guinea pigs weighing 350 g each were used in this experiment. A small piece of Gelform containing 0.04 mg of E. coli derived endotoxin was set on the round window 24 hours after intraperitoneal injection of 0.02 mg endotoxin. Morphological changes in the cochlea were observed at 24 hours (previous report), 48 hours, 72 hours and 7 days after the introduction of the endotoxin into the middle ear. As the results of the morphological changes of cochlea at 24 hours after the introduction of the endotoxin were reported in previous paper we present only an outline of these. Inflammatory cell infiltration and bleeding were observed in both endolymphatic and perilymphatic spaces. Inflammatory cells also infiltrated the stria vascularis, spiral ligament, spiral prominence and organ of Corti. Almost all of the inflammatory cells were neutrophils. Blood sludge was observed in all of the strial capillaries of the upper three turns. The hair cells were intact in every turn except for having small vacuoles. Intermediate cells and marginal cells of the stria vascularis were shrunken. At 48 hours after the introduction of the endotoxin into the middle ear, the changes in the stria vascularis were almost the same as at 24 hours. However the infiltrated inflammatory cells changed from neutrophils to macrophages. Macrophages had phagocytosed many neutrophils. The hair cells had many large vacuoles. At 72 hours, the enlargement of the intercellular space in the stria vascularis disappeared and damage to the hair cells decreased although many macrophages were still observed. At 7 days, the cochlea was morphologically normal.

Morphological changes in the inner ear induced by bacterial endotoxin

Escherichia coli-derived endotoxin was introduced into the middle ears of 10 guinea pigs 24 hr after intraperitoneal injection of the same endotoxin. The cochleae were removed 24 hr after the introduction of the endotoxin into the middle ears and observed by light and electron microscopy. Inflammatory cell infitration and bleeding were observed in both endolymphatic and perilymphatic spaces. Inflammatory cells also infiltrated the stria vascularis, spiral ligament, spiral prominence and the organ of Corti. Blood sludge was observed in almost all of the strial capillaries of the upper three turns, but in few of the basal turns. The hair cells were intact in every turn except for a small number of degenerated mitochondria. Intermediate cells of the stria vascularis were shrunken, and some of them showed degenerative changes. Marginal cells had also shrunken, but they were less shrunken than the intermediate cells. The shrinking of both cells caused the enlargement of the intercellular space of the stria vascularis.

Large Doses of Topical Lidocaine during Microvascular Surgery Are Not Associated with Toxic Blood Concentrations

Large Doses of Topical Lidocaine during Microvascular Surgery Are Not Associated with Toxic Blood Concentrations

Alterations in Capillary Permeability of Stria Vascularis of Guinea Pigs following Decapitation

Ten minutes after an intravenous injection of HRP, guinea pigs were killed by decapitation. The bullas were removed and opened, and the cochleas were fixed by perilymphatic infusion with glutaraldehyde. Blood shudging and considerable HRP leagage were observed in the capillaries of the stria vascularis. When blood was replaced with plasma expander, blood sludging did not appear after decapitation because few blood cells remained in the capillaries. Moreover, HRP leakage was scarecely observed in the strial capillaries. Even if the strial capillaries were contracted by the decapitation, HRP leakage did not occur without blood sludging. The high pressure between capillary endothelium and blood cells produces many marginal bolds, which efficiently transport HRP out of the capillaries.