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A L Linton

Publications and source records attributed to A L Linton.

At least 19 recordsLinked to original sources
PubMed1990

Guidelines for medical practice: 2. A possible strategy.

The recognition that much current medical practice is based on incomplete scientific evidence has led to calls for the generation of guidelines for optimal patterns of practice. These guidelines must be developed from a synthesis of existing scientific data ideally obtained from randomized clinical trials. However, at present we may have to rely on less satisfactory data and the views of experts in the field. The primary purpose of these initiatives must be to improve patient care. The Ontario Medical Association has made recommendations on how such guidelines should be produced, and in a recent survey a substantial majority of family physicians supported them. There is general agreement that the coordinating body should be independent of government and other interested parties. In addition, the medical profession must have the primary role, and a number of medical organizations should also be represented. We propose a possible structure for a group charged with developing guidelines for medical practice at a provincial level and on an experimental basis. Recommendations are made on its membership, function and relationship with other organizations. The identification and diffusion of justifiable, scientific practice patterns will help reduce waste of scarce resources, maintain the role of the profession as guardian of the quality of care and ultimately benefit the patient.

Canada↗
PubMed1990

Guidelines for medical practice: 1. The reasons why.

Various external special interest groups are promoting attempts to better measure and control the performance of the medical profession, primarily to restrain costs. We can neither afford to ignore the rising costs nor reject efforts by provincial licensing authorities to improve supervision of the quality of care. Furthermore, there is increasing public interest in the outcome of medical treatment and a suspicion that some care may be unnecessary or inappropriate. Much of what physicians do is not based on impeccable or complete scientific evidence, and we have not established a method whereby science can consistently be translated into practice. Optimal practice patterns must be defined to improve the quality of care and to maximize the efficiency with which scarce resources are used. Careful scientific evaluation of data is particularly necessary with the arrival of new drugs and technology. Sensible, flexible guidelines produced by appropriate panels will help promote improved practice. Rigid standards must be avoided to allow for individual consideration and scientific innovation. The recognized difficulties of influencing clinical practice by precept or education and the problems imposed by rapidly changing scientific knowledge are two hurdles to be overcome. Licensing bodies must identify and enforce minimal standards, but optimal practice patterns are better devised by a broader segment of the profession. Intervention by third-party payers, as is prevalent in the United States, intrudes upon physician autonomy and reduces access to care. Physicians must support the development of guidelines for optimal medical practice based on the best existing data and focused on improving the quality of care.

Canada↗
PubMed1989

The protective effect of thromboxane synthetase inhibition on renal function in systemic sepsis.

To study the role of thromboxane in systemic sepsis and renal failure, peritonitis was induced surgically in 22 sheep, leading to local and systemic sepsis. A selective thromboxane synthetase inhibitor, U63,557A (Upjohn Co, Kalamazoo, MI) was given before surgery in five animals and 30 minutes after surgery in five animals. A typical picture of volume-loaded, normotensive, vasodilated septic shock developed in all animals. Twenty four hours after induction of sepsis, the control group showed a marked reduction in glomerular filtration rate (GFR), urine volume, and urinary sodium excretion. Pretreated animals showed no change in GFR and a smaller reduction in urine volume and sodium excretion. The posttreatment group showed no change in any parameters of renal function. Plasma renin activity, urinary TXB2 excretion, and urinary 6-keto PGF1 alpha excretion increased after 24 hours only in the control group. Urinary TXB2 excretion was reduced by 80% in animals given U63,557A before surgery. The results indicate a significant protective effect of U63,557A on renal function during septic shock, probably related to reduced thromboxane synthesis, with no apparent deleterious systemic effects. The results support a role for thromboxane in the pathogenesis of acute renal failure in systemic sepsis.

Animals↗
PubMed1988

Vasoactive hormones in the renal response to systemic sepsis.

The pathophysiology of renal dysfunction in generalized sepsis remains unknown. In this study, 24 hours after surgical induction of peritonitis in 20 volume-loaded sheep, three patterns of renal function were seen. In group 1 (n = 8), glomerular filtration rate (GFR) decreased by 70%, urine volume by 85%, absolute sodium excretion by 95%, and fractional sodium excretion by 83%. Group 2 (n = 4) exhibited similar sodium retention but GFR did not fall. Group 3 (n = 8) showed no change in GFR or urine volume and only minimally reduced sodium excretion. Mean arterial pressure fell 17% in group 1 only; central venous pressure, pulmonary capillary wedge pressure, and plasma volume were maintained at or above presepsis values in all groups. Cardiac index was either increased or unchanged, and renal plasma flow was maintained in all groups; there was thus no hemodynamic evidence to suggest volume contraction. Histologic examination showed only minor changes with no consistent pattern. Renal functional changes correlated with other manifestations of severe sepsis--GFR and sodium retention correlated significantly with increased cardiac index, decreased systemic vascular resistance, pulmonary arterial hypertension, leukopenia, hypoproteinemia, and hypoglycemia. All of these changes were most marked in group 1. In groups 1 and 2, plasma renin activity (PRA) increased and urinary kallikrein excretion decreased. PRA correlated inversely with GFR, urine volume, and sodium excretion; urinary kallikrein excretion correlated positively with urine volume and sodium excretion. Urinary excretion of 6-keto-PGF1 alpha was increased in groups 1 and 2 and correlated inversely with mean arterial pressure in group 1 animals. During sepsis, urinary thromboxane B2 excretion continued at presepsis values in all groups. The results suggest that unusual reciprocal changes in activity of the renin-angiotensin and renal kallikrein-kinin systems may play a role in the renal response to sepsis. PGI2 synthesis is increased and may affect systemic hemodynamics and renal function; the role of thromboxane A2 in this context is unknown.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Association between renal and sympathetic responses to nonhypotensive systemic sepsis.

We investigated the association between plasma catecholamines and the renal response to nonhypotensive sepsis. Arterial plasma catecholamines were measured in 16 sheep, before and 24 h after surgical induction of peritonitis. Animals were volume loaded with lactated Ringer's solution (8 L/24 h) before and after surgery; non became hypotensive. For analysis, animals were retrospectively divided into those with increased serum creatinine after 24 h of sepsis (group 1, n = 8) and those without (group 2, n = 8). Group 1 showed increased cardiac index and decreased systemic vascular resistance typical of severe sepsis, with decreased glomerular filtration rate (GFR), oliguria, sodium retention, increased plasma renin activity (PRA), decreased urinary kallikrein excretion, and increased urinary 6-keto-prostaglandin-F1 alpha excretion. Group 2 showed insignificant hemodynamic disturbance, and no significant renal response. Plasma catecholamines were equal in both groups at baseline. In group 1, there were uniform increases after 24 h in plasma norepinephrine (474 +/- 115 to 1183 +/- 158 [SEM] pg/ml; p less than .01) and plasma epinephrine (108 +/- 8 to 309 +/- 70 pg/ml; p less than .05). In group 2, neither plasma norepinephrine (343 +/- 59 to 330 +/- 56 pg/ml) nor plasma epinephrine (116 +/- 16 to 116 +/- 13 pg/ml) changed significantly. Plasma norepinephrine correlated inversely with GFR; plasma epinephrine correlated with PRA. The sympathetic nervous system may be involved in the renal response to nonhypotensive sepsis, both directly and via effects on other vasoactive hormone systems.

Acute Kidney Injury↗
PubMed1988

Nephrotoxicity of high- and low-osmolality contrast media.

Nephrotoxicity of radio-opaque contrast media (CM) is generally believed to involve toxic injury of proximal tubular cells. Measurement of urinary tubular enzyme excretion has been advocated as a sensitive marker of such toxic injury. It has been claimed that the new low-osmolality or nonionic CM reduce the incidence of nephrotoxicity but this remains uncertain. We studied 23 patients with normal renal function undergoing coronary angiography; patients were randomized into three groups receiving either diatrizoate (1,800 mmol/kg H2O), ioxaglate (600 mmol/kg H2O) or iohexol (850 mmol/kg H2O). Urinary excretion of a panel of enzymes increased significantly in all groups by 20 h (p less than 0.05 to less than 0.005). Alanine aminopeptidase excretion at 20 h was greater after the administration of high osmolality ionic CM than with the others but all three CM produced a similar pattern of enzyme excretion. No significant change in glomerular filtration rate was found in any group so the significance of the enzymuria remains uncertain.

Adult↗
PubMed1987

Acute effect of a thromboxane synthetase inhibitor on renal function in unanaesthetized sheep.

1. Eleven healthy, unanaesthetized sheep were given either a single intravenous bolus infusion of U63,577A (Upjohn), a selective thromboxane synthetase inhibitor, at a dose of 30 mg/kg (group 1, n = 6), or vehicle alone (group 2, n = 5). Animals were maintained in metabolic cages during the study, and received 150 ml of water/h and 7.5 mmol of sodium/h as Ringers lactate by intravenous infusion for 24 h before and during the study. During two 1 h control urine collections via bladder catheter, urine volume and sodium excretion closely paralleled these infusion rates. 2. In the first hour after injection of U63,577A, there were significant two- to three-fold increases in urine volume, urinary sodium excretion and fractional sodium excretion, compared with the control collections. During the subsequent 4 h, urine volume, urinary sodium excretion, and fractional sodium excretion fell to values significantly lower than in the control period. Creatinine clearance was reduced 1, 2 and 4 h post injection and returned to control values at 5 h. Urinary excretion of thromboxane B2 was significantly reduced compared with control values during the 5 h after injection of U63,577A. Excretion of 6-keto-prostaglandin F1 alpha did not change. Plasma renin activity was significantly increased 1, 3 and 5 h after injection of U63,577A. Vehicle controls showed no change in any of the above parameters. 3. The results indicate that in healthy conscious sheep, sodium and water replete, U63,577A has a transient but significant diuretic and natriuretic effect, followed by sodium and water retention and increased plasma renin activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

AG-ARF.

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Acute Kidney Injury↗