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Biomedical subjects

R J Anderson

Publications and source records attributed to R J Anderson.

At least 343 records · Page 19Linked to original sources
PubMed1982

Cardiovascular function in patients with progressive systemic sclerosis (scleroderma).

Sixteen patients with progressive systemic sclerosis (PSS), including 3 with the "CREST" (calcinosis, Raynaud's, esophageal dysfunction, sclerodactyly, and/or telangiectasias) variant, were evaluated with resting M-mode echocardiography and noninvasive measurements of cardiac output at rest and during submaximal exercise to determine the nature and extent of any cardiovascular impairment. No patient had arterial hypertension, significant renal impairment, clinical evidence of large vessel coronary artery disease, or severe pulmonary dysfunction. The duration of disease was 1 to 12 years (9 to 30 for patients with the CREST variant). Echocardiographic abnormalities included increased right ventricular dimension (3 patients), reduced left ventricular ejection fraction (3 patients), and pericardial effusion (3 patients). Cardiac index (CI) and stroke volume index (SVI) at rest were similar for patients and controls. Patients and controls were exercised to similar heart rates (130 +/- 3 vs 124 +/- 4; p, NS). Total peripheral resistance (TPR) was higher for patients (1123 +/- 81 vs 810 +/- 44 dyn X s X cm-5) and their mean SVI failed to increase significantly compared with sitting rest values (30 +/- 2 vs 35 +/- 3 ml/m2). The control subjects had the expected increase in SVI (36 +/- 2 vs 51 +/- 5; p less than 0.01). Ten patients with an abnormal hemodynamic response to exercise had a normal echocardiographic circumferential fiber shortening (VCF) or ejection fraction (EF) at rest. The data indicate that PSS patients have a greater degree of cardiovascular dysfunction than would be predicted from clinical data and laboratory evaluation of cardiovascular and pulmonary function at rest. Multiple mechanisms, including right and left ventricular dysfunction and abnormal vasoconstrictor activity, are likely to contribute to the reduction in exercise capacity seen in patients with PSS.

Adult↗
PubMed1982

Plasma antidiuretic hormone in acute respiratory failure.

The role of antidiuretic hormone (ADH) in the pathogenesis of renal impaired water excretion in acute respiratory failure has not been clearly delineated. Plasma sodium concentration and plasma ADH levels (radioimmunoassay) were therefore serially measured in 13 patients with acute respiratory failure (10 with acute exacerbations of chronic lung disease and three with acute lung disease) and eight "control" patients admitted ot the intensive care unit with suspected myocardial infarction. None of the patients had systemic hemodynamic, hepatic or renal dysfunction. ADH levels were significantly elevated in patients with acute respiratory failure (15.1 +/- 5.2 pg/ml versus 5.7 +/- 1.9 pg/ml, p less than 0.05) when compared with levels in control patients. The elevated ADH levels occurred despite significantly lower plasma sodium concentration (133 +/- 1 meq/liter versus 138 +/- 2 meq/liter, p less than 0.05) compared wit control values. Moreover, markedly increased ADH values (range 1.1 to 13.0 pg/ml) were often encountered in patients with acute respiratory failure despite significant hyposmolality (263 to 275 mOsm/kg H2O). This was not observed in any control patients. These results suggest that patients with acute respiratory failure are susceptible to water retention and hyposmolality due to nonosmotic release of antidiuretic hormone.

Acute Disease↗
PubMed1982

Prevention of reserpine rigidity by alpha-2 adrenergic antagonists.

Since alpha adrenergic antagonists are known to protect rats from the extrapyramidal effects of reserpine, the purpose of this study was to examine the relative contribution of alpha-2 receptors in modifying the reserpine-induced syndrome. Rats were pretreated with either clonidine, yohimbine, phentolamine, methysergide or SKF-7265. Thirty minutes later they were given reserpine (20 mg/kg) and evaluated using eleven categories of behavioral responses for three hours. Yohimbine, an alpha-2 antagonist, was the most effective agent in protecting against the reserpine effects. Phentolamine and SKF-7265, which block both alpha-1 and alpha-2 receptors, were also effective. Clonidine, an alpha-2 agonist, and methysergide a serotonin antagonist, were not. In all cases the alpha blocking drugs prevented the motor responses but did not alter the autonomic responses induced by reserpine. The results show not only the efficacy of alpha adrenergic antagonists in protecting against reserpine rigidity but more importantly that the blockade of alpha-2 receptors may be the functionally important action. These results are consistent with the view that some descending motor pathways are controlled by an adrenergic mechanism and suggest that alpha-2 receptors are an important component.

Adrenergic alpha-Antagonists↗
PubMed1982

Renal concentration defect following nonoliguric acute renal failure in the rat.

The mechanism of impaired renal concentrating ability following nonoliguric ischemic acute renal failure was studied in the rat. Fifty min of complete occlusion of the renal artery and vein with contralateral nephrectomy resulted in reversible, nonoliguric acute renal failure. Eight days following induction of acute renal failure, a defect in 30 hr dehydration urine osmolality was present when experimental animals were compared with uninephrectomized controls (1,425 +/- 166 versus 2,267 +/- 127 mOsm/kg water respectively, P less than 0.001). Comparable postdehydration plasma vasopressin levels in experimental and control animals and an impaired hydro-osmotic response to exogenous vasopressin in experimental animals documented a nephrogenic origin of the defect in urine concentration. Lower urinary excretion of prostaglandin E2 in experimental animals and a failure of cyclo-oxygenase inhibition with 10 mg/kg of indomethacin to improve dehydration urine osmolality suggested that prostaglandin E2 antagonism of vasopressin action did not contribute to the concentration defect. Postdehydration inner medullary (papillary) interstitial tonicity was significantly reduced in experimental animals versus controls (870 +/- 85 versus 1,499 +/- 87 mOsm/kg water respectively, P less than 0.001). To determine if this decreased interstitial tonicity was due to vascular mechanisms, papillary plasma flow was measured and found to be equivalent in experimental and control animals. To examine a role for biochemical factors in the renal concentration defect, cyclic nucleotide levels were measured in cytosol and membrane fragments. A decrease in vasopressin and sodium fluoride-stimulated adenylate cyclase was found in outer medullary tissue of experimental animals. In contrast, vasopressin-stimulated adenylate cyclase activity was comparable in the inner medullary tissue of control and experimental animals. Our study suggests a defect in generation of renal inner medullary interstitial solute as a mechanism of the impaired urinary concentration observed in this model of acute renal failure.

Acute Kidney Injury↗
PubMed1982

Role of alpha-2 adrenergic affinity in the action of a non-sedative antispasticity agent.

Muscle hypertonus of central origin can be effectively reversed by either dopamine agonists or alpha-adrenergic antagonists. Because of its efficacy in reversing reserpine rigidity (a syndrome resembling Parkinsonism), SKF-7265 was examined to determine whether its action was mediated through alpha-adrenergic or dopaminergic receptors. The pharmacologic blocking activity of SKF-7265 was assessed by measuring blockade of the cardiovascular agonist responses induced by norepinephrine, epinephrine, isoproterenol, acetylcholine and histamine. The binding affinity of SKF-7265 was determined by displacement of 3H-spiperone from rat corpus striatum tissue and 3H-clonidine and 3H-WB-4101 displacement from rat cerebral cortical tissue. Using the cardiovascular responses, SKF-7265 was devoid of beta-adrenergic or cholinergic blocking effects and did not produce any behavioral or reflex deficits in awake animals. Receptor binding studies showed that SKF-7265 had equal affinity for alpha-1 and alpha-2 adrenergic receptors and little affinity for dopamine receptors. It is concluded that the efficacy which has been reported for the SKF-7265 induced reversal of reserpine rigidity and its potential value as an antispasticity agent may be attributed to its relatively high affinity for alpha-2 adrenergic receptors.

Acridines↗
PubMed1982

Refractive errors in patients with fundus flavimaculatus.

A total of 59 patients (118 eyes) with fundus flavimaculatus who had atrophic macular lesions were examined for refractive error. Myopic refractions of greater than -0.1 dioptre were seen in 12% of a normal population and in 76% of our patient population. The spherical equivalent refractive errors described a single-peaked skewed distribution with a mean of -1.12 dioptres, which is 2.12 dioptres more myopic than that of a normal population. In addition astigmatic refractive errors of greater than +0.5 dioptres were found in 42% of this patient population, which is considerably more than the 18.6% observed in a normal population.

Adolescent↗
PubMed1982

Effects of DDAVP and AVP on sodium and water balance in conscious rat.

Many aspects of the physiological adaptation to chronic vasopressin and hypotonic fluid administration remain unclear. We therefore infused vasopressin [either 1-desamino-8-D-arginine vasopressin (DDAVP) at 0.112 ng/h or arginine vasopressin (AVP) at 2.4 mU/h] and hypotonic fluid (0.22% NaCl at 3.1 ml/h) into conscious unrestrained rats for 4-6 days. To determine if a decrease in the hydrosmotic effect of vasopressin occurred, urinary osmolality, flow rate, and free water reabsorption were measured sequentially in vasopressin-treated and control animals (receiving 0.22% NaCl alone). Progressive increases in urine flow and decreases in urine osmolality and free water reabsorption occurred in vasopressin-treated animals. This decreased hydrosmotic effect was noted with both DDAVP and AVP and could be dissociated from hormonal degradation and urinary prostaglandin E2 excretion. Sodium and water balance were measured to assess the determinants of the hypotonic state following chronic vasopressin and hypotonic fluid. In DDAVP-treated animals, sodium balance remained constant and hyponatremia resulted from water retention alone. In AVP-treated animals, a greater degree of hyponatremia was observed and resulted from combined positive water balance and negative sodium balance. The difference in sodium balance observed when DDAVP- and AVP-treated animals were compared could not be attributed to differences in either magnitude of water retention or filtered load of sodium.

Animals↗
PubMed1982

Water metabolism after cisplatin in the rat.

A polyuric state is often observed after cis-dichlorodiammine platinum (cisplatin). To study the mechanism of this polyuria we gave 5-6 mg/kg cisplatin to conscious rats and observed polydipsia and a polyuric form of mild acute renal failure. A defect in renal concentrating ability was observed 1 and 8 days after cisplatin. Animals demonstrated diminished postdehydration plasma vasopressin at 1 but not at 8 days after cisplatin, and exogenous vasopressin corrected the renal concentration defect at 1 but not at 8 days after cisplatin. To assess the role of polydipsia in the concentration defect, water intake in cisplatin-treated animals was matched to pair-fed controls. Prevention of polydipsia improved the polyuria but not the concentration defect seen 8 days after cisplatin. To assess intrarenal factors in the renal concentration defect, postdehydration interstitial solute was measured and was significantly lower in cisplatin-treated than in control animals. To determine whether the diminished interstitial solute was due to vascular mechanisms, inner medullary plasma flow was measured and was identical in cisplatin-treated and control rats. Treatment with cisplatin also resulted in decreased excretion of a water load. We conclude that either impaired synthesis or release of vasopressin is the cause of the impaired renal concentration seen 1 day after cisplatin. Eight days after cisplatin, the renal concentration defect is due in part to decreased interstitial tonicity.

Animals↗
PubMed1982

Role of renal nerves, angiotensin II, and prostaglandins in the antinatriuretic response to acute hypercapnic acidosis in the dog.

Although clinical studies suggest that chronic hypercapnic acidosis may be associated with renal sodium retention, little information is available on the effect of acute hypercapnic acidosis on renal sodium excretion. We, therefore, increased PCO2 from 23 to 74 mm Hg in anesthetized dogs and observed a marked antinatriuresis as absolute sodium excretion (235 to 60 muEq/min, P less than 0.001) and fractional excretion of sodium (4.0 to 1.2 %, P less than 0.02) decreased significantly. This decrease in sodium excretion occurred independent of consistent changes in renal perfusion pressure, PO2, glomerular filtration rate, renal blood flow, extraction of P-aminohippuric acid, and filtration fraction. The antinatriuretic response to acute hypercapnic acidosis could be attenuated significantly by surgical renal denervation, intrarenal phenoxybenzamine, and by intrarenal infusion of 1-sarcosine,8-glycine angiotensin II. Administration of 10 mg/kg indomethacin enhanced the antinatriuretic response to hypercapnic acidosis in denervated kidneys. These results suggest that renal alpha-adrenergic nerves and the renal angiotensin system result in an antinatriuretic effect during acute hypercapnic acidosis. Renal prostaglandins or related substances may serve to attenuate this antinatriuretic response.

Acidosis↗
PubMed1982

Alterations in nerve and muscle compound action potentials after acute acrylamide administration.

The early deficits of neurotoxicity induced by acrylamide were examined in rats by comparing nerve and muscle action potentials before and 24 hr after exposure to acrylamide (25, 50 or 100 mg/kg). No changes were seen in the nerve action potential amplitude or duration. The 25 mg/kg dose produced a more variable nerve conduction velocity. There was also a significant broadening of the muscle compound action potential. Neither of these effects were seen in the fasted controls. However, the lengthening of the relative refractory period of the muscle action potential was highly correlated with losses in body weight in the treatment groups and was identical to changes seen in control animals which were fasted for 24 hr. The slowed conduction of the muscle action potential may be a precursor of the nerve terminal damage which results from chronic exposure. Changes in the muscle refractory period, on the other hand, appear to be secondary to the loss in body weight which accompanies acrylamide administration.

Action Potentials↗
PubMed1982

Physician and pharmacy student expectations of pharmacy practice.

This study was initiated to examine the attitudes of some of the future health care providers, family practice residents, toward various ambulatory pharmacy services. Pharmacy students were then asked to predict what the resident attitudes would be and the results were compared. This project addressed the following questions: (i) What are the expectations of family practice residents of what today's pharmacists should be doing? and (ii) How accurately can pharmacy students judge what the responses of the residents will be? The survey results indicated that the family practice residents' perceptions of certain pharmacist behaviors rated significantly higher than how the pharmacy students thought they would respond. Such behaviors included: (i) maintain and review patient profiles; (ii) counsel patients; (iii) take medication/allergy histories; (iv) provide therapeutic information to physicians; and (v) stock a wide variety of generic drugs. Most of these behaviors reflect direct involvement of the pharmacist in disseminating information to the patient and/or physician. Other expanded roles of the pharmacist such as triage, refill determination, reimbursement for consultation services, and chronic care management were given low priority.

Attitude of Health Personnel↗