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Biomedical subjects

M J Hogan

Publications and source records attributed to M J Hogan.

At least 55 records · Page 3Linked to original sources
PubMed1993

Mediastinal paraganglioma: a surgical experience.

Between October 1960 and January 1991, 5 male and 9 female patients (mean age, 44 +/- 19 years) were seen at the Mayo Clinic because of mediastinal paraganglioma. Nine patients presented with hypertension. In these and an additional patient, the tumors were biochemically active. In 13 patients, the mediastinal mass was localized preoperatively. All patients with functioning tumors received alpha-adrenergic and beta-adrenergic blockade preoperatively. Total resection was performed in 11 patients and partial resection in 2. In 1 patient, the tumor was found at postmortem examination. Five lesions were grossly invasive and nine were noninvasive. Blood pressure returned to normal in 6 of the 8 hypertensive patients whose tumors were totally removed. In 4, catecholamine excretion normalized as well. Tumor multicentricity occurred in 6 patients. In 7 patients, the disease took a malignant course (metastases in 5 and progression of unresectable lesions in 2). The probability of 10-year survival after resection was 50% in the group with malignant tumors, and there were no deaths in the group with benign lesions. Analysis of the DNA cellular content showed no correlation between the ploidy pattern and the behavior of the disease.

Adolescent↗
PubMed1992

In vivo distribution of CGS-19755 within brain in a model of focal cerebral ischemia.

The blood-brain barrier permeability of the competitive N-methyl-D-aspartate receptor antagonist CGS-19755 [cis-4-(phosphonomethyl)-2-piperidine carboxylic acid] was assessed in normal and ischemic rat brain. The brain uptake index of CGS-19755 relative to iodoantipyrine was assessed using the Oldendorf technique in normal brain. The average brain uptake index in brain regions supplied by the middle cerebral artery was 0.15 +/- 0.35% (mean +/- SEM). The unidirectional clearance of CGS-19755 from plasma across the blood-brain barrier was determined from measurements of the volume of distribution of CGS-19755 in brain. These studies were performed in normal rats and in rats with focal cerebral ischemia produced by combined occlusion of the proximal middle cerebral artery and ipsilateral common carotid artery. In normal rats the regional plasma clearance across the blood-brain barrier was low, averaging 0.015 ml 100 g-1 min-1. In ischemic rats this clearance value averaged 0.019 ml 100 g-1 min-1 in the ischemic hemisphere and 0.009 ml 100 g-1 min-1 in the nonischemic hemisphere. No significant regional differences in plasma clearance of CGS-19755 were observed in either normal or ischemic rats except in cortex injured by electrocautery where a 14-fold increase in clearance across the blood-brain barrier was measured. We conclude that CGS-19755 crosses the blood-brain barrier very slowly, even in acutely ischemic tissue.

Animals↗
PubMed1992

Reversibility of nimodipine binding to brain in transient cerebral ischemia.

Using autoradiography, we have measured the in vivo binding of [3H]nimodipine to brain in a rat model of reversible cerebral ischemia. Ischemia was induced by simultaneous occlusion of the middle cerebral artery (MCA) and ipsilateral common carotid artery by microaneurysm clips. Rats were studied after 15 min of ischemia (ischemic group) or after 45 min of reperfusion following 15 min of ischemia (reperfused group). Regional cerebral blood flow (CBF) was determined autoradiographically using [14C]iodoantipyrine in both ischemic (n = 6) and reperfused (n = 6) groups. During ischemia blood flow in the territory of the MCA was depressed and recovered to normal only in the distal territory of the MCA following reperfusion. [3H]Nimodipine binding in the ischemic group (n = 12) was elevated in ischemic brain regions and declined significantly (p < 0.01) in these regions in the reperfused group (n = 11). The ratio of the volume of cortex showing increased binding to the total volume of the forebrain was 0.113 +/- 0.025 (mean +/- SD) in the ischemic group and declined to 0.080 +/- 0.027 following reperfusion (p < 0.005). In general, infarct was only observed in regions showing persistent elevation of nimodipine binding following reperfusion as determined by histology performed in a separate group of rats (n = 8) after 24 h of reperfusion. We conclude that increased nimodipine binding to ischemic tissue is initially reversible with prompt reestablishment of CBF and is a sensitive indicator of early and reversible ischemia-induced cerebral dysfunction.

Animals↗
PubMed1992

Time course of cerebral blood flow and histological outcome after focal cerebral ischemia in rats.

BACKGROUND AND PURPOSE: The relation between time-dependent changes in cerebral blood flow and the appearance of infarction after focal cerebral ischemia is still a matter for debate. The aim of this study was to measure perfusion after simultaneous occlusions of the left middle cerebral artery and ipsilateral common carotid artery in rats and correlate it with the timing and distribution of histological changes. METHODS: We studied histological and cerebral blood flow changes 5 minutes and 4, 24, and 48 hours after the onset of focal ischemia. Blood flow was determined autoradiographically using [14C]iodoantipyrine. A coronal template subdivided into regions of interest was applied to the autoradiographs and the histological data. RESULTS: In some regions of the nonoccluded hemisphere, cerebral blood flow 5 minutes after occlusion fell below 50% of normal. Many ischemic structures showed stable blood flow for 48 hours after occlusion, confirming that in this model reperfusion is minimal. Infarction occurred eventually in all areas in which blood flow at 5 minutes fell below 10% of that in control rats, but infarction appeared earlier in regions in which blood flow at 5 minutes was below 5% of that in control rats. When blood flow at 5 minutes rose above 12% of that in control rats, the occurrence of infarction became unpredictable. CONCLUSIONS: Despite the general dependence of infarction on perfusion levels, blood flow was not a reliable indicator of those regions committed to infarction.

Animals↗
PubMed1992

Evaluating an intern/residency program.

When faced with the task of program evaluation, many directors of medical education may find themselves overwhelmed. This article presents suggestions for conducting an evaluation, including the six basic elements to consider before embarking on such an undertaking. With an emphasis on selecting a model framework as a guide for conducting a program evaluation, this article examines one model--Stufflebeam's CIPP model--in depth.

Internship and Residency↗
PubMed1991

In vivo binding of nimodipine in the brain: I. The effect of focal cerebral ischemia.

We report the regional variation in [3H]nimodipine binding in vivo during focal cerebral ischemia. After intravenous injection, 30 min of circulation of [3H]nimodipine was sufficient to establish a secular equilibrium of distribution in the brain. Rats sustained left middle cerebral and common carotid artery occlusions for 5 min, and 4, 24, and 48 h (n greater than or equal to 6 epr group). They were decapitated 30 min after injection of 250 microCi of [3H]nimodipine and their brains were submitted to autoradiography. The concentrations of [3H]nimodipine in plasma and brain structures, corrected for metabolism of nimodipine, were used to calculate the regional volumes of distribution (V) in the ischemic left (L) and control right (R) hemispheres. Log (VL/VR) was then defined as the group mean of the logarithms of the left-to-right ratio of V of [3H]nimodipine. In the lateral caudate, binding of [3H]nimodipine on the ischemic side was highest within 5 min of occlusion. Log (VL/VR) in this region for the combined sham-operated and normal control rats and those after 5 min and 4 and 24 h of ischemia were -0.014 +/- 0.025, 0.137 +/- 0.056*, -0.201 +/- 0.367, and -0.049 +/- 0.370 (mean +/- SD, *represents p less than 0.01 compared with controls). By contrast, in the superior frontal cortex, values for log (VL/VR) in the same sequence were -0.016 +/- 0.025, 0.028 +/- 0.056, 0.284 +/- 0.228*, and 0.224 +/- 0.069*, thus showing a significant rise in [3H]nimodipine binding only at 4 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

In vivo binding of nimodipine in the brain: II. Binding kinetics in focal cerebral ischemia.

We report the binding characteristics of [3H]nimodipine to normal and ischemic brain in vivo. We used the 1,4-dihydropyridine, nimodipine, to label the L-type voltage-sensitive calcium channel in focal cerebral ischemia after occlusion of both the middle cerebral and ipsilateral common carotid arteries in rats. Varying concentrations of [3H]nimodipine were infused 3.5 h after the onset of ischemia and circulated for 30 min before the brain was obtained for autoradiography and determination of regional nimodipine content. In separate sets of experiments, the metabolites of nimodipine were determined and the conditions for equilibrium of nimodipine distribution were established. Increased nimodipine uptake was observed in ischemic regions. This increased binding was saturable and specific with an affinity constant, KD, of 0.45 nM and a maximal regional binding capacity, Bmax, ranging from 3.1 to 10.9 pmol/g. Only binding to ischemic tissue was specific and saturable whereas that in nonischemic tissue was nonspecific. In vivo binding of nimodipine may be used to identify cell membrane depolarization and calcium channel activation in focal cerebral ischemia.

Animals↗
PubMed1991

Accurate attenuation correction for a 3D PET system.

An accurate attenuation correction has been developed for a small-volume three-dimensional positron emission tomography (PET) system. Transmission data were measured as twenty-four 2D slices which were reconstructed and combined to form a 3D attenuation image. Emission data were reconstructed using a backproject-then-filter technique, and each event was corrected for attenuation at backprojection time by a reprojection through the attenuation image. This correction restores the spatial invariance of the point response function, thus allowing a valid deconvolution and producing an undistorted emission image. Scattering corrections were not applied to either the transmission or the emission data but simulation studies indicated that scattering made only a small contribution to the attenuation measurement. Results are presented for two phantoms, in which transmission scans of 57,500 and 18,700 events/slice were used to correct emission images of 5.2 and 2.8 million events. Although the attenuation images had poor statistical accuracy and a resolution of 13 mm, the method resulted in accurate attenuation-corrected images with no degradation in image resolution (which was 3 mm for the first emission image), and with little effect on image noise.

Image Processing, Computer-Assisted↗
PubMed1990

Primary aldosteronism: diagnosis and treatment.

The syndrome of primary aldosteronism produces few signs or symptoms. The diagnosis should be suspected when either spontaneous hypokalemia or easily provoked hypokalemia is found in a patient with hypertension. Hypokalemia in association with inappropriate kaliuresis, low plasma renin activity, and a high plasma aldosterone concentration/plasma renin activity ratio are the findings on initial screening tests that should suggest primary aldosteronism. The diagnosis must be confirmed by demonstrating nonsuppressible aldosterone excretion in conjunction with normal cortisol excretion. The choice of therapy is based on distinguishing unilateral from bilateral adrenal disease. With a unilateral adrenal adenoma, surgical removal reverses the hypokalemia and frequently cures the hypertension. In most patients with bilateral adrenal hyperplasia who are treated surgically, however, hypertension persists; thus, the initial treatment in these patients should be pharmacologic.

Adenoma↗
PubMed1988

Lupus anticoagulant, antiphospholipid antibodies and migraine.

The records of fifteen patients referred for neurological assessment and found to have lupus anticoagulant or elevated anticardiolipin antibodies were reviewed. The mean age for females in the group was 29.4 years and for males was 35. A diagnosis of migraine, either as an acute or chronic problem, was made in 10 (66%) of these patients. Seven of the 15 patients had ischemic stroke and two patients had other thrombotic complications associated with lupus anticoagulant. Three of the nine female patients with migraine had histories of spontaneous abortions. All migraine patients experienced transient or more prolonged neurological deficits with their headaches. An association between lupus anticoagulant and migraine can only be suggested. Data on the incidence of migraine in patients with lupus anticoagulant in the general medical population does not exist. Furthermore the prevalence of lupus anticoagulant in migraine sufferers is unknown. Therefore further studies are required to investigate this possible association.

Adult↗
PubMed1984

Evaluation of a test using saralasin to differentiate primary aldosteronism due to an aldosterone-producing adenoma from idiopathic hyperaldosteronism.

We evaluated a new method utilizing saralasin to differentiate primary aldosteronism due to an aldosterone-producing adenoma from idiopathic hyperaldosteronism. The test is based on the marked difference in sensitivity to angiotensin II of aldosterone-producing adenomas and hyperplastic adrenal glands and the partial angiotensin II agonist property of saralasin in low-renin states. Saralasin was infused into 14 patients with primary aldosteronism and the plasma aldosterone responses determined. Plasma aldosterone concentration increased in all eight patients with idiopathic hyperaldosteronism, whereas there was no increase in plasma aldosterone in six patients who had a solitary adenoma. We concluded that saralasin may be a clinically useful, noninvasive tool to distinguish patients with an aldosterone-producing adenoma from those who have idiopathic hyperaldosteronism.

Adenoma↗
PubMed1984

Drug overdose during pregnancy: an overview from a metropolitan poison control center.

Suicide attempts during pregnancy usually present as intentional drug overdoses after interpersonal conflicts. During a recent four-year period, 119 (0.07%) of all 179,893 telephone inquiries at a metropolitan poison control center involved drug overdoses by 111 pregnant women. This was usually the first such attempt and telephone notification occurred primarily within the first hour. The ingested substance was known in 109 (98%) cases and consisted mostly of an excess of a single drug. The 50 different types of over-the-counter and prescription medications consisted primarily of analgesics (most notably acetaminophen), vitamins or iron, sedatives, antibiotics, and antihistamines or decongestants. No maternal deaths were reported. Signs or symptoms were nonexistent or mild in 61 (55%) women, and major or life-threatening in 50 (45%) women. Compliance with recommendations given by telephone and referral to the primary physician or emergency room was good, especially when major symptoms or life-threatening illnesses were apparent. Close emotional support and a search for depression during pregnancy and the postpartum period are recommended.

Adolescent↗
PubMed1983

Oral glucose tolerance test compared with a mixed meal in the diagnosis of reactive hypoglycemia. A caveat on stimulation.

Reactive hypoglycemia is being diagnosed with increasing frequency. We compared plasma glucose, insulin, glucagon, epinephrine, and norepinephrine responses to an oral glucose tolerance test and to a mixed meal containing equivalent carbohydrate in 33 patients who had been referred to our institution with a presumed diagnosis of reactive hypoglycemia and in 2 patients who had insulinomas. In addition, a control group of 36 normal volunteers underwent the meal study. During the meal studies, electroencephalograms were obtained. Despite provocation of hypoglycemia by the oral glucose tolerance test, no consistent relationship between hypoglycemia and symptoms was observed. Despite similar symptoms, hypoglycemia did not develop after the meal test in the 33 patients without insulinomas. Both patients with insulinoma became hypoglycemic after ingestion of the meal. When a physiologic stimulus such as a meal is used to duplicate the daily dietary experience of patients, reactive hypoglycemia in the absence of a pancreatic pathologic lesion is an uncommon occurrence.

Adolescent↗
PubMed1981

Plasma clonidine concentration and pharmacologic effect.

Analysis of sequential plasma samples in 14 hypertensive subjects receiving their usual oral dose of clonidine (0.1 to 0.6 mg twice daily) indicated that clonidine plasma concentration increased for the first 2 hr and then decreased and stabilized over the next 12 hr. Percent fall in diastolic blood pressure, but not side effects, correlated well with plasma concentration. Our study indicates a potential role for plasma clonidine determination in the treatment of patients with hypertension. It also demonstrates that clonidine can probably be given at 12-hr intervals and be effective.

Adult↗
PubMed1981

The plasma aldosterone response to angiotensin II infusion in aldosterone-producing adenoma and idiopathic hyperaldosteronism.

To determine if the adrenal sensitivity to angiotensin II in patients with an aldosterone-producing adenoma differs from that in patients with idiopathic hyperaldosteronism, we infused graded doses of angiotensin II into 17 patients with primary aldosteronism and measured their plasma aldosterone concentrations after each dose. At a rate of 0.5 ng angiotensin II/kg.min, the mean increase in the plasma aldosterone concentration in the 8 patients from whom an aldosterone-producing adenoma was subsequently removed was 4 +/ 2.4 ng/dl (mean +/- SE), which was significantly less (P less than 0.01) than the mean increase (23 +/- 4.8 ng/dl) in the 9 patients with idiopathic hyperaldosteronism. The threshold dose of angiotensin II in the patients with aldosterone-producing adenoma was 1.0 +/- 0.24 ng/kg.min, significantly greater (P less than 0.05) than the threshold dose (0.3 +/- 0.07 ng/kg.min) in the patients with idiopathic hyperaldosteronism. We conclude that the sensitivity of aldosterone-producing adenomas to angiotensin II is significantly less than that of the hypersecreting adrenal tissue in patients with idiopathic hyperaldosteronism. This difference in adrenal sensitivity might in part explain the difference in the response of plasma aldosterone concentrations to upright posture in these two subsets of aldosteronism with low renin activity.

Adenoma↗