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Biomedical subjects

M J Hogan

Publications and source records attributed to M J Hogan.

At least 37 records · Page 2Linked to original sources
PubMed1999

Neonatal vascular catheters and their complications.

There has been an evolution in vascular access in the neonate. Newer types of materials and catheters, such as PICC lines and ECMO catheters, are now available. The frequency of line placement has increased, and radiologists now perform many of these procedures. This places the radiologist in the position of not only diagnosing complications, but actually causing them. Knowledge of these complications can help the practitioner avoid them and diagnose them as quickly as possible when they occur.

Catheterization, Central Venous↗
PubMed1999

Lungs in infants and young children: improved thin-section CT with a noninvasive controlled-ventilation technique--initial experience.

Three sedated young children underwent thin-section computed tomography (CT) of the chest while breathing and during controlled respiratory pauses induced by means of a step increase in positive-pressure ventilation applied via a face mask. Motion-free inspiratory and expiratory thin-section CT images were successfully acquired during 8-12-second respiratory pauses. This simple, reproducible technique produced thin-section CT images that were clearer and more clinically useful than those obtained during quiet tidal breathing.

Child, Preschool↗
PubMed1998

Cortical spreading depression activates trophic factor expression in neurons and astrocytes and protects against subsequent focal brain ischemia.

We recently reported that cortical spreading depression (CSD), used to precondition rat brain, reduced cortical infarction volume resulting from focal cerebral ischemia by middle cerebral artery occlusion (MCAO) 3 days later. The mechanisms underlying this protective effect by CSD remains to be explored. In this study, we confirm that CSD is neuroprotective when KCl is applied epidurally rather than intracortically. Neocortical infarct volume was 101.3+/-48.5 mm3 and 45.3+/-44.1 mm3 in the sham and CSD group, respectively (p<0.05). Using image analysis, we identified the cortical region spared from infarction by the prior CSD. We then determined the distribution of brain-derived neurotrophic factor (BDNF) and basic fibroblast growth factor (bFGF) mRNA and the time course of their expression in groups of animals treated with CSD and their controls. We also examined the response of astrocytes to CSD using glial fibrillary acidic protein (GFAP) as a marker. In situ hybridization (done at 0, 3, 12, 24, 72 or 168 h after CSD) showed significant elevation of BDNF mRNA in the cortex immediately after CSD in a distribution surrounding the spared cortex, while bFGF mRNA rose 12 h after CSD and appeared more within the core of the ischemic region. Immunohistochemistry (done at 1, 3 or 7 days after CSD) demonstrated GFAP in the neocortex, with a peak at 3 days after CSD. Heat shock protein 72 (HSP72) expression was not affected by CSD. We concluded that upregulation of trophic factors and activation of glial cells may contribute to the neuroprotection induced by CSD.

Animals↗
PubMed1998

Regional activation of L-type voltage-sensitive calcium channels in experimental thiamine deficiency.

During pyrithiamine-induced thiamine deficiency (PTD), specific regions of the brain develop histological damage. The basis of this selective vulnerability is unknown but the mechanism may involve a glutamate-mediated excitotoxic process in affected structures, leading to alterations in membrane potential and disturbances in calcium homeostasis. In this study, we have examined the volume of distribution of [3H]nimodipine, an L-type voltage-sensitive calcium channel (VSCC) antagonist, in the brain of the PTD rat. An increase in specific binding of [3H]nimodipine was detected only in the posterior thalamus at the symptomatic stage, immediately following the loss of righting reflexes (P < 0.0001). There was also an increase in nonspecific binding in the medial geniculate and inferior colliculi. Replenishment with thiamine at the symptomatic stage returned [3H]nimodipine binding to normal levels. These findings provide evidence that depolarization and activation of L-type VSCCs occur in the posterior thalamus and may contribute to the appearance of histological lesions in this structure during experimental thiamine deficiency.

Animals↗
PubMed1998

Preamputation MR imaging in meningococcemia and comparison to conventional arteriography.

Meningococcemia is a life-threatening infection which produces purpura fulminans and extremity gangrene in its most severe form. In patients with gangrene, amputation is usually necessary. The amputations frequently need revision as ischemic changes in the underlying soft tissues and bone are difficult to evaluate at the time of surgery. These ischemic changes often have non-vascular distributions and progress over time. We present two patients in whom MR imaging and MR angiography were performed prior to planned amputation. These cases demonstrate the potential utility of MR imaging in this setting, and compare the MR angiographic results to conventional arteriography in one of these patients.

Amputation, Surgical↗
PubMed1998

Neonatal total parenteral nutrition ascites from liver erosion by umbilical vein catheters.

BACKGROUND: A preterm infant was found to have total parenteral nutrition (TPN) ascites after infusion through a low umbilical vein catheter (UVC). Objective. To evaluate the clinical and imaging findings of neonates with TPN ascites after infusion through UVCs. MATERIALS AND METHODS: Eight patients with TPN ascites were identified over three years. Charts were abstracted for clinical data. Plain-film, ultrasound (US), and contrast studies through the UVCs were examined to determine UVC placement, presence of liver injury, and confirmation of intraperitoneal extravasation from the UVC. RESULTS: All eight patients with TPN ascites presented with hypotension and abdominal distension. All had UVCs overlying the liver on plain film. Catheters were in place a mean of 8.9 days prior to TPN extravasation. US in four patients showed hepatic parenchymal damage around the UVC tip. Contrast studies in six patients showed intraperitoneal spill. CONCLUSION: While low UVC placement may sometimes be clinically unavoidable, TPN administered through abnormally positioned UVCs is not without risk.

Ascites↗
PubMed1997

Massive hemoptysis as the presenting manifestation in a child with histoplasmosis.

A previously healthy and asymptomatic 7-year-old white boy presented with a history of two episodes of hemoptysis productive of bright red blood in the 5 days preceding admission. After admission he developed massive hemoptysis that, on bronchoscopy, was noted to be emanating from the right lower lobe. An emergency right lower lobe resection was done. Pathological examination revealed hilar adenopathy and peripheral lesions with caseating granulomas containing yeast, morphologically consistent with Histoplasma capsulatum.

Amphotericin B↗
PubMed1997

Cystic periventricular leukomalacia of the corpus callosum.

Periventricular leukomalacia (PVL) is a common finding during neurosonography of preterm infants. Secondary thinning of the corpus callosum is seen following PVL, typically from loss of hemispheric white matter tracts. We report a case of direct involvement of the corpus callosum with PVL, its pathogenesis, and its potential as a cause of corpus callosal thinning.

Corpus Callosum↗
PubMed1997

In vivo uptake of [3H]nimodipine into brain during cortical spreading depression.

We report autoradiographic measurements of the in vivo uptake of [3H]nimodipine during the nonischemic depolarization of cortical spreading depression (CSD) in rat brain. [3H]Nimodipine uptake in brain was determined regionally in rats undergoing CSD (n = 8) and was significantly increased in cortex (14 +/- 7%) and hippocampus (10 +/- 6%) on the stimulated side relative to the contralateral hemisphere when compared with the same measurements in a control group (n = 8). A similar measurement using the physiologically inert radiotracer [14C]iodoantipyrine to control for potential effects of CSD on radioligand distribution showed a minimal increase (2.4 +/- 0.7%) of radiotracer uptake in cortex after CSD. This increase was significantly less than that observed in the [3H]nimodipine uptake studies. We hypothesize that increased in vivo [3H]nimodipine uptake in CSD identifies regions of depolarization and thus infers activation of the L-type voltage sensitive calcium channels.

Animals↗
PubMed1997

In vivo uptake of [3H]nimodipine in focal cerebral ischemia: modulation by hyperglycemia.

Cell membrane depolarization and tissue acidosis occur rapidly in severely ischemic brain. Preischemic hyperglycemia is recognized to increase ischemic tissue acidosis and the present studies were undertaken to correlate depolarization and tissue acidosis during acute focal cerebral ischemia and hyperglycemia. We used a dual-label autoradiography method to simultaneously measure the in vivo distribution of [3H]nimodipine and [14C]DMO (5,5-dimethyl-2,4-oxazolidinedione) in brain to identify regions of ischemic depolarization and measure regional net tissue pH. Regional cerebral blood flow (CBF) was measured in separate studies. Measurements were made 30 minutes after combined middle cerebral artery and ipsilateral common carotid artery occlusion in normoglycemic and hyperglycemic rats. Tissue pH in the ischemic cortex was depressed to 6.76 +/- 0.11 in normoglycemic rats (n = 12) and 6.57 +/- 0.13 in hyperglycemic rats (n = 12), with significantly greater acidosis in the hyperglycemic group (P < 0.001). In contrast the ratio of [3H]nimodipine uptake in the ischemic cortex relative to the contralateral nonischemic cortex was significantly greater in normoglycemic (1.83 +/- 0.45) than hyperglycemic (1.40 +/- 0.50) rats (P < 0.05). Within this region of ischemic cortex CBF was 31 +/- 22 mL/100 g in normoglycemic rats (n = 8) and 33 +/- 22 mL/100 g/min in hyperglycemic rats (n = 9). Cerebral blood flow did not differ between these two groups in any region. Thus hyperglycemia reduced the extent of ischemic depolarization within the cortex during the first 30 minutes of focal cerebral ischemia. This effect may be related to the increased tissue acidosis or to other factors that may lessen calcium influx and preserve cellular energy stores in the ischemic cortex of the hyperglycemic rats.

Animals↗
PubMed1996

Cortical spreading depression protects against subsequent focal cerebral ischemia in rats.

The possibility that cortical spreading depression (CSD) may have neuroprotective action during subsequent focal cerebral ischemia was examined in rats. Three days before the imposition of focal cerebral ischemia CSDs were elicited by applying potassium chloride (KC1) for 2 h through a microdialysis probe implanted in the occipital cortex. Control animals were handled identically except that saline was infused instead of KC1. Focal ischemia was produced by the intraluminal suture method and cortical and subcortical infarct volumes were measured 7 days later. Neocortical infarct volume was reduced from 124.8 +/- 49.5 mm(3) in the controls to 62.9 +/- 59.5 mm(3) in the animals preconditioned with CSD (p = 0.012). There was no difference between the two groups in the subcortical infarct volume or in CBF, measured by the hydrogen clearance method, during or immediately after the ischemic interval. Our data indicate that preconditioning CSD applied 3 days before middle cerebral artery occlusion may increase the brain's resistance to focal ischemic damage and may be used as a model to explore the neuroprotective molecular responses of neuronal and glial cells.

Animals↗
PubMed1996

A practical guideline for management of hypertension in patients with diabetes.

Hypertension is common in patients with non-insulin-dependent diabetes mellitus and is also an early sign of diabetic nephropathy in those with insulin-dependent diabetes. Hypertension contributes to the progression of both macrovascular disease and nephropathy in patients with diabetes. Certain antihypertensive agents can adversely affect carbohydrate and lipid metabolism. Angiotensin-converting enzyme inhibitors and calcium channel blockers may slow the progression of renal complications in patients with diabetes. The pharmacologic approaches to treatment of hypertension in patients with diabetes potentially differ from those in nondiabetic persons. On the basis of a review of the recent literature related to antihypertensive therapy for patients with diabetes, we describe an empiric approach to treatment of hypertension in such patients. The proposed approach must be modified as new data from randomized clinical trials become available.

Antihypertensive Agents↗
PubMed1995

In vitro binding of [3H]nimodipine and [3H]CGS-19755 to rat brain in focal cerebral ischemia.

Focal cerebral ischemia results in increased in vivo binding of calcium channel antagonists to both the L-type voltage sensitive calcium channel (VSCC) and the N-methyl-D-aspartate (NMDA) receptor-linked calcium channel. It was the aim of this study to investigate the effect of focal cerebral ischemia on the in vitro binding of calcium channel antagonists to rat brain. Quantitative autoradiography was used to measure regional in vitro binding of the L-type VSCC antagonist [3H]nimodipine and the competitive NMDA receptor antagonist [3H]CGS-19755 to rat brain following 4 h of irreversible focal cerebral ischemia. [3H]Nimodipine binding to the nonischemic hemisphere was characterized by one binding site with regional binding affinity (KD) estimates ranging from 221 to 482 pM and maximal binding site densities (BMAX) ranging from 13.2 (9.6-17.5) pmol/g tissue (estimate and 95% confidence interval) in CA1 to 32.5 (26.5-39.9) pmol/g tissue in dentate. [3H]CGS-19755 binding to the nonischemic hemisphere was characterized by KD estimates ranging from 59 to 97 nM and BMAX values ranging from 143 (108-192) pmol/g tissue in cortex to 569 (515-641) pmol/g tissue in CA1. For [3H]CGS-19755 a model of two binding sites was applicable in several brain regions. No difference in binding site densities or binding affinities between ischemic and paired nonischemic structures (cortex and striatum) was observed with either ligand. In vitro binding of [3H]nimodipine and [3H]CGS-19755 to ischemic brain failed to identify ischemic-induced changes in calcium channel function previously reported by in vivo binding methods.

Animals↗
PubMed1994

In vivo binding of [3H]nimodipine in rat brain after transient forebrain ischemia.

We report the regional variation in relative in vivo binding of the L-type voltage sensitive calcium channel (VSCC) antagonist [3H]nimodipine to brain following transient forebrain ischemia in the rat. At 30-min of reperfusion after 20 min of forebrain ischemia, [3H]nimodipine binding was significantly increased in striatum, CA3 and CA4, and dentate relative to binding in sham-operated rats, suggesting that VSCCs were responding to ischemic depolarization. Two h following ischemia, binding in all brain structures returned to normal levels indicating repolarization of cell membranes. At 24 h of recirculation, increased [3H]nimodipine binding was again observed in striatum and dentate. Binding remained elevated in the striatum and dentate, and increased binding became evident in the CA1 region of the hippocampus after 48 h of reperfusion. With the exception of the dentate gyrus, the second rise in [3H]nimodipine binding anticipated or coincided with the observed regional ischemic cell changes. These observations in global cerebral ischemia support previous work indicating that in vivo binding of [3H]nimodipine to the L-type VSCC may be an early and sensitive indicator of impending ischemic injury. Such measurements may be of use in identifying vulnerable brain regions and defining a therapeutic window of opportunity in models of cerebral ischemia.

Animals↗
PubMed1994

Calcium-mediated mechanisms of ischemic injury and protection.

Our understanding of calcium's role in cerebral ischemia continues to evolve from the initial recognition that it may be harmful to the ischemic cell. A multitude of experiments have supported the hypothesis that excessive influx of calcium into the cell under ischemic conditions is a major mechanism of cell injury and death. Pharmacological intervention to restore cellular calcium homeostasis is protective in many models of cell anoxia. Principle routes of calcium entry are the voltage-sensitive (VSCC) and N-methyl-D-aspartate linked receptor operated (ROCC) calcium channels. Regional variations in channel densities have been described and it is now known that these classes of channels are located in different regions of the neurons. Activation of both channel types has been identified in in vivo models of cerebral ischemia. Although the ROCC is predominant in number, the VSCC appears to activate at higher cerebral blood flow values suggesting that it is an earlier conduit for calcium than the glutamate-driven ROCC. Intracellular calcium is well recognized as a second messenger system and there is increasing appreciation that it induces immediate early genes (IEG). Since IEGs function as transcriptional regulating factors, the differential expression of specific target genes may be of importance for determining death or survival of the ischemic tissue.

Animals↗
PubMed1994

Age-related variability in elbow joint capsule thickness in asymptomatic children and adults.

The purpose of this study was to establish normal ultrasonographic measurements for elbow joint capsule thickness in children. Transverse posterior ultrasonographic images of 53 elbow joints in asymptomatic patients were digitized, and off-line measurements were performed and compared to the corresponding scale present on each image to yield a reliable measurement in millimeters. Joint capsule thickness measurements regressed with age. Significant differences existed between three age groups. Joint capsule thickness is under 1 mm in children 1 month to 2 years of age, increased significantly to just over 1 mm from 2 to 15 years of age, and approached 2 mm in thickness at and after 15 years of age.

Adolescent↗