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Biomedical subjects

J Atkinson

Publications and source records attributed to J Atkinson.

At least 127 records · Page 7Linked to original sources
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↗
PubMed1981

Contrast sensitivity function of preschool children.

A procedure specifically adapted for children of preschool age has been used to measure contrast sensitivity in emmetropic children aged 3 to 5 years. Mothers of the children acted as adult observers using the same procedure. The results show that the contrast sensitivity function of adults and children is very similar, sensitivity for the children being slightly lower than that for adults at all spatial frequencies. The sensory and cognitive factors involved in these differences are discussed.

Adult↗
PubMed1981

Does the Catford drum give an accurate assessment of acuity?

Adult emmetropes and myopes were tested with the Catford drum and the results compared with subjective (Landolt C) acuity. For he emmetropes the Catford drum was found to overestimate visual acuity by a factor of approximately 4. For myopes, and emmetropes viewing through plus lenses, the discrepancies were much larger. Since the Catford drum not only overestimates acuity but will do so by a factor which varies for different visual disorders, caution is needed in clinical interpretation of results obtained with it.

Adult↗
PubMed1980

Cortical binocularity in infants.

The primate visual cortex, including that of man, receives separate input from each eye and these interact in binocular cortical neurones. This organization is known to be vulnerable to disruption in early life. To understand the development of human visual cortex, and to detect and assess disorders of binocular function at the earliest possible age, a robust method is needed for detecting binocular interactions in the infant's visual system. We have done this by recording cortical visual evoked responses (VERs) to the onset and offset of binocular correlation in a large-screen dynamic random dot display. We report here that, in general, the human infant has a functional binocular visual cortex by 3 months of age, with some individuals showing cortical binocularity at an earlier age.

Age Factors↗
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↗
PubMed1979

Contrast sensitivity of the human neonate measured by the visual evoked potential.

Visual evoked potentials (VEPs) were recorded from a total of 97 1- to 10-day-old infants, with phase-reversing sinusoidal grating stimuli. The grating contrast or spatial frequency for which 50% of infants gave a statistically significant VEP was taken as a measure of threshold. This procedure yielded an estimate of neonatal acuity of 0.85 cycles/degree and an optimal contrast threshold of 50%. VEPs from an older infant showed good agreement with behavioral measures of sensitivity on the same individual. Comparison of the neonatal VEP results with behavioral data from 5-week-old infants, suggests little change in visual performance over the first month of life.

Evoked Potentials↗
PubMed1978

Infant astigmatism measured by photorefraction.

Photorefraction of a sample of 93 infants of ages 1 day to 12 months showed that 63 percent of the subjects had astigmatism of 0.75 diopter or greater, and 12 percent greater than 2 diopters. Seventy percent of these astigmatisms were in the horizontal-vertical meridians. By comparison, only 8 percent of a sample of 26 adults tested by the same method showed astigmatism (all 0.75 to 1 diopter). The high incidence of infant astigmatism has implications for critical periods in human visual development and for infant acuity.

Adult↗
PubMed1978

Comparison of effects of quinidine and dihydroquinidine on canine heart.

Various cardiac effects of quinidine and dihydroquinidine were tested in isolated dog hearts and in vivo in dogs. No significant differences were found in the negative inotropic, chronotropic, and dromotropic effects. Dihydroquinidine was more potent than quinidine in decreasing coronary arterial pressure.

Animals↗