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Biomedical subjects

J Atkinson

Publications and source records attributed to J Atkinson.

At least 163 records · Page 9Linked to original sources
PubMed1992

Orientation selectivity in infancy: behavioural evidence for temporal sensitivity.

One-month-old infants were tested with a habituation-recovery paradigm to determine whether they could discriminate phase-shifting grating patterns that switched between two orientations, three or eight times a second, from grating patterns that only shifted in phase. The infants were found to discriminate patterns switching orientation at the lower temporal rate of 3 reversals s-1, but not 8 reversals s-1. This finding supports the idea that orientation-selective mechanisms improve in their temporal sensitivity during early infancy. Where they can be compared, the results from behavioural and electrophysiological studies agree as to the course of this development.

Child↗
PubMed1992

Changes in infants' ability to switch visual attention in the first three months of life.

The abilities of 1-month-old and 3-month-old infants to shift their gaze from a central target to a peripheral target were compared in four experiments. In experiment 1 targets matched in mean luminance to the background were presented to infants in the periphery at varying levels of contrast. The contrast thresholds for target detection were found to be significantly different for 1-month-olds compared with 3-month-olds. With targets set close to these contrast thresholds, correct refixations and the latency for shifting attention were examined in experiment 2. Two conditions were used: a peripheral target was presented against a homogeneous background (noncompetition); and in the second condition, the patterned target appeared at one of two lighter peripheral windows set against a darker background (competition). Although there was no difference between the two age groups in the latency for shifting visual attention, 1-month-olds were found to make more directional errors in the competition condition. The competition effect of two potential targets on latencies was examined in experiment 3. In the competition condition, two identical peripheral patterned targets were presented to the infants. The 3-month-olds refixated more quickly to one of the double targets in the competition condition than to a single peripheral target, whereas 1-month-olds were slowed down by a double target display. Finally, in experiment 4 the ability of the infants to process and disengage from a central stimulus and to refixate towards a similar peripheral target was examined. This type of competition disrupted both the direction of the first eye movement and the latency to shift attention in both age groups. However, the effect was significantly greater for the 1-month-olds. Taken together, the results of these experiments demonstrate the greater disruption of fixation-shift behaviour in 1-month-olds compared with 3-month-olds when competing visual stimuli are used. This developmental change is explained in terms of maturation of executive cortical orienting systems over the first months of life.

Age Factors↗
PubMed1992

Haemodynamic effects of the calcium facilitator Bay K-8644 in rats following vascular calcium overload.

1. The haemodynamic effects of the Ca2+ facilitator Bay K-8644 (Bay) were studied in a model of calcinosis induced by acute treatment with vitamin D3 and nicotine administration over 4 days with 13 days of recovery. 2. Calcium content of the left ventricular myocardium increased 8-9 fold, while aortic Ca2+ levels increased up to 12-fold in treated animals. There were minimal changes in the ECG and no change in the level of plasma alpha-hydroxy-butyrate-dehydrogenase, a cardiac specific enzyme which increases during ischaemia. Significant increases in pulse pressure (PP) were seen in anaesthetized and conscious calcinotic rats, with no increase in cardiac output index (DABF) or systemic vascular resistance. However, aortic rigidity (AORI) was significantly elevated in the calcinotic group under anaesthesia. 3. In both control and calcinotic rats, pressor responses to i.v. Bay were exclusively mediated by an increase in aortic blood flow (DABF) as lower body vascular resistance (TLBVR) did not change. The increase in DABF at low doses (0.1-1 microgram kg-1) of Bay probably resulted from an increase in venous return induced by the agonist, as Bay had little effect on cardiac contractility over this dose range (as estimated by left ventricular dp/dtmax) and did not cause tachycardia. At higher doses (10-1000 micrograms kg-1), Bay significantly increased LV dp/dt. Bay caused dose-related increases in AORI in pithed calcinotic rats, but a decrease in AORI in control animals. 4. The calcinosis model, which incorporates a recovery period to obviate the acute effects of nicotine and/or vitamin D3 treatment, results in long-term tissue calcium accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Haemodynamic effects of a new dihydropyridine calcium entry blocker, S-12968-(-), in a rat model of cardiovascular calcium overload.

1. The haemodynamic effects of S-12968-(-), a new dihydropyridine calcium entry blocker (enantiomer of S-11568), were compared with those of the stereoisomer, S-12967-(+), nifedipine, and sodium nitroprusside. 2. A first experiment was performed in conscious, young male rats chronically implanted with femoral artery and vein cannula and repeated in rats previously treated with vitamin D3 and nicotine. Such treatment produces marked vascular calcium overload, especially of the compliance arteries, with no overt sign of toxicity as far as can be judged from the plasma profile. 3. In conscious rats the hypotensive effects of S-12968-(-), nifedipine and sodium nitroprusside were of similar potency. The falls in blood pressure produced by nifedipine and sodium nitroprusside were accompanied by reflex tachycardia which was less marked in the vascular calcium overload model. S-12968-(-) did not induce reflex tachycardia. S-12967-(+) increased blood pressure in both models. 4. A second experiment was performed in open-chest pentobarbitone-anaesthetized rats with electromagnetic flowprobes on the ascending aorta. In controls the falls in blood pressure produced by low doses (0.1 and 0.3 mg kg-1, i.v.) of S-12968-(-) were accompanied by falls in total peripheral resistance. The higher dose (1 mg kg-1, i.v.) of S-12968-(-) produced no change in total peripheral resistance, and in rats pretreated with vitamin D3 and nicotine, cardiac output fell. 5. In conclusion, S-12968-(-) appears to have a dual action and to lower blood pressure at higher doses at least in part by a cardiac effect. This phenomenon is more pronounced in rats pretreated with vitamin D3 and nicotine.6. S-12967-(+) resembles a calcium channel activator in this model.

Animals↗
PubMed1992

Chronic antihypertensive treatment with captopril plus hydrochlorothiazide improves aortic distensibility in the spontaneously hypertensive rat.

1. Adult male spontaneously hypertensive rats (SHR) were given captopril plus hydrochlorothiazide mixed in the diet for 10 weeks. Calculated daily doses were 44 mg kg-1 per day for captopril, and 22 mg kg-1 per day for hydrochlorothiazide. Separate groups received captopril or hydrochlorothiazide alone, at similar doses, or no treatment. A final group of WKY normotensive rats received no drug. 2. Systolic arterial blood pressure, measured at regular intervals throughout the 10 weeks' period was lowered but not normalized, in groups receiving either captopril plus hydrochlorothiazide, or captopril alone, but not in the group receiving hydrochlorothiazide alone. 3. Following pentobarbitone anaesthesia, systolic arterial blood pressure, measured in the femoral artery, was found to be lower in all treated groups, but the greatest effect was observed in SHR previously treated with captopril plus hydrochlorothiazide. Aortic pulse wave velocity was also lower in treated SHR, and once again the greatest decrease was observed in the group previously treated with captopril plus hydrochlorothiazide. 4. Following pithing, systolic arterial blood pressures were similar in all SHR groups. Aortic pulse wave velocity was lower in pithed rats previously treated with captopril and hydrochlorothiazide. 5. In conclusion, antihypertensive treatment of SHR produces falls in blood pressure and pulse wave velocity, an indicator of aortic distensibility. Results in pithed rats suggest that treatment with the combination of captopril plus hydrochlorothiazide may increase aortic distensibility independently of blood pressure.

Animals↗
PubMed1992

Extracorporeal membrane oxygenation in lambs through umbilical vessel perfusion: cardiac and hepatic complications.

Twin lambs were delivered by ceasarean section near term, aralyzed, sedated and randomly assigned to either mechanical ventilation or umbilical arteriovenous ECMO for 48 hours. Umbilical arteriovenous ECMO provided adequate gas exchange with minimal or no ventilation of the native lungs. However, at autopsy, animals treated with umbilical ECMO showed right heart dilation and liver necrosis or hemorrhage compared to their twins treated with mechanical ventilation.

Animals↗
PubMed1992

Sulfasalazine-induced pulmonary disease.

We report the findings in two patients with sulfasalazine-induced pulmonary disease. The first patient developed pulmonary interstitial fibrosis after more than 4 yr of treatment for Crohn's disease. Pulmonary symptoms and chest roentgenographic and pulmonary function abnormalities gradually reversed after stopping the drug. No specific treatment was given. The second patient, who had rheumatoid arthritis without pulmonary disease, received the drug for 1 yr without experiencing any problems. Readministration seven months later resulted in the development of an acute interstitial pulmonary disease. Discontinuing the drug and treatment with corticosteroids produced rapid improvement. We discuss these patients in relation to other reports of sulfasalazine-induced pulmonary toxicity, highlighting their atypical features.

Acute Disease↗
PubMed1992

Vascular calcium overload. Physiological and pharmacological consequences.

Pronounced vascular calcium overload, especially of compliance arteries, is an important aspect of aging, and of various age-related vascular diseases such as hypertension and atherosclerosis. The development of new drugs specifically aimed at attenuating the evolution and/or pathological consequences of vascular calcium overload is hindered by the paucity of animal models available. Although several laboratory animals exhibit vascular calcium overload, this evolves slowly and is far less marked than in man. Nevertheless, Fleckenstein and associates (1989) suggested a suitable animal model involving the treatment of young rats with vitamin D3 and nicotine; such treatment produces pronounced vascular calcium overload within a few weeks. This paper describes the cardiovascular effects of such treatment, and our preliminary attempts to pharmacologically modify vascular calcium overload and its cardiovascular consequences.

Animals↗
PubMed1992

Effect of chronic treatment with the calcium entry blocker, isradipine, on vascular calcium overload produced by vitamin D3 and nicotine in rats.

Treatment of young rats with vitamin D3 and nicotine produced a 35-fold increase in the calcium content of the aorta and a 4-fold increase in the calcium content of the mesenteric arterial bed. Blood pressure was not modified. In vitro, aortic rings and mesenteric arterial bed preparations from such animals showed diminished vasoconstrictor responses to norepinephrine. After precontraction with norepinephrine, the endothelium-dependent vasodilator, carbachol, produced vasorelaxation. This latter effect was attenuated in aortic rings and mesenteric arterial bed preparations from animals previously treated with vitamin D3 and nicotine, but the vasodilator effect of sodium nitroprusside (which is independent of the endothelium) was unchanged. Prolonged treatment with the calcium entry blocker, isradipine, at a dose (1 mg/kg, i.p.) which had no effect on blood pressure, prevented calcium overload of the mesenteric arterial bed, but did not modify aortic calcium overload. Isradipine treatment had no effect on vasoconstrictor responses to norepinephrine in vitro. Such treatment did, however, restore the endothelium-dependent vasodilator effect of carbachol in the mesenteric arterial bed (but not in aortic rings). In conclusion, in a rat model of vascular calcium overload produced by administration of vitamin D3 plus nicotine, chronic treatment with a low dose of the calcium entry blocker, isradipine, restored the endothelium-dependent vasorelaxant effect of carbachol in the mesenteric arterial bed, but not in the aorta.

Animals↗
PubMed1992

Clinical significance of mild rejection of the cardiac allograft.

BACKGROUND: The clinical status of heart transplant patients during mild rejection (lymphocytic infiltrate without myocyte necrosis) has not been previously reported. This study examined the frequency and outcome of mild rejection associated with allograft dysfunction sufficient in magnitude to be evident on clinical exam (two or more abnormal findings) and/or two-dimensional echocardiography. METHODS AND RESULTS: The study population consisted of 59 patients, 50 men and nine women 14-61 years old (mean, 1.7 +/- 0.8 years) with a mean follow-up of 1.7 +/- 0.8 years after transplant. All were receiving cyclosporine, azathioprine, and prednisone. A total of 108 episodes of mild rejection were detected (frequency, 1.8 episodes per patient). Detailed records of clinical findings were available for 94 episodes. Thirty-five (37%) of these 94 mild rejections were associated with allograft dysfunction: hypotension, n = 4; elevated jugular venous pressure, n = 14; S3, n = 13; rales, n = 10; sinus rate > or = 110 beats per minute, n = 25; atrial fibrillation, n = 5; bradycardia < 60, n = 1; and systolic dysfunction on echo, n = 14. Treatment with high-dose steroids was clinically indicated in eight mild rejection episodes (9%) with allograft dysfunction. Of the remaining 86 untreated episodes, eight (30%) of 27 with allograft dysfunction versus six (10%) of 53 without allograft dysfunction progressed to moderate rejection on subsequent biopsy (chi 2 = 5.15, p = 0.02). Episodes with allograft dysfunction occurred earlier than those without dysfunction (15.4 +/- 2.8 weeks versus 34.4 +/- 5.5 weeks, p = 0.01) when baseline immunosuppression was higher. CONCLUSIONS: Our findings indicate that 1) mild rejection is frequently associated with cardiac allograft dysfunction; 2) nine percent of mild rejection episodes may be accompanied by severe allograft dysfunction or arrhythmias, requiring aggressive treatment; 3) mild rejection associated with allograft dysfunction occurs earlier than that without allograft rejection; 4) untreated, mild rejection episodes with allograft dysfunction progress to moderate rejection more frequently than those without allograft dysfunction. These episodes require increased surveillance for progression.

Arrhythmias, Cardiac↗
PubMed1992

[Effect of isosorbide dinitrate on vasomotricity-cytosolic calcium coupling during aging in the rat].

Simultaneous measurement of vasomotricity and variations of cytosolic calcium concentrations (mobilisation of intracellular calcium) on a preparation of a normotensive Wistar rat caudal artery allowed analysis of the vasomotricity-cytosolic calcium coupling with respect to age and after administration of isosorbide dinitrate. Vasomotricity was evaluated from changes in perfusion pressure (delta P) of arterial segments perfused at a steady flow state. These segments were exposed to a fluorescent probe, fura 2, the variations of the intensity of emission of which, at wave lengths of 340 and 380 nm, reflect variations in cytosolic calcium concentration (delta R%). The "efficacy" of the vasomotricity-cytosolic calcium coupling was estimated from the delta P/delta R% ratio. In the rat, ageing is accompanied by a reduction in vasomotricity and efficacy of the coupling during noradrenalin stress testing. However, these two parameters recorded during contractions induced by the calcium in a depolarising medium do not change with age. Isosorbide dinitrate reduces vasoconstriction and the delta P/delta R% ratio during noradrenalin stimulation in the young rat. The effect is less pronounced in older rats. Isosorbide dinitrate also reduced the vasomotricity and efficacy of coupling but to a lesser degree during vaso-constriction induced by the calcium in a depolarising medium, without changing the mobilisation of intracellular calcium irrespective of the age of the animals. In conclusion, ageing seems to affect the vasomotricity-cytosolic calcium coupling mainly during receptor stimulation (noradrenalin) rather than during depolarising stimulation (calcium in a depolarising medium). Isosorbide dinitrate acts mainly on the same depolarising stimulation, independent of age.

Aging↗
PubMed1991

The role of endogenous norepinephrine release in potassium-evoked vasoconstriction of the rat tail artery.

Potassium-containing solutions are often used to study the sequence of events leading from excitation to vasoconstriction. In densely innervated vessels, such as the rat tail artery, potassium-induced vasoconstriction may be mediated via smooth muscle depolarization and release of endogeneous norepinephrine. The relative contribution of these two mechanisms--a 'direct' depolarization of the vascular smooth muscle cell membrane, and an 'indirect' sympathomimetic action--to the vasoconstrictor response was studied in the present paper. Perfusion/superfusion of the rat tail artery in vitro with potassium-containing solutions had different effects depending on the concentration used. A change in potassium concentration from 4.7 to 20 mM had no effect on either perfusion pressure or norepinephrine overflow. From 30 to 70 mM, potassium produced increasing amounts of norepinephrine overflow. Experiments with phentolamine and reserpine showed that this norepinephrine overflow contributed for up to half of the vasoconstrictor response observed. A second norepinephrine-independent mechanism was also involved but the latter appeared to be incapable of producing sustained contraction. At concentrations of potassium above 50-70 mM, the results of experiments with (+/-)-propranolol suggest that the norepinephrine released by potassium has a beta-adrenoceptor-mediated vasorelaxant effect.

Animals↗
PubMed1991

Decrease in endothelium-dependent relaxation in the mesenteric arterial bed following vascular calcium overload produced by vitamin D3 and nicotine in rats.

Treatment of young rats with vitamin D3 plus nicotine, which has been proposed as a model of cardiovascular calcium overload, produced an increase in the calcium content of the mesenteric arterial bed and lowered in vitro vasoconstrictor responses to norepinephrine and serotonin. Attenuation of the vasoconstriction induced by norepinephrine by the endothelium-dependent vasodilators, carbachol and histamine, was diminished, but the effects of sodium nitroprusside and papaverine were unchanged. The vitamin D3 plus nicotine model may be useful for the study of the involvement of calcium overload in vascular endothelial dysfunction.

Animals↗
PubMed1991

Differences between the in vitro vasoconstrictor responses of the tail artery to potassium and norepinephrine between spontaneously hypertensive, renovascular hypertensive, and various strains of normotensive rats.

Isolated tail arteries removed from spontaneously hypertensive, renovascular hypertensive, or various strains of normotensive rats were perfused/superfused with norepinephrine or potassium, or subjected to electrical field stimulation. Responses in spontaneously hypertensive and outbred normotensive rat tail artery preparations were similar. Tail artery segments from renovascular hypertensive or normotensive rats of the inbred Wistar-Kyoto strain showed smaller responses to all three stimuli. Thus, in certain in vitro arterial preparations, the apparent increase in vascular reactivity observed when comparing spontaneously hypertensive rats with inbred Wistar-Kyoto rats may be due to a decrease in vascular reactivity in the Wistar-Kyoto rat strain.

Animals↗
PubMed1991

The preparation and acute antihypertensive effects of a nanocapsular form of darodipine, a dihydropyridine calcium entry blocker.

We have addressed two problems associated with the use of dihydropyridine calcium entry blockers in antihypertensive therapy, namely, potent vasodilation and short half-lives, by incorporating the representative blocker, darodipine, into a nanocapsular vehicle. In awake, renovascular hypertensive rats, darodipine nanocapsules lowered blood pressure when given orally or intramuscularly, and the initial fall in blood pressure was less marked than that observed with the same dose of darodipine dissolved in polyethylene glycol 400 (PEG). Intramuscular administration of the nanocapsular form of darodipine had an antihypertensive effect which lasted for at least 24 hr.

Animals↗
PubMed1991

Three cases of disputed paternity in dogs resolved by the use of DNA fingerprinting.

DNA fingerprinting with the probes 33.15 and alpha-globin 3'HVR has been used to resolve three cases of disputed paternity in dogs. For each pedigree it was necessary to establish which bands in the DNA fingerprints of the offspring were of paternal origin, and then establish which putative sire carried all these bands. In the first case, a litter of Rhodesian Ridgebacks, twelve DNA bands were informative in establishing paternity. In the second case, a litter of Afghan hounds, five DNA bands established paternity, Lastly, in a litter of Border collies, five DNA bands established paternity. In each case a single dog only sired the entire litter.

Journal Article↗
PubMed1991

Effects of the angiotensin I converting enzyme inhibitor perindopril on cerebral blood flow in awake hypertensive rats.

As chronic hypertension shifts the lower limit of cerebral blood flow (CBF) autoregulation to higher pressure levels, we studied the effects of the angiotensin converting enzyme (ACE) inhibitor, perindopril on mean arterial pressure (mean BP), basal CBF, and CBF autoregulation in awake renovascular hypertensive (2 kidneys, 1 clip model) and spontaneously hypertensive rats (SHR). Blood pressure was measured via a chronically implanted arterial cannula and CBF by hydrogen clearance. Chronic renovascular hypertension, like spontaneous hypertension, caused a marked shift in the lower limit of CBF autoregulation but did not alter basal CBF. In SHR, acute administration of perindopril did not diminish CBF in spite of the fact that BP fell to a level below the lower limit of CBF autoregulation (determined by hypotensive hemorrhage). Chronic treatment of renovascular hypertensive rats with perindopril normalized BP and restored CBF autoregulation.

Angiotensin-Converting Enzyme Inhibitors↗