Changes In Capillary Morphology Research Articles

YOLOv8-Based System for Nail Capillary Detection on a Single-Board Computer.

Nail capillaroscopic examination is an inexpensive and easily applicable method to identify capillary morphological changes in patients with conditions such as systemic sclerosis and Raynaud's. The detection of changes in capillaries makes an important contribution to diagnosing these diseases. Capillary morphology is important in the symptoms of these diseases, and capillary diameter, visibility, distribution, length, microbleeds, blood flow, and density are important indicators in capillaroscopic evaluation. Manual examination to determine these parameters is subjective, causes inconsistent results, and is labor-intensive and time-consuming. To overcome these problems, a YOLOv8s-based system was proposed in this paper to detect the number, thickness, and density of capillaries in the nail bed. The system's components include database systems that store the analysis results, artificial intelligence-based software that runs on the SBC (Single-Board Computer), and recorded microscope images. mAP and F1_score parameters were used to evaluate the system's performance, and values of 0.882 and 0.83 were obtained. The proposed system is promising in improving the diagnosis process of diseases such as systemic sclerosis and Raynaud's by providing objective measurements and the early diagnosis and monitoring of diseases.

Nailfold Capillaroscopy: A Comprehensive Review on Its Usefulness in Both Clinical Diagnosis and Improving Unhealthy Dietary Lifestyles.

Since the 1970s, the utility of nailfold capillaroscopy (NFC) in diagnosing rheumatological disorders such as systemic sclerosis has been well established. Further studies have also shown that NFC can detect non-rheumatic diseases such as diabetes, glaucoma, dermatitis, and Alzheimer disease. In the past decade, nailfold capillary morphological changes have also been reported as symptoms of unhealthy lifestyle habits such as poor diet, smoking, sleep deprivation, and even psychological stress, all of which contribute to slow blood flow. Therefore, studying the relationships between the morphology of nailfold capillaries and lifestyle habits has a high potential to indicate unhealthy states or even pre-disease conditions. Simple, inexpensive, and non-invasive methods such as NFC are important and useful for routine medical examinations. The present study began with a systematic literature search of the PubMed database followed by a summary of studies reporting the assessment of morphological changes detected by NFC, and a comprehensive review of NFC's utility in clinical diagnosis and improving unhealthy dietary lifestyles. It culminates in a summary of dietary and lifestyle health promotion strategy, assessed based on NFC and other related measurements that indicate healthy microvascular blood flow and endothelial function.

Quantitative histomorphometry of capillary microstructure in deep white matter.

White matter lesions represent a major risk factor for dementia in elderly people. Magnetic Resonance Imaging (MRI) studies have demonstrated cerebral blood flow reduction in age-related white matter lesions, indicating that vascular alterations are involved in developing white matter lesions. Hypoperfusion and changes in capillary morphology are generally linked to dementia. However, a quantitative study describing these microvascular alterations in white matter lesions is missing in the literature; most previous microvascular studies being on the cortex. The aim of this work is to identify and quantify capillary microstructural changes involved in the appearance of deep subcortical lesions (DSCL). We characterize the distribution of capillary diameter, thickness, and density in the deep white matter in a population of 75 elderly subjects, stratified into three equal groups according to DSCL: Control (subject without DSCL), Lesion (sample presenting DSCL), and Normal Appearing White Matter (NAWM, the subject presented DSCL but not at the sampled tissue location). Tissue samples were selected from the Cognitive Function and Aging Study (CFAS), a cohort representative of an aging population, from which immunohistochemically-labeled histological images were acquired. To accurately estimate capillary diameters and thicknesses from the 2D histological images, we also introduce a novel semi-automatic method robust to non-perpendicular incidence angle of capillaries into the imaging plane, and to non-circular deformations of capillary cross sections. Subjects with DSCL presented a significant increase in capillary wall thickness, a decrease in the diameter intra-subject variability (but not in the mean), and a decrease in capillary density. No significant difference was observed between controls and NAWM. Both capillary wall thickening and reduction in capillary density contribute to the reduction of cerebral blood flow previously reported for white matter lesions. The obtained distributions provide reliable statistics of capillary microstructure useful to inform the modeling of human cerebral blood flow, for instance to define microcirculation models for their estimation from MRI or to perform realistic cerebral blood flow simulations.

The macular capillary morphology in diabetic patients by optical coherence tomography angiography

Objective To observe the macular capillary morphology in diabetic patients. Methods A total of 61 patients (104 eyes) with diabetes mellitus (DM group) and 31 healthy controls (41 eyes) were enrolled in the study. According to the degree of diabetic retinopathy (DR), the DM group was divided into non-DR (NDR) group, non-proliferative DR (NPDR) group, and proliferative DR (PDR) group. There were 13 patients (23 eyes), 21 patients (34 eyes) and 27 patients (47 eyes) in each group, respectively. According to whether there was diabetic macular edema (DME), the DM patients were divided into DME group and non-DME group, each had 20 patients (28 eyes) and 41 patients (76 eyes), respectively. The age (F=2.045) and sex (χ2=2.589) between the control group, the NDR group, the NPDR group and PDR group were not statistically significant (P=0.908, 0.374). The 3 mm × 3 mm region in macula was scanned by optical coherence tomography angiography (OCTA), and the retinal capillary morphological changes of superficial capillary layer (SCL) and deep capillary layer (DCL) were observed. Chi-square test and t test were used to compare data among different groups. Results There was no abnormal change of retinal capillary morphology in control group. Microaneurysms and foveal avascular zone (FAZ) integrity erosion can be found in NDR group. There were microaneurysms, FAZ integrity erosion, vascular tortuosity bending, capillary non-perfusion and venous beading in NPDR and PDR groups. The microaneurysms of DCL were significantly more than that of the SCL (t=4.759, P<0.001). The eyes with microaneurysms in NDR group, NPDR group, and PDR group showed significant differences (χ2=44.071, P<0.001), and the eyes with FAZ integrity erosion among these three groups also showed significant differences (χ2=30.759, P<0.001). Compared with NPDR group and PDR group, there were significant differences in vascular tortuosity bending and capillary non-perfusion (vascular tortuosity bending: OR=0.213, 95%CI 0.070−0.648, P=0.004; capillary non-perfusion: OR=0.073, 95%CI 0.022−0.251, P<0.001), and there was no significant difference in venous beading (OR=0.415, 95%CI 0.143−1.208, P=0.102). SCL blood flow density in the 4 groups (control, NDR, NPDR and PDR group) was 49.233±1.694, 48.453±2.581, 45.020±4.685 and 40.667±4.516, respectively. While the difference between the control and NDR group was not significant, the differences between other pairs (control vs NPDR/PDR, NDR vs NPDR/PDR, NPDR vs PDR) were significant. The ratio of FAZ integrity erosion and non-perfusion of DME group was significantly higher than those of non-DME group (vascular tortuosity bending: OR=7.719, 95%CI 1.645−36.228, P=0.004; capillary non-perfusion: OR=14.560, 95%CI 3.134−67.646, P<0.001). Conclusions OCTA can distinctively detect the abnormal retinal capillary changes of SCL and DCL in diabetic patients. Even in DM patients without diabetic retinopathy, OCTA can detect abnormal blood vessels. Key words: Diabetic retinopathy; Regional blood flow; Tomography, optical coherence; Foveal avascular zone

Primary Raynaud's phenomenon and nailfold videocapillaroscopy: age-related changes in capillary morphology.

This study aimed to detect by nailfold videocapillaroscopy (NVC) the presence of age-related capillary morphological patterns in a large cohort of subjects affected by primary Raynaud's phenomenon (PRP). NVC was performed in 877 patients affected by PRP, divided into three age groups: <35, 35-55 and >55years. The following qualitative parameters were assessed and compared in the three groups of patients: apical dilations, irregular (non-homogeneous) dilations, venous branch dilations, microhaemorrhages, tortuosities and subpapillary venous plexus visibility. Patients with either irregular dilations or venous branch dilations were found significantly younger than those without (p<0.0001). The presence of either irregular or venous branch dilations seems to exclude the presence of apical dilations. Patients with microhaemorrhages were found significantly younger than those without (p=0.05), and 81% of patients without microhaemorrhages did not show irregular and venous branch dilations. The subpapillary venous plexus seems more visible in subjects with age<35, as well as in those with age>55years (p<0.0001). A statistically significant negative correlation was found between presence of apical and irregular dilations (p<0.0001), apical dilations and venous branch dilations (p=0.02), apical dilations and tortuosities (p=0.0005), microhaemorrhages and tortuosities (p<0.0001) and venous branch dilations and tortuosities (p=0.02). Finally, a statistically significant positive correlation was found between irregular and venous branch dilations (p<0.0001), irregular dilations and microhaemorrhages (p<0.0001) and venous branch dilations and microhaemorrhages (p<0.0001). In conclusion, our study detected different age-related morphological capillary changes mainly in younger patients with PRP, as well as statistically significant correlations between the presence of different capillary variables.

Capillary dysfunction: its detection and causative role in dementias and stroke.

In acute ischemic stroke, critical hypoperfusion is a frequent cause of hypoxic tissue injury: As cerebral blood flow (CBF) falls below the ischemic threshold of 20 mL/100 mL/min, neurological symptoms develop and hypoxic tissue injury evolves within minutes or hours unless the oxygen supply is restored. But is ischemia the only hemodynamic source of hypoxic tissue injury?Reanalyses of the equations we traditionally use to describe the relation between CBF and tissue oxygenation suggest that capillary flow patterns are crucial for the efficient extraction of oxygen: without close capillary flow control, “functional shunts” tend to form and some of the blood’s oxygen content in effect becomes inaccessible to tissue.This phenomenon raises several questions: Are there in fact two hemodynamic causes of tissue hypoxia: Limited blood supply (ischemia) and limited oxygen extraction due to capillary dysfunction? If so, how do we distinguish the two, experimentally and in patients? Do flow-metabolism coupling mechanisms adjust CBF to optimize tissue oxygenation when capillary dysfunction impairs oxygen extraction downstream?Cardiovascular risk factors such as age, hypertension, diabetes, hypercholesterolemia, and smoking increase the risk of both stroke and dementia. The capillary dysfunction phenomenon therefore forces us to consider whether changes in capillary morphology or blood rheology may play a role in the etiology of some stroke subtypes and in Alzheimer’s disease.Here, we discuss whether certain disease characteristics suggest capillary dysfunction rather than primary flow-limiting vascular pathology and how capillary dysfunction may be imaged and managed.

Neurovascular coupling during cortical spreading depolarization and -depression.

Cortical spreading depolarizations (CSDs) are self-propagating waves of transient loss of neuronal transmembrane ion gradients, followed by prolonged suppression of neuronal activity (spreading depression). CSDs emerge spontaneously in animal models of traumatic brain injury,1 subarachnoid hemorrhage,2 and in focal ischemia3 where they are associated with infarct growth.4 In humans, CSDs have been demonstrated in traumatic brain injury,5 subarachnoid hemorrhage,6,7 and malignant hemispheric stroke,8 and they are believed to be the brain mechanism underlying migraine aura.9 CSDs are associated with dramatic changes in cerebral blood flow (CBF). During the depolarization phase of CSDs induced in healthy and well-perfused brain tissue in animal models, an early hyperemic response is observed, typically followed by prolonged oligemia after the neuronal repolarization. Despite the initial CBF increase, tissue hypoxia may develop in more distant territories of capillary supply.10,11 Similar CBF changes have been observed in patients with migraine aura.12–14 In the injured brain, CSDs can be accompanied by severe initial CBF reduction instead of a CBF increase during the depolarization phase, termed spreading ischemia.15 When this inverse hemodynamic response is observed, the energy-dependent recovery from CSD is delayed in a characteristic fashion, indicating a severe mismatch between oxygen supply and demand2 and a high risk of tissue damage.16 In rat and cat models of focal ischemia, CSD-related CBF transients range from monophasic, positive CBF responses in peri-ischemic tissue, over biphasic transients in mildly ischemic tissue, to negative CBF transients in more severe ischemia.17–19 During CSD in animal models, capillary flow patterns become severely disturbed.10,20,21 The passage of a CSD causes erythrocytes in some capillaries to reduce their speed, whereas other capillaries reveal 4-fold increases in flow or higher. …

The Role of the Microcirculation in Delayed Cerebral Ischemia and Chronic Degenerative Changes after Subarachnoid Hemorrhage

The mortality after aneurysmal subarachnoid hemorrhage (SAH) is 50%, and most survivors suffer severe functional and cognitive deficits. Half of SAH patients deteriorate 5 to 14 days after the initial bleeding, so-called delayed cerebral ischemia (DCI). Although often attributed to vasospasms, DCI may develop in the absence of angiographic vasospasms, and therapeutic reversal of angiographic vasospasms fails to improve patient outcome. The etiology of chronic neurodegenerative changes after SAH remains poorly understood. Brain oxygenation depends on both cerebral blood flow (CBF) and its microscopic distribution, the so-called capillary transit time heterogeneity (CTH). In theory, increased CTH can therefore lead to tissue hypoxia in the absence of severe CBF reductions, whereas reductions in CBF, paradoxically, improve brain oxygenation if CTH is critically elevated. We review potential sources of elevated CTH after SAH. Pericyte constrictions in relation to the initial ischemic episode and subsequent oxidative stress, nitric oxide depletion during the pericapillary clearance of oxyhemoglobin, vasogenic edema, leukocytosis, and astrocytic endfeet swelling are identified as potential sources of elevated CTH, and hence of metabolic derangement, after SAH. Irreversible changes in capillary morphology and function are predicted to contribute to long-term relative tissue hypoxia, inflammation, and neurodegeneration. We discuss diagnostic and therapeutic implications of these predictions.

Oxidized low-density lipoprotein alters the effect of matrix stiffness on the formation of endothelial networks and capillary lumens.

Abstract Formation of new blood vessels is essential for vascular repair and remodeling, and it is known that biomechanical properties of extracellular matrix play a major role in this process. Our earlier studies have also shown that exposing endothelial cells to oxidized modification of low-density lipoproteins (oxLDL) increases endothelial stiffness and facilitates their ability to form cellular networks, suggesting that it facilitates endothelial angiogenic potential. The goal of this study, therefore, was to test the interrelationship between matrix stiffness and oxLDL in the regulation of angiogenesis. Our results show that, as expected, an increase in matrix stiffness inhibited endothelial network formation and that exposure to oxLDL significantly facilitated this process. We also show, however, that oxLDL-induced facilitation of endothelial networks was observed only in stiff (3 mg/mL) but not in soft (1 mg/mL) collagen gels, resulting in blunting the effect of matrix stiffness. Also unexpectedly, we show that an increase in matrix stiffness results in a significant increase in the number of capillary lumens that are formed by single cells or pairs of cells, suggesting that while endothelial connectivity is impaired, formation of single-cell lumens is facilitated. oxLDL facilitates lumen formation, but this effect is also matrix dependent and is observed only in soft gels and not in stiff gels. Finally, an increase in both matrix stiffness and oxLDL exposure results in changes in capillary morphology, with the formation of larger capillary lumens. Overall, our study suggests that oxLDL plays an important role in formation of new capillaries and their morphology and that this effect is critically dependent on the extracellular environment's compliance, thereby underlining the importance of the interdependence of these parameters.

The Role of the Cerebral Capillaries in Acute Ischemic Stroke: The Extended Penumbra Model

The pathophysiology of cerebral ischemia is traditionally understood in relation to reductions in cerebral blood flow (CBF). However, a recent reanalysis of the flow-diffusion equation shows that increased capillary transit time heterogeneity (CTTH) can reduce the oxygen extraction efficacy in brain tissue for a given CBF. Changes in capillary morphology are typical of conditions predisposing to stroke and of experimental ischemia. Changes in capillary flow patterns have been observed by direct microscopy in animal models of ischemia and by indirect methods in humans stroke, but their metabolic significance remain unclear. We modeled the effects of progressive increases in CTTH on the way in which brain tissue can secure sufficient oxygen to meet its metabolic needs. Our analysis predicts that as CTTH increases, CBF responses to functional activation and to vasodilators must be suppressed to maintain sufficient tissue oxygenation. Reductions in CBF, increases in CTTH, and combinations thereof can seemingly trigger a critical lack of oxygen in brain tissue, and the restoration of capillary perfusion patterns therefore appears to be crucial for the restoration of the tissue oxygenation after ischemic episodes. In this review, we discuss the possible implications of these findings for the prevention, diagnosis, and treatment of acute stroke.

Quantitative nailfold video capillaroscopy in patients with idiopathic inflammatory myopathy

To quantify nailfold capillary density and dimensions in patients with idiopathic inflammatory myopathy (IIM) and compare them with those in healthy controls; to look for associations with microvascular disease in IIM; and to determine whether nailfold capillary density and dimensions change over time. Nailfold video microscopy (x300 magnification) was performed on 24 patients with IIM and 35 healthy controls. Capillary density and dimensions (total width and apical width) were quantified. Patients were clinically assessed and disease activity recorded using the Myositis Disease Activity Assessment Tool. Disease severity and physical function were assessed using the myositis damage index and Stanford HAQ, respectively. Findings were analysed using linear and logistic regression, adjusted for age and sex. In a subgroup of 16 patients with IIM and 27 controls, the process was repeated 6-12 months later and the results were analysed using Student's t-test. Capillary density was lower and dimensions were higher in patients with IIM compared with healthy controls (P < 0.001 for all). Anti-Jo-1 antibody was associated with reduced capillary density. In the longitudinal cohort, the mean change in capillary density was -1.4 in patients vs -0.4 in controls (P = 0.07). Mean change in capillary dimensions did not differ between patients and controls, but some patients demonstrated pronounced changes in capillary morphology over time. Reduced capillary density and increased dimensions in patients with IIM can be quantified using nailfold capillaroscopy, suggesting that nailfold capillaroscopy may be useful as an outcome measure of microvascular disease in studies of IIM.

Microcirculatory Dysfunction in Chronic Venous Insufficiency (CVI)

The elevated ambulatory pressure in the peripheral venous system of chronic venous insufficiency (CVI) patients manifests itself not only in the form of disturbed macrocirculation but also and particularly in microangiopathic changes. For this reason, it is closely correlated with trophic disorders of the skin and can ultimately lead to ulceration. Using microcirculation research techniques, we are able to provide clear evidence of a typical microangiopathy in chronic venous insufficiency. Fifty CVI in Widmer stages I, II, and III were examined with fluorescence video microscopy, intravital video capillaroscopy, transcutaneous oxygen partial pressure measurement, TcpO2 and laser Doppler flowmetry. The effects of compression therapy with individually fitted compression stockings on capillary morphology were studied over a period of 4 weeks in 20 CVI patients in Widmer stages I and II. The capillary pressure was measured during simulated muscle contraction using a servo-null micropressure system. We periodically drew blood from the dorsalis pedis vein and a brachial vein of 11 healthy test persons and 8 patients with stage III CVI during experimental venous hypertension in order to evaluate the expression pattern of leukocyte adhesion molecules involved in inflammation: LFA-1 (CD11a), Mac-1 (CD11b), p150,95 (CD11c), CD18, VLA-4 (CD49d), and L-selectin (CD62L). In the same patients, we used immunohistochemical methods to examine clinically unaffected skin and the skin near an ulcer, focusing on the adhesion molecules ICAM-1, VCAM-1, and E-selectin. The microangiopathic changes observed with worsening clinical symptoms include a decrease in the number of capillaries, glomerulus-like changes in capillary morphology, a drop in the oxygen content (tcpO2) of the skin, increased permeability of the capillaries to low-molecular-weight substances, increased laser Doppler flux reflecting elevated subcutaneous flow, and diminished vascular reserve. These microangiopathic changes worsen in linear proportion to the clinical severity of chronic venous insufficiency. In patients with venous ulcerations, the baseline expression of LFA-1 and VLA-4 on lymphocytes, Mac-1 expression on the myeloid cell line, and L-selectin expression on all three cell lines was not significantly different form that in healthy controls. During orthostatic stress, there was a significant reduction in the expression of L-selectin in blood cells collected at foot level in the controls (p=0.002), but not in the patients. Clinical improvement by compression therapy was accompanied by an increase in the number of nutritive capillaries, while the diameter of the capillaries and the dermal papillae was reduced. When ulcers healed in a short period (<6 weeks), we observed a concomitant increase in the number of capillaries (p<0.05). Microangiopathy appears before tropic disorders of the skin develop. Even trophically normal skin areas may have dilated nutritive capillaries, an early sign of disturbed skin perfusion. These changes represent a plausible explanation for the development and to recurrency tendency of venous ulcers. The reduced expression of lymphocytic L-selectin in healthy controls during the orthostatic stress test may be an indication that the cells are activated by venous stasis. Clinically effective therapeutic measures improve the impaired microcirculation of the skin in the ankle area.

Microcirculation of the Fingernail Fold in Capd Patients: Preliminary Observations

To study changes in the peritoneal microcirculation during continuous ambulatory peritoneal dialysis (CAPD) by studying change in the microcirculation of the fingernails of CAPD patients. A university department. A cross-sectional study of 10 nondiabetic patients on CAPD. Hemorrheological tests of fingernail microcirculation using equipment built at our university. Microcirculation was characterized by estimation of capillary density, red blood cell (RBC) column diameter, torque index, and RBC flow velocity semiquantitatively using videocapillaroscopy at the fingernail fold and plasma viscosimetry. Findings were correlated with treatment duration, peritoneal clearance, state of capillary morphology and hemodynamics, and lipid and fibrinogen levels. Treatment duration was significantly correlated (p < or = 0.05) with low-density lipoprotein (LDL) (r = 0.776) and clearances of urea (r = -0.583), uric acid (r = -0.666), and potassium (r = -0.764). Changes in capillary morphology were correlated to clearances of urea (r = 0.643) and uric acid (r = 0.701). The fibrinogen concentration increases plasma viscosity (r = 0.799) and deteriorates the capillary state (r = -0.706). In addition, plasma viscosity correlates to cholesterol (r = 0.620, NS) and LDL (r = 0.781), but not to high-density lipoprotein and triglycerides. CAPD treatment results in lipid abnormalities and high fibrinogen levels that may cause microvascular damage and poor perfusion. These interactions may explain the deterioration of peritoneal transport in some CAPD patients.

Nailfold capillary circulation in osteoarthritis.

Nailfold capillaries in 28 patients with OA affecting the distal interphalangeal joints were compared to 23 age- and sex-matched controls without OA. Patients with OA showed a significantly lower density of capillaries in their nailfolds and significantly more capillary morphological abnormalities including haemorrhage, 'drop out', dilatation and irregularity. There was a trend for OA patients to have warmer fingers with reduced finger to brachial blood pressure ratios. There were significant correlations between nailfold capillary numbers and average joint tenderness and between capillary morphological changes and joint swelling. These results reveal a relationship between interphalangeal joint OA and nailfold capillary abnormalities and density. As changes in microcirculation may be pertinent to the pathogenesis of OA, further studies which could explore possible causal relationships are warranted.

Exercise-induced focal skeletal muscle fiber degeneration and capillary morphology.

The relationship between exercise-induced focal muscle fiber degeneration and changes in capillary morphology was investigated in male Wistar rats. Untrained animals ran on a treadmill for 1 h at submaximal intensity and were killed 0, 6, or 24 h after running. Nonexercised rats served as controls. In situ perfused soleus muscles were prepared for electron microscopy. Micrographed cross sections were quantitatively analyzed for parameters indicative of capillary blood flow or transcapillary exchange. Capillary lumina were ovally rather than circularly shaped, and no indications for obstruction of blood flow at the capillary level were found. Endothelial cells and their organelles had a normal appearance in all groups. However, immediately after exercise, capillaries showed a decreased thickness of their endothelium and basal membrane, probably caused by dehydration. Six hours after exercise, muscle fibers were swollen (28% increase in cross-sectional area), resulting in a slightly increased diffusion distance. This fiber swelling was not associated with an increase in muscle water content, a finding for which no explanation could be found. Twenty-four hours after the animals ran, capillaries located near degenerated muscle fibers had an increased cross-sectional luminal area and an increased luminal circumference. This effect decreased gradually with increasing distance from the degenerated fiber area. The present morphometric results do not support the hypothesis that changes in capillary morphology primarily contribute to exercise-induced focal muscle fiber degeneration.

Beagle puppy model of intraventricular hemorrhage. Effect of superoxide dismutase on cerebral blood flow and prostaglandins.

Intraventricular hemorrhage (IVH) represents a major problem for preterm neonates and is thought to occur secondary to alterations in cerebral blood flow (CBF) to damaged germinal matrix tissues. Many investigators believe that both local CBF and changes in capillary morphology and permeability may be partially controlled by prostaglandins. To evaluate this hypothesis, the authors have studied the effects of superoxide dismutase (SOD), a known free-radical scavenger, on newborn beagle pups that were randomly assigned by computer to four groups consisting of either SOD- or saline-pretreated animals that underwent either insult by hemorrhagic hypotension/volume reexpansion or no insult. Prostaglandin levels were determined prior to and 60 minutes following the administration of the solutions, and carbon-14 iodoantipyrine autoradiography was performed for determination of CBF. It was demonstrated that, although SOD significantly decreased the incidence of IVH in this model (p less than 0.05), it caused no alterations in baseline CBF or prostaglandin levels. In addition, SOD did not prevent either the systemic blood pressure changes or the alterations in CBF found in response to a hemorrhagic hypotensive insult. The authors propose that neonatal IVH results from a combination of factors, one of which is prostaglandin-mediated alterations in CBF to a damaged capillary matrix.