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Biomedical subjects

G R Hogan

Publications and source records attributed to G R Hogan.

At least 37 records · Page 2Linked to original sources
PubMed1985

Incidence of seizures that follow rehydration of hypernatremic rabbits with intravenous glucose or fructose solutions.

Hypernatremic dehydration was induced in rabbits during a 3- to 5-day period resulting in mean plasma sodium concentrations of 187 meq/liter. The animals were then rehydrated during a 4-h period by intravenous administration of a 2.5% glucose or fructose solution. The water content of four regions of brain sample showed a significant (P less than 0.05) increase in brain water content above normal in the rehydrated groups. Brain water content was significantly (P less than 0.01) greater in those animals with seizures compared with those without seizures, suggesting the importance of water intoxication in the pathogenesis of seizure activity. Changes in muscle Na, K, Cl, and water content were not similar to those of brain, indicating that muscle content of these substances was not an accurate reflection of the brain content specific time. The incidence of seizures was significantly (P less than 0.05) greater when glucose solution was used for rehydration (49%) compared with the use of fructose solution (25%). The mechanism(s) by which fructose resulted in a lower incidence of seizures is not known. The frequency of seizure activity was directly proportional to the rate of administration of intravenous solutions utilized to correct hypernatremia. In addition, the specific carbohydrate of the solution appeared to play an important role in the pathophysiology of the development of seizures.

Animals↗
PubMed1985

Ulnar neuropathy at the wrist: case report and review of literature.

We present a case of pure motor ulnar neuropathy with sparing of the hypothenar muscles and a review of 55 published cases of ulnar neuropathy at the wrist in which the clinicoanatomic correlation was clearly delineated. We propose a classification of ulnar neuropathies at the wrist divided into five types based on clinical findings, electrophysiologic studies, and clinicoanatomic correlations. Type I: a mixed motor and sensory neuropathy, occurring just outside or within the proximal end of Guyon's canal. II: a pure sensory neuropathy, where the lesion involves the superficial branch of the ulnar nerve (UN) at the wrist but distal to the branch to the m. palmaris brevis. III: a pure motor neuropathy due to a lesion of the deep branch of the UN just distal to the superficial branch but proximal to the branch to the hypothenars. IV: a pure motor ulnar neuropathy with sparing of hypothenars; this lesion occurs on the deep branch of the UN distal to the origin of the superficial branch and distal to the branch going to the hypothenars. V: a distal motor neuropathy in which the lesion occurs just proximal to the branches going to the first dorsal interosseus and adductor pollicis muscles.

Adult↗
PubMed1984

Neonatal Citrobacter meningitis: pathogenesis of cerebral abscess formation.

In 2 premature infants with brief survival, the major pathological feature of Citrobacter meningitis consisted of vasculitis and infarction with necrosis and liquefaction of large portions of the white matter of the hemispheres. Areas of decreased density demonstrated on computed tomographic head scan represented infarction with necrosis, liquefaction, and cavitation and not a classic abscess. This finding has clinical significance, because surgical drainage of liquefied infarcts is rarely indicated and could further damage the relatively preserved cortex.

Brain Abscess↗
PubMed1984

The incidence of seizures after rehydration of hypernatremic rabbits with intravenous or ad libitum oral fluids.

Hypernatremic dehydration (mean plasma sodium, 184 mEq/L) was produced over a 3-5 d period in 71 rabbits. The dehydrated animals were divided into groups and rehydrated by intravenous (4, 6, and 8 h duration) or oral (4 and 24 h duration) solutions in amounts calculated to return plasma Na to 140 mEq/L. Plasma was obtained serially from each animal for electrolyte and osmolality determinations during dehydration and rehydration. Samples of brain hemisphere and cortex were obtained for chemical analysis from every animal immediately after death. The incidence of seizures was significantly less (P less than 0.025) in rabbits rehydrated orally when compared with rabbits rehydrated by the intravenous route. Brain water content was significantly greater in rabbits rehydrated intravenously when compared with normal rabbits and rabbits rehydrated orally. In addition, the amount of brain water was greater in rabbits with seizures when compared with those which did not have seizure manifestations. The mechanism underlying the significant reduction in seizures when the animals were rehydrated orally may relate to an integration of drinking behavior with rehydration status. Administration of oral fluids may provide an effective method of therapy for some patients with hypernatremic dehydration.

Administration, Oral↗
PubMed1984

Meningococcal meningitis in children: clinical comparison of disease produced by the minor and major serologic groups of Neisseria meningitidis.

Since 1972, there has been an increased incidence of meningococcal disease due to the minor serologic groups, "serogroups," of Neisseria meningitidis. Few cases, however, have been reported in pediatric patients. We present 24 cases of meningococcal meningitis, ten of them (42%) due to serogroups X, Y, and Z N meningitidis. We believe these cases to be the largest group of pediatric patients with such meningitis thus far reported. The clinical disease produced by the minor serogroups was indistinguishable from that produced by the major serogroups. Our experience supports previous published reports that severe meningococcal disease does occur with the minor serogroups of N meningitidis, and this increasing incidence may be of major importance if vaccination programs are to be effective in controlling epidemic meningococcal disease.

Adolescent↗
PubMed1982

Variation of lead-induced lethality in estradiol-treated mice.

Studies were undertaken to test the female sex hormone beta-estradiol for its ability to modify lethality in young adult female and male mice exposed to lead acetate. Mice were injected with beta-estradiol on d -1 and 0, and immediately after the second injection lead acetate was administered at four subgroup dosages ranging from 75 to 600 mg/kg body weight. Control mice were injected with only lead acetate. On d 4, 6, and 8 after Pb, the median lethal dosages (LD50s) were calculated from the observed mortality ratios by a method of moving averages. LD50 values were considerably lower for the Pb- and beta-estradiol-injected groups than for the controls. Data from these experiments indicate that the beta-estradiol treatments render both female and male mice more vulnerable to the lethal effects of lead acetate.

Animals↗
PubMed1979

Lead-induced leukocytosis in female mice.

Lead acetate was shown to stimulate a striking leukocytosis in young adult female mice. The effect was manifest 4 days after lead injection and continued throughout the following 4 days. At the higher treatment level, lead induced an increase of 300% for both monocytes and neutrophils. The leukocytosis was due primarily to the elevated levels of neutrophils as suggested by a decrease in the ratios of peripheral agranulocytes to granulocytes. No differences from normal leukocyte cytology were observed in blood samples collected from animals receiving lead.

Animals↗
PubMed1979

Aflatoxin B1; its role in the etiology of Reye's syndrome.

Seven cases of Reye's syndrome in which aflatoxin B1 was isolated from the blood or liver or both are presented. In two cases aflatoxin B1 was found in the blood during the acute phase of the disease; a finding not previously reported. In six cases aflatoxin B1 was recovered from autopsy specimens of liver. A number of case reports linking aflatoxin B1 to Reye's syndrome have appeared in the literature but until now only one case had been reported from the United States. Aflatoxin B1 and its possible role in the etiology of Reye's syndrome is discussed. It is concluded that Reye's syndrome is the result of multiple interrelated factors.

Aflatoxins↗
PubMed1977

Single lead acetate insult, testosterone therapy, and erythropoiesis in mice.

Lead acetate (PbAc) was tested for its effects on the production and release of erythrocytes-that is, erythropoiesis-in ICR mice. Dose-survival data indicate that a dosage of 20 mg PbAc/100 g body weight represents the maximum tolerable treatment level. No differences in survival at the various levels of the salt were observed with regard to sex or age. For erythropoietic effects of PbAc, mice were injected on day O, and radioiron (59Fe) incorporation percentages were determined at daily intervals through day 8 for both erythrocytes and splenic tissue. Control mice received isotonic saline as the injectate. On day 3, the percentages obtained from PbAc-treated mice showed a decline, reaching their minimum value by day 4. Recovery from erythropoietic suppression appeared to be complete by day 6 or 7; no positive overshoots in 59Fe percentages were found following recovery. These trends were typical for both peripheral red blood cells and spleen. Testosterone was administered to mice receiving saline or PbAc on two consecutive days (days -1 and O). Radioiron uptake percentages for females receiving testosterone and saline showed an abrupt increase on day 4. No accelerative effect due to testosterone was found in recipient males. For females treated with testosterone and PbAc, the radioiron percentages for erythrocytes and spleen paralleled those for females receiving saline only. Male mice treated with both androgen and PbAc demonstrated 59Fe percentages typical of males treated with PbAc alone.

Animals↗
PubMed1977

Neurological evaluation of the newborn.

The neurological examination is an integral part of the evaluation of the newborn infant. In too many instances the infant is dismissed from the nursery as 'normal' when,in fact, little or no effort has been expended to determine the body's neurological status. The neurological deficits overlooked often do not become overt until a much later age. Early detection can prevent the mental anguish that plagues the parents who must be told that their 'normal' infant has significant neurological problems. In some instances early diagnosis may lead to a better ultimate prognosis. We have presented a simple scheme for the neurological evaluation of the full-term infant and hope that it will be useful in encouraging pediatricians to assess neurological status.

Cephalometry↗
PubMed1976

Hypernatremia--problems in management.

Hypernatremia may be produced under several different circumstances but most frequently is the result of excessive water loss with diarrhea and the excessive solute load secondary to inappropriate preparation of formula. The clinical manifestations vary and depend primarily on the degree of dehydration and the rate at which the hyperosmolar state has been reached. The management of the patient will, of course, depend upon the mechanism of hypernatremia and degree of dehydration and/or hypovolemia that is present. It seems clear that the exact nature of the rehydrating solution is not of major importance. The volume is of great concern but most vital seems to be the rate of rehydration. If rehydration is accomplished too rapidly the child becomes edematous, develops increased intracranial pressure, stupor, and convulsions. If fluids are given slowly and at a well regulated rate, these complications can usually be avoided. The patient should be monitored regularly with electrolytes, careful determination of weights, and records of intake and output. The rate of rehydration should be monitored to assure that the planned schedule of 24 to 72 hours (depending on the severity of the problem) is followed. Approximately 10 to 15 per cent of children with serum sodium of 160 mEq per liter or greater will have permanent neurological deficits.

Brain Diseases↗