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Biomedical subjects

F MacPherson

Publications and source records attributed to F MacPherson.

7 recordsLinked to original sources
PubMed1998

Future financial neonatal shock.

In a changing economic climate, the neonatologist must be aware of all of the forces that can affect the practice of neonatology. In addition to clinical issues, billing and reimbursement must take into account physician work and common procedural terminology (CPT) codes, which accurately describe the medical services and procedures delivered. An understanding of this coding and resource-based work unit system is necessary to prevent financial loss. The influence of managed care, capitation, fixed per-case reimbursement, practice guidelines and care maps have already seriously affected clinical practice patterns. The neonatologist must be proactive in negotiating contracts using historic information and outcome data to define and defend the quality of care provided.

Abstracting and Indexing↗
PubMed1993

Comparison of eating disorders and other dietary/weight groups on measures of perceived control, assertiveness, self-esteem, and self-directed hostility.

Anorexic and bulimic patients were compared to obese dieters, nonobese dieters, and normal controls on measures of perceived control, assertiveness, self-esteem, self-directed hostility, and psychiatric caseness. The anorexic and bulimic groups both scored significantly differently in the expected direction from the other three groups on all measures. There were no significant differences between the anorexic and bulimic groups and in turn, no significant differences among the obese, nonobese dieters, and normal controls. Results are in keeping with the notion that perceived control, low assertiveness, low self-esteem, and self-directed hostility are characteristics of eating disorder patients that differentiate them from individuals who display dietary/weight features, as well as from normal controls.

Adult↗
PubMed1991

Angiotensin II causes vascular hypertrophy in part by a non-pressor mechanism.

Angiotensin II, when given in low doses, raises blood pressure slowly. When tested in vitro on vascular smooth muscle cells, it has mitogenic and trophic effects; it is not known if it has these effects in vivo. Our purpose was to determine whether vascular hypertrophy develops during slow pressor infusion of angiotensin II and, if so, whether it is pressure induced. Three experiments were done in rats infused subcutaneously with angiotensin II (200 ng/kg/min) by minipump for 10-12 days. Experiment 1: Angiotensin II gradually raised systolic blood pressure (measured in the tail) from 143 +/- 2 to 208 +/- 8 mm Hg (mean +/- SEM), significantly suppressing plasma renin and increasing threefold (NS) plasma angiotensin II. There was no loss of peptide in the pump infusate when tested at the end of the experiment. Experiment 2: In the perfused mesenteric circulation, vasoconstrictor responses to norepinephrine, vasopressin, and KCl were enhanced in rats given a slow pressor infusion of angiotensin II, but sensitivity of responses was not altered. This combination of changes suggests that vascular hypertrophy develops during slow pressor infusion of angiotensin II. Experiment 3: Vessel myography was done after angiotensin II infusion with and without a pressor response. Angiotensin II raised systolic blood pressure, increased heart weight, and produced myographic changes of vascular hypertrophy in the mesenteric circulation, increasing media width, media cross-sectional area, and media/lumen ratio. Hydralazine given with angiotensin II prevented the rise of pressure and the cardiac effect but not the vascular changes. Two-way analysis of variance showed that angiotensin II significantly increased media width, media cross-sectional area, and media/lumen ratio, all independent of hydralazine. Thus, although hydralazine inhibits the pressor and cardiac effects of angiotensin II, suggesting a pressor mechanism for the cardiac change, it does not inhibit structural vascular change, which suggests that at least part of the effect has a non-pressor mechanism.

Angiotensin II↗
PubMed1991

Structural changes during the early onset of experimental hypertension: trophic influences of the renin-angiotensin system.

All forms of established hypertension are characterised by hypertrophy of the heart and blood vessels. Although these structural alterations are a normal adaptation to raised blood pressure, it has been suggested that hypertrophy may develop by a mechanism independent of pressure. Some investigators claim that in the young spontaneously hypertensive rat, hypertrophy of the blood vessels and heart is present at a time before the rise in pressure. Evidence also exists to support the role of angiotensin II in directly influencing growth within the vasculature. The present study confirms that hypertrophy of the mesenteric resistance vessels is present in the 3-week old spontaneously hypertensive rat. However, enhanced vascular structure was also associated with a higher mean arterial blood pressure. No increase in activity of the renin-angiotensin system could be detected. These observations raise doubts as to whether hypertrophy of the blood vessels can develop independently of raised pressure.

Animals↗
PubMed1990

Vascular hypertrophy, renin and blood pressure in the young spontaneously hypertensive rat.

1. Cardiovascular reactivity, blood vessel morphology, blood pressure and the activity of the renin-angiotensin system were determined in the 3-week-old spontaneously hypertensive (SHR), Wistar-Kyoto (WKY) and outbred Wistar (WIS) rat. 2. In an isolated perfused mesenteric artery preparation the SHR had a significantly increased maximum response to KCl and noradrenaline (P less than 0.02) compared with the WKY. Using a myograph, vascular structure was measured over a range of resistance arteries and showed a significant correlation between lumen diameter and both media cross-sectional area and thickness, with the regression line for the SHR shifted upwards indicating both increased media area and thickness. This was associated with a slight, but significant, narrowing of the lumen (P less than 0.01) and an increased media/lumen ratio (0.049 +/- 0.01, 0.034 +/- 0.007, 0.036 +/- 0.008 for SHR, WKY and WIS, respectively, means +/- SD P less than 0.001). The SHR had a greater heart/body weight ratio than either the WKY or the WIS (P less than 0.001). 3. Both mesenteric artery and membrane protein content were higher in the SHR, indicating an increase in cell size or number. 4. Plasma renin activity (means +/- SD) was lower in the SHR (1.0 +/- 0.7 pmol of angiotensin I h-1 ml-1) than in the WKY (2.2 +/- 1.2 pmol of angiotensin I h-1 ml-1, P less than 0.001) but not different from that in the WIS (1.2 +/- 0.8 pmol of angiotensin I h-1 ml-1). Mesenteric artery vascular renin concentration was also lower in the SHR (P = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMedDate not supplied

Angiotensin II receptor antagonist losartan has persistent effects on blood pressure in the young spontaneously hypertensive rat: lack of relation to vascular structure.

The persistent effects on blood pressure of the angiotensin II receptor antagonist losartan and the converting enzyme inhibitor captopril were compared in the young spontaneously hypertensive rat (SHR). Losartan (DuP753/MK954, 15 mg/kg/day) and captopril (100 mg/kg/day) were given in the drinking water of 3-week-old SHRs for 4- and 10-week durations. Blood pressure was measured during treatment and after treatment was stopped until the age of 30 weeks. Both losartan and captopril given for 4 and 10 weeks prevented the development of hypertension during treatment and redevelopment of hypertension after treatment was stopped. Treatment for 10 weeks was more effective than for 4 weeks in lowering long-term pressure. Four weeks of treatment did not affect the mesenteric resistance artery media/lumen (m1/l1) ratio. In contrast, both losartan and captopril given for 10 weeks resulted in large and significant reductions in m1/l1 [5.3 +/- 0.8 and 5.63 +/- 0.8 vs 7.7 +/- 0.8 x 10(-2) (SD), p less than 0.001]. In losartan-treated rats, plasma renin and angiotensin II concentration were increased between 4- and 7-fold at the end of both treatment periods. These findings show losartan to be an effective antihypertensive agent and support data implicating angiotensin II in the early events leading to hypertension in this model. The abilities of losartan and captopril to affect blood pressure without affecting vascular structure suggest that the latter is a poor predictor of long-term hypertensive levels in the SHR.

Aging↗