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Biomedical subjects

J Atkinson

Publications and source records attributed to J Atkinson.

At least 109 records · Page 6Linked to original sources
PubMed1983

Optics of photorefraction: orthogonal and isotropic methods.

Analysis of the optics of photorefractively computed ray tracing shows that, for short camera-to-subject distances, the function relating image size to defocus of the eye is not symmetrical for errors of focus in front of and behind the camera. This asymmetry is exploited in the new method of isotropic photorefraction, in which the supplementary cylinder lenses of the original orthogonal photorefractors are replaced by defocusing of the camera lens itself. By comparing photographs taken with the camera focused in front of and behind the subject, the sign of the eyes' defocus (myopic or hyperopic relative to the camera) can be determined. The axis of any astigmatism is readily apparent as the direction in which the photorefractive images are elongated. The method is well adapted for the refractive screening of infants and young children.

Astigmatism↗
PubMed1983

The onset of binocular function in human infants.

Visual evoked potentials (VEP) elicited by a dynamic random-dot correlogram were used to assess the development of cortical binocular function in infant subjects. In a group of newborn infants who showed a VEP for a comparable non-binocular stimulus, none showed evidence of binocular function. A further group of infants were tested longitudinally, starting between 35-50 days. The median age for the first evidence of binocular function in this group was 91 days, with individual variation from 54 to at least 105 days.

Aging↗
PubMed1982

Effects of vestibular stimulation in seizure-prone children. An EEG study.

Concern that vestibular stimulation may induce seizures in seizure-prone children has been based on hearsay and unconfirmed clinical impressions of practicing therapists. To clarify this issue, we took electroencephalographic recordings of seizure-prone children before, during, and after specific vestibular stimulation. Ten children with seizure histories, 5, to 15 years of age, were exposed to warm and cold caloric vestibular stimuli. Electroencephalographic activity was recorded before, during, and after each vestibular stimulus; recordings were rated and compared prevestibular and postvestibular stimulation. Electronystagmographic recordings were also taken. Results show that vestibular stimulation does not accentuate the abnormal brain wave pattern in seizure-prone children. Six of 10 subjects had a significant reduction in paroxysmal activity (p less than .02). Possible explanations for clinical reports of vestibular induced seizures are given, with suggestions for precautions when applying vestibular stimulation to seizure-prone children.

Adolescent↗
PubMed1982

Evaluation of a diabetes education programme.

An education programme was evaluated for 140 insulin-dependent diabetics and their family members from 1978 to 1980. Dietary, biochemical and other assessments were made before and 6 months after the programme. As a group, the diabetics were initially in good metabolic control and this was maintained, or improved, over the study period. The programme recommended a diet in which complex carbohydrate constituted at least 45% of energy intake and fat was limited to 30%. The diabetics and their family members significantly increased their consumption of complex carbohydrate and decreased fat intake. On this regimen, diabetics did not gain weight and their relatives lost weight. There were also improvements in knowledge of the disorder and in perceptions of susceptibility to complications and barriers to compliance.

Attitude to Health↗
PubMed1982

'Preferential looking' for monocular and binocular acuity testing of infants.

A method is described for obtaining rapid and reliable estimates of acuity in infants, for both monocular and binocular viewing. The method depends on 'preferential looking', where the infant prefers to look at a striped pattern rather than a blank screen of matched mean luminance. A staircase procedure for testing is followed, with observations being recorded by a 'blind' observer (who does not know on which of the 2 screens the striped pattern is displayed). Monocular acuity estimates have been obtained for a group of infants 3 to 4 months old with normal refractions. Many of these infants show similar acuity values in the 2 eyes, with a few showing reliable differences between the eyes. To check reliability of the method a comparison of 2 independent interleaved staircase estimates of the same eye have been made. In general this check shows highly consistent estimates for a given eye of a given infant. Nearly all infants show slightly higher acuity estimates for binocular viewing than for monocular. The possible reasons for this difference are discussed. The clinical use of such a method is reported for a number of cases. The method has been found to be useful in a variety of clinical conditions where other available tests are not possible on young infants.

Child, Preschool↗
PubMed1982

The role of plasma and renal renin in the rise in blood pressure following unilateral renal artery constriction.

Constriction of the artery to the remaining kidney of control rats uninephrectomized 24 h previously induced a sixfold rise in plasma renin level from 11 +/- 1 to 60 +/- 11 ng AI ml-1 h-1, a 43% decrease of renal cortical renin level, and a 21% rise of mean arterial pressure from 119 +/- 2 to 144 +/- 3 mm Hg. Constriction of the artery to a renin-depleted kidney (with a renin level which was 5% of normal) was not followed by any significant increase in plasma renin level or mean blood pressure. Renin-depleted kidneys were produced by removing the clipped kidney from two-kidney one-clip hypertensive rats, 24 h before the experiment. Such a maneuver induces renin depletion but does not completely normalize blood pressure. When a large dose of frusemide (50 mg/kg i.p.) was injected immediately following removal of the clipped kidney, mean arterial pressure (117 +/- 7 mm Hg) returned to control values 24 h later but again constriction of the remaining renal artery failed to induce a rise in plasma renin level or mean arterial pressure. By 7 days after removal of the clipped kidney, plasma renin level and mean arterial pressure were normal and clipping of the remaining kidney (in spite of the fact that kidney renin level was still low) now produced a wave of renin release and an increase in mean arterial pressure. These results suggest that the initial, rapid increase in mean arterial pressure following unilateral renal artery constriction is dependent on an increase in plasma renin level. Our results from animals with kidneys of varying renin levels suggest the existence of a cortical renin content of about 20% of normal below which the kidney is incapable of responding to renal artery constriction with significant renal release. Complete recovery of the renin (and blood pressure) response to clipping occurred when the renin content had reached about 75% of normal.

Animals↗
PubMed1982

Interaction between the renin-angiotensin and beta adrenergic nervous systems in drinking and pressor responses after renal artery constriction.

Constriction of the remaining renal artery of a uninephrectomized rat produced an increase in plasma renin level, a decrease in renal cortex renin level, an increase in blood pressure and a drinking response. Simultaneous infusion with the angiotensin II antagonist, saralasin, potentiated the rise in plasma renin level and blocked the rise in blood pressure. Drinking was only partially attenuated. Pretreatment with l-propranolol had no effect on the changes in plasma or kidney renin levels, but the increase in blood pressure was potentiated and the drinking response was attenuated. It is concluded that the pressor and drinking responses to renal artery constriction are partially mediated by the beta adrenergic nervous system.

Angiotensin II↗
PubMed1981

Renin release by renin-depleted rats following hypotensive haemorrhage and anesthetics.

1. Renin-depletion, described as a decrease in renal cortex and plasma renin levels, was produced by clipping one renal artery of a rat and leaving the contralateral kidney in place (two kidney one clip hypertension), One month later the clipped kidney was removed and after 24 h recovery such rats were found to be renin depleted: renal cortex and plasma renin levels were 8 and 63% of normal respectively. 2. Such renin depleted rats were incapable of releasing renin (as judged by increase in plasma renin level) in response to severely hypotensive haemorrhage and had very blunted renin release responses to pentobarbital and urethane anesthesia (59 and 17% of normal respectively). 3. Our results confirm the hypothesis that a low renal renin status is associated with low basal and stimulated renin release. We suggest that the renin depleted rat may be a useful model for the study of the role of the renin angiotensin system in phenomena such as blood pressure compensation following hypotensive haemorrhage and drinking induced by beta-adrenoreceptor agonists.

Anesthetics↗
PubMed1980

Influence of streptozotocin-induced diabetes on blood pressure and on renin formation and release.

I.v. injection of 40 mg/kg or 65 mg/kg streptozotocin reliably induced diabetes in female Sprague-Dawley rats, but failed to induced hypertension within the following 42 days. In most animals injected with the higher dose and in some animals injected with the lower dose the tail blood flow was permanently impaired so that no blood pressure signals could be obtained by tail plethysmography. This phenomenon occurred also when the drug was injected into the jugular vein and thus was not due to a local effect of streptozotocin. 15 days after 65 mg/kg streptozotocin, the mean arterial pressure of the rats was similar to that of controls, when measured inthe awake state (carotid cannula) or under ether anaesthesia. 42 days after streptozotocin, under pentobarbital anaesthesia, the blood pressure was again normal in the animals given 40 mg/kg of the drug and depressed in the animals given 65 mg/kg of the drug 42 days previously. The increase of blood pressure induced by 1 microgram/kg (-)-noradrenaline i.v. was similar in the latter group of animals and in controls. The renal cortical renin concentration was much lower than in controls 42 days after either dose of streptozotocin, while the plasma renin activity was normal (40 mg/kg) or increased 65 mg/kg). The low renal renin content may have been due to the diabetic state, rather than to the drug itself. Adrenal medullary dopamine-beta-hydroxylase activity was increased 42 days after the higher dose of streptozotocin.

Adrenal Medulla↗
PubMed1979

The renal effects of clonidine in unanesthetized rats.

Clonidine s.c. (0.01-0.3 mg/kg), in unanesthetized rats, caused an initial rise (+20 mm Hg), followed by a continuous fall of BP and a dose-dependent natriuresis and diuresis for up to 2 h. Glomerular filtration rate (GFR) (CIn) increased during the first 20 min, while effective renal plasma flow (ERPF) (CPAH) remained normal. Subsequently, between 20 and 60 min after injection, ERPF (CPAH) decreased considerably while GFR had reverted to its normal value. In saline-infused rats clonidine diuresis was accompanied by an "inappropriate" positive free water clearance. Pentobarbital anesthesia suppressed the initial BP peak and the diuresis. Phenoxybenzamine (1 mg/kg i.v.) was antinatriuretic in saline diuresis; the effect of phenoxybenzamine + clonidine on diuresis and salt excretion represented the sum of the effects of both drugs, but phenoxybenzamine enhanced the clonidine-induced increase of GFR. Neither haloperidol (1 mg/kg i.v.) nor bulbocapnine (3 mg/kg i.v.) interfered with the renal effects of clonidine. Clonidine s.c. caused hyperglycemia and glucosuria which did not account for the natriuresis. Clonidine thus appears to increase the GFR and "filtration fraction" (FF) by a phenoxybenzamine-insensitive rise of glomerular ultrafiltration, to depress ERPF by alpha-adrenergic afferent vasoconstriction, to induce natriuresis by a tubular action not blocked by phenoxybenzamine and to exert an antivasopressin effect, either by depressing pituitary vasopressin secretion or the renal response to vasopressin.

Animals↗
PubMed1979

Effect of chronic clonidine treatment and its abrupt cessation on mean blood pressure of rats with a normal or an elevated blood pressure.

1. Clonidine (6 mg of base/l of water) was given as drinking fluid to normotensive rats or rats with established or early hypertension. 2. Spontaneous hypertensive rats (6 months old: average dose of clonidine, 0.6 mg 24 h-1 kg-1) showed a sustained fall in blood pressure over 3 weeks. 3. The same clonidine solution given for 6 weeks to two-kidney Goldblatt rats with early-stage hypertension (average dose of clonidine: 1 mg 24 h-1 kg-1) or spontaneously hypertensive rats (clonidine dose: 1 mg) induced a fall in mean blood pressure, but no change in normotensive rats. 4. Replacement of clonidine by water induced hypertension and lability which led to death in hypertensive but not in normotensive rats.

Animals↗
PubMed1979

The role of circulating renin in drinking in response to isoprenaline.

1. In nephrectomized rats, S.C. (0.12 mg. kg body wt.(-1)) or intracerebroventricular (I.C.V.: 0.03 mg. kg(-1)), isoprenaline failed to elicit drinking. However, when preceded (5-20 min) by a non-dipsogenic dose of I.V. pig renin, S.C. isoprenaline induced a marked, and I.C.V. isoprenaline a smaller drinking response. 2 hr after I.V. renin, S.C. isoprenaline no longer caused drinking.2. Pig renin did not enhance drinking in response to 0.12 mg. kg(-1) isoprenaline S.C. in intact or sham-operated rats.3. Isoprenaline (0.12 mg. kg body wt.(-1), S.C.) caused a larger fall of blood pressure in unanaesthetized nephrectomized than in intact unanaesthetized rats, but it was not the resulting hypotension that interfered with the nephrectomized rats' ability to drink, since intact rats with similar falls in blood pressure drank avidly in response to large doses of isoprenaline.4. Since the rate of inactivation of pig renin in nephrectomized rats was not modified by isoprenaline, drinking in nephrectomized animals in response to renin+isoprenaline was not attributable to increased plasma renin levels.5. Since isoprenaline induces drinking in the presence of circulating renin, but in the absence of renin release from kidneys, renin plays a permissive role in isoprenaline-induced drinking. Angiotensin and isoprenaline may interact at the level of intracranial receptors.

Animals↗
PubMed1979

Hexobarbital blood levels and effects on EEG in the presence and absence of caffeine.

The interaction of caffeine and hexobarbital in the rat with spinal cord transection was studied. Duration of hexobarbital effect on the brain was taken as the time from the injection of hexobarbital (i.v.) to the return of pre-injection cortical voltage. Hexobarbital distribution and elimination was estimated by application of a two-compartmental model to values for blood hexobarbital concentration (determined by a direct gas chromatographic method after extraction). Caffeine caused a shift in the dose-response curve for hexobarbital but no changes in hexobarbital distribution and elimination. Results are interpreted on the basis of a central interaction of caffeine with hexobarbital at a brain receptor level.

Animals↗