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Biomedical subjects

P E Arnold

Publications and source records attributed to P E Arnold.

At least 19 recordsLinked to original sources
PubMed1991

Emmetropisation, squint, and reduced visual acuity after treatment.

In a sample of children used to assess the value of optical correction of hypermetropia from the age of 6 months the refraction of the most hypermetropic meridian frequently became less than 3.5 D as the children grew. When this occurred, the incidence of squint was significantly less (p less than 0.001) and the last known acuity after treatment was significantly better (p less than 0.001) than when it did not. This process of emmetropisation appears to have been impeded by the consistent wearing of hypermetropic spectacle correction from the age of 6 months.

Eyeglasses↗
PubMed1990

Results of a randomised trial of treating abnormal hypermetropia from the age of 6 months.

Children who were abnormally hypermetropic at the age of 6 months were randomly allocated treatment with spectacles or no treatment. The eventual incidence of squint was the same in both groups (approximately 24%). The last known visual acuity of the two groups was not significantly different either. Therefore there is no indication to screen infants with a view to preventing squint/amblyopia by optical correction of hypermetropia. If, however, the children allocated treatment are divided into two subgroups--those who wore glasses consistently and those who probably or certainly did not do so--the incidence of squint was the same, but the last known acuities of those who consistently wore glasses may be better than those who did not do so. This suggests that it may yet prove possible to prevent severe amblyopia.

Eyeglasses↗
PubMed1986

Effects of angiotensin II on plasma antidiuretic hormone and renal water excretion.

The effects of intravenous (i.v.) and intracarotid (IC) angiotensin II (AII) infusion on systemic and renal hemodynamics, renal water excretion, and plasma antidiuretic hormone (ADH) levels were examined in six conscious dogs under water loaded and hydropenic conditions. In the first group of seven studies, AII in a mean dose of 12.7 ng/kg/min was administered i.v. to water loaded dogs. The infusion induced a significant increase in mean arterial pressure (MAP, 99 to 118 mm Hg, P less than 0.001), and significant reductions in both glomerular filtration rate (GFR, 67 to 57 ml/min, P less than 0.05) and para-aminohippurate clearance (CPAH, 280 to 212 ml/min, P less than 0.005) occurred. Despite this decrement in renal hemodynamics, urine remained maximally dilute (Uosm, 58 to 61 mOsm/kg H2O, NS). Furthermore, plasma ADH was suppressed maximally after water load and did not increase after i.v. AII infusion. The IC infusion of AII (mean dose 5.8 ng/kg/min) produced similar changes in hemodynamics; plasma ADH remained undetectable. When AII was administered i.v. to hydropenic animals (mean dose 8.3 ng/kg/min), MAP again increased (86 to 111 mm Hg, P less than 0.001) as GFR (81.3 to 68.6 ml/min, NS) and CPAH (291 to 223 ml/min, P less than 0.05) declined modestly. In these animals, Uosm decreased significantly (1429 to 1114 mOsm/kg H2O, P less than 0.005) and plasma ADH did not change significantly (1.66 to 1.88 pg/ml, NS). When IC AII (4 ng/kg/min) was repeated in hydropenic dogs pretreated with indomethacin, neither Usom (1787 to 1664 mOsm/kg H2O, NS) nor plasma ADH were altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1986

Prediction of amblyopia and squint by means of refraction at age 1 year.

In this series amblyopia, uncorrectable by spectacles and occlusion, was highly likely (48%) if a child had +3.50 or more dioptres of meridional hypermetropia at age 1 year. 45% of children with this refraction also had a squint. All those who remained with severely defective acuity in spite of treatment had either +3.50 or more dioptres of meridional hypermetropia or 4 or more dioptres of meridional myopia at age 1 year. These children were identifiable in the 3.7% of the population at age 1 year who showed high refractive errors. Squint as such was not so accurately predictable. Of those children with squint 71% had less than +3.50 dioptres of meridional hypermetropia at age 1 year--an incidence of 4.4% of the population. Apart from two 'congenital myopes' only 16% of these had residual amblyopia after treatment, and their last known acuity was never less than 6/12. Astigmatism in infancy or later is not significantly associated with squint or amblyopia.

Amblyopia↗
PubMed1986

Screening for visual defects in preschoolchildren.

There is no evidence to support the suggestion that a widespread programme of vision screening at age 3 1/2 should be instituted. Some of the practical problems and defects of such a programme are outlined. If the issues raised are to be resolved by further research, identification of preschoolchildren who have visual problems will be facilitated by a screening procedure involving refraction and possibly a cover test.

Amblyopia↗
PubMed1986

Reduced osmotic and nonosmotic release of vasopressin after meclofenamate in the conscious dog.

Both in vivo as well as in vitro experiments suggest that prostaglandins (PG) may influence arginine vasopressin (AVP) release. Recent studies on conscious dogs have shown that cyclooxygenase inhibition with meclofenamate reduces basal AVP release as well as AVP release in response to hypoxia. The current experiments were performed in order to test whether PG synthesis inhibition affects osmotic- and nonosmotic-stimulated AVP release in a similar manner. Osmotic AVP release was tested by slowly infusing hypertonic saline intravenously in water-diuresing dogs and serially sampling plasma for AVP concentration. Experiments were performed both with and without meclofenamate (2 mg/kg and 2 mg X kg-1 X h-1 iv) pretreatment. AVP release to a comparable osmotic stimulus was greatly reduced after meclofenamate administration. Nonosmotic AVP release was tested by inducing systemic hypotension with an intravenous infusion of nitroprusside. Hypotension was associated with an increase in AVP concentration, which was partially blunted after meclofenamate administration. Experiments performed with only a saline vehicle administered showed no decrease in AVP release in response to comparable hypotension. The findings of these studies suggest that endogenous PG may be involved in both osmotic and nonosmotic AVP release in the conscious dog.

Animals↗
PubMed1986

Adenine nucleotide metabolism and mitochondrial Ca2+ transport following renal ischemia.

Mitochondrial Ca2+ accumulation and mitochondrial respiratory dysfunction have been observed after renal ischemia. The present study examined the effects of ischemia and reperfusion on cellular energy production and mitochondrial Ca2+ transport after 50 min of bilateral renal artery and vein clamping in the anesthetized rat. Prior to reflow, tissue ATP and total adenine nucleotide levels were severely reduced. These nucleotide levels recovered towards normal but remained lower than control values throughout 24 h of reperfusion. Energy-linked mitochondrial Ca2+ uptake was unmeasurable, mitochondrial Ca2+ efflux was increased and the mitochondria were unable to maintain a steady-state free Ca2+ concentration prior to reflow. Three hours of reperfusion was associated with a normalization of mitochondrial Ca2+ uptake, release, and steady-state buffering. However, progressive deterioration subsequently occurred in these processes. Thus the mitochondrial Ca2+ accumulation previously observed during the later stages of postischemic reperfusion (3-24 h) is due neither to an increase in the rate of active Ca2+ uptake nor to a decrease in the rate of Ca2+ release. The present results therefore suggest that passive mitochondrial Ca2+ accumulation may occur during the later stages of reperfusion, probably due to a progressive increase in the cytosolic Ca2+ concentration.

Adenine Nucleotides↗
PubMed1985

In vitro versus in vivo mitochondrial calcium loading in ischemic acute renal failure.

Progressive mitochondrial Ca2+ accumulation and respiratory dysfunction have been observed during reperfusion after renal ischemia. The present study demonstrated that normal mitochondria, isolated in the presence of high Ca2+ concentrations, are capable of accumulating large amounts of Ca2+ in vitro and exhibit depressed respiratory rates. Since mitochondria isolated from reperfused ischemic tissue may be exposed to high concentrations of Ca2+ during the isolation procedure, the present study examined the effect of in vitro versus in vivo mitochondrial Ca2+ loading on mitochondrial function during ischemic acute renal failure (ARF) in anesthetized rats. When ruthenium red was added during isolation to prevent mitochondrial Ca2+ exchange with the medium, mitochondrial Ca2+ increased from 10.8 +/- 0.3 to 65.6 +/- 11.6 nmol/mg (P less than 0.001) after 24 h of postischemic reperfusion; this resulted in a 47% reduction in the acceptor-control ratio (ACR) from 4.19 +/- 0.09 to 2.70 +/- 0.13 (P less than 0.001). These data were compared with an increase in mitochondrial Ca2+ from 52.5 +/- 2.9 to 167.6 +/- 25.4 nmol/mg (P less than 0.001) and a 95% fall in ACR (3.84 +/- 0.40 to 1.15 +/- 0.08, P less than 0.001) at 24 h of reperfusion when no ruthenium red was added. However, at each time point examined, in vivo mitochondrial Ca2+ accumulation was shown to account for 50% or more of the mitochondrial respiratory dysfunction observed during ischemic ARF.

Acute Kidney Injury↗
PubMed1984

Mitochondrial calcium accumulation and respiration in ischemic acute renal failure in the rat.

Changes in mitochondrial (Mito) calcium (Ca++) and Mito respiration have been demonstrated 24 hr after a renal ischemic insult. The Ca++ accumulation has been suggested to contribute to impaired Mito function; alternatively, the Mito Ca++ accumulation could be a late event resulting from cell death. The present aim was, therefore, to determine the sequence of changes in Mito function in ischemic acute renal failure (ARF) induced by 45 min of bilateral renal pedicle clamping in the rat. Animals were studied at the end of clamping, 1, 4, and 24 hr after reflow. By 24 hr, the serum creatinine level had risen progressively to almost ten times control values and fractional excretion of sodium and water were increased. Mito respiration (state 3, adenosine diphosphate-stimulated; acceptor control ratio, state 3/state 4; and uncoupled, FCCP) was severely depressed immediately after 45 min of clamping but improved significantly at 1 and 4 hr after reflow although remaining below sham-operated controls. At 24 hr, when ischemic ARF was established, Mito respiration was again severely depressed. Mito Ca++ was increased slightly but significantly at the end of clamping and increased progressively at 1, 4, and 24 hr after reflow. The Mito Ca++ accumulation was not only demonstrated to occur very early after the ischemic insult, but was relatively selective since it was not associated with Mito Mg++ accumulation. Moreover, the increased Mito Ca++ during reperfusion (1, 4, and 24 hr) demonstrated a significant correlation with the decreased state 3 respiration and the rising serum creatinine level (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1984

Protection of mitochondrial function by mannitol in ischemic acute renal failure.

The effect of isotonic mannitol to provide protection against ischemic renal injury was examined in the dog. Mannitol treatment attenuated the fall in glomerular filtration rate at both 1 and 24 h after the ischemic insult. The functional changes were associated with profound cellular protection, since normal mitochondrial respiration, mitochondrial calcium uptake and release rates were preserved, and excessive mitochondrial calcium accumulation was prevented. These effects at the cellular level appear critical to the protective effect of mannitol after ischemia and are most likely due to prevention of cell swelling.

Acute Kidney Injury↗
PubMed1984

Protective effect of intrarenal calcium membrane blockers before or after renal ischemia. Functional, morphological, and mitochondrial studies.

The present study examined whether a pre- or postischemic infusion of verapamil (V) or a postischemic infusion of nifedipine (N), drugs which block calcium (Ca++) influx across plasma membranes, provides protection against ischemic acute renal failure (ARF) in dogs. Renal hemodynamics and excretory function were examined 1 h (initiation phase) and 24 h (maintenance phase) after a 40-min intrarenal infusion of norepinephrine (NE). In each case, the uninfused contralateral kidney served as control. Four groups were studied: (a) dogs receiving NE alone; (b) dogs receiving an intrarenal infusion of V for 30 min before NE (V + NE); (c) dogs in which intrarenal V was infused for 2 h, beginning immediately after completion of NE infusion (NE + V); and (d) dogs in which intrarenal N was infused for 2 h, beginning immediately after completion of NE infusion (NE + N). Glomerular filtration rate (GFR) in the NE kidneys, as assessed by inulin clearance, at 1 and 24 h averaged 2.4 +/- 1.1 and 5.0 +/- 2.0 ml/min, respectively, as compared with control kidney GFRs of 28.0 +/- 3.5 and 43.8 +/- 5.0 ml/min, respectively (both at least P less than 0.01). In the V + NE group, GFR at 1 and 24 h averaged 15.0 +/- 5.5 and 31.0 +/- 4.5 ml/min, respectively, both at least P less than 0.05 as compared with values from NE kidneys. GFRs in the NE + V group averaged 15.0 +/- 2.4 and 16.3 +/- 3.6 ml/min at 1 and 24 h, both at least P less than 0.02 as compared with values from NE kidneys. GFR in the NE + N group averaged 18.6 +/- 6.0 ml/min at 24 h (P less than 0.05 as compared with GFRs in the NE kidneys). In addition, function of cortical mitochondria (Mito) was examined at the end of the 40-min NE infusion and after 1 and 24 h of reperfusion in the NE alone and NE + V groups. Mito respiration, assessed by acceptor control ratios, was reduced at each period in the NE alone kidneys. After 24 h, these Mito had accumulated Ca++ and exhibited reduced Ca++ uptake and increased Ca++ release rates. Mito from NE + V kidneys respired normally, did not accumulate Ca++, and exhibited no alterations in Ca++ uptake or release. Light and electron microscopy also demonstrated morphological protection of V against tubular necrosis and cell injury. Mito from the NE + N kidneys also respired normally and did not accumulate significant amounts of Ca++. The results of the present studies therefore demonstrated that chemically dissimilar calcium entry blockers exert substantial functional, cellular, and morphological protection against experimental ischemic ARF. These findings are compatible with the hypothesis that increased cytosolic Ca++ is critically important in the maintenance of renal vasoconstriction and the development of cellular necrosis with subsequent tubular obstruction in NE-induced ischemic ARF. V or N may provide protection against renal injury by retarding any increase in cytosolic Ca++ in renal vasculature and epithelium.

Acute Kidney Injury↗
PubMed1983

Prevention of ischemic acute renal failure with impermeant solutes.

Studies were performed to evaluate the effect of solute permeability and extracellular osmolality in protecting against ischemic acute renal failure. The functional protective effect of a 1-min intrarenal perfusion (prior to intrarenal norepinephrine 0.75 micrograms . kg-1 . min-1) of a hypertonic permeant solute (hypertonic saline, 1,400 mosmol/kg H2O) and an isotonic impermeant solute (isotonic mannitol, 280 mosmol/kg H2O or isotonic polyethylene glycol, IPEG, 300 mosmol/kg H2O) was evaluated. Three hours after ischemia, the glomerular filtration rate was significantly lower in hypertonic saline group vs. either the isotonic mannitol- or IPEG-treated animals (2.4 vs. 8.9 and 10.4 ml/min, respectively; both P less than 0.05). Mean renal blood flow was similar in all three groups. The effects of hypertonic saline and IPEG on glomerular filtration pressure and tubular obstruction were also evaluated. Stop-flow pressure, as an index of glomerular filtration pressure, was higher in the IPEG- vs. the hypertonic saline-treated animals (40 vs. 35 mmHg, P less than 0.001). Although proximal tubular pressure was increased in both groups, transglomerular hydrostatic pressure was higher in the IPEG vs. the hypertonic saline group (13 vs. 6 mmHg, P less than 0.01). Tubular microperfusion studies demonstrated increases in proximal tubular pressure in the hypertonic saline but not the IPEG studies. The present results indicate that isotonic, impermeant solutes provide functional protection against ischemic acute renal failure. The beneficial effect of impermeant solute is mediated, at least in part, by better maintenance of transglomerular hydrostatic pressure and prevention of secondary tubular obstruction.

Acute Kidney Injury↗
PubMed1983

Role of mitochondria in ischemic acute renal failure.

Ischemic ARF is characterized by progressive mitochondrial accumulation of Ca++ which is inversely correlated with the level of oxidative phosphorylation. At least two possibilities exist which would be compatible with these data 1) depressed respiration leads to Ca++ accumulation or 2) increased mitochondrial Ca++ leads to reduced mitochondrial respiration. We favor the latter hypothesis for the reasons outlined above; furthermore, this conclusion is supported by the observations of Lehninger, made some 20 years ago: first, that either oxidative phosphorylation or mitochondrial Ca++ accumulation can be accomplished by intact mitochondria but that these events cannot occur simultaneously and second, that Ca++ accumulation takes precedence over oxidative phosphorylation. Our observation made during post-ischemic reflow that mitochondrial Ca++ accumulation occurs to a significant degree, strongly suggest a potential role for mitochondrial Ca++ overload in the pathogenesis of ARF. Nevertheless, this is not an irreversible pathogenetic process. Clearly, impermeant solutes, vasodilators and Ca++ membrane blockers will alter the natural history of this injury and prevent the severity of the functional defect. A common mechanism of action may involve direct or indirect modification of cellular Ca++ overload in renal vascular and epithelial tissue. The vascular smooth muscle may then revert to a less constricted state with a subsequent more rapid recovery of renal blood flow and that the renal epithelial cell death may be minimized thereby reducing tubular obstruction.

Acute Kidney Injury↗
PubMed1983

Insulin pump.

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Humans↗