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Biomedical subjects

P F Rogers

Publications and source records attributed to P F Rogers.

At least 19 recordsLinked to original sources
PubMed2001

Ntau-methylhistidine excretion is a valid index of myofibrillar protein breakdown in the guineapig (Cavia porcellus).

The recovery of radioactivity in the urine of guineapigs following a bolus intravenous dose of chromatographically pure 14C-Ntau-methylhistidine was measured in order to test whether the excretion of Ntau-methylhistidine (Ntau-MH) is a valid index of myofibrillar protein breakdown in these animals. Four male and four female guineapigs were dosed and after 7 days, 91.65+/-2.82% and 3.58+/-0.91% of injected radioactivity was recovered in the excreta and tissues, respectively. The average total recovery of 95.2+/-3.0% was not significantly different from 100%. Male guineapigs excreted the radioactivity more slowly than females (70% of the dose excreted within 74 h vs 39 h, respectively) but cumulative excretion at 7 days was the same for each sex. Chromatographic analysis of the urine showed almost all of the radioactivity to be associated with a single peak corresponding to Ntau-MH, indicating a lack of significant metabolism. These data show that although the clearance of 14C-Ntau-MH is slower than in rats or humans the urinary excretion of Ntau-MH is a valid index for myofibrillar protein degradation in the guineapig.

Actins↗
PubMed1993

Combined effects of dietary fish oil and sodium restriction on blood pressure in enalapril-treated hypertensive rats.

Sodium restriction and fish oil supplementation are effective dietary measures for preventing or treating mild hypertension. However, their usefulness as an adjunct to drug treatment of hypertension requires further evaluation. In the present study, we examined the influence of dietary sodium and fish oil on the antihypertensive effect of the angiotensin converting enzyme (ACE) inhibitor enalapril in stroke-prone spontaneously hypertensive rats (SHRSP). Rats were fed experimental diets containing fish oil or olive oil (5% w/w) and low (0.04% w/w) or normal (0.23% w/w) sodium from 1 to 4 months of age. Tail-cuff blood pressure (BP) rose by 8.4 and 4.3 mm Hg/week, respectively, in untreated and enalapril-treated (2.5 mg/kg/day, orally) rats fed the olive oil/normal sodium diet. Feeding fish oil further reduced the rise in enalapril-treated rats to 2.8 mm Hg/week. When sodium intake was also restricted, the BP rise was almost prevented (1.1 mm Hg/week). In older rats with established hypertension, the low sodium/fish oil diet also potentiated the blood pressure reduction by enalapril (tail-cuff BP fell by 61 mm Hg compared to 25 mm Hg with enalapril alone). These observations were confirmed by direct BP recording in conscious rats following the implantation of aortic catheters. Factorial analysis revealed a highly significant antihypertensive effect of fish oil in both young and adult SHRSP receiving enalapril, and a further interactive effect of dietary sodium restriction with fish oil feeding in young rats. The antihypertensive effects of the dietary interventions were associated with further reductions of cardiac hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Chronic central administration of enalaprilat lowers blood pressure in stroke-prone spontaneously hypertensive rats.

Earlier studies on the cardiovascular effects of intracerebroventricular (i.c.v.) administration of angiotensin converting enzyme (ACE) inhibitors implicate angiotensin II (AII) present in the central nervous system in the pathogenesis of hypertension. We have now examined whether central AII contributes to the maintenance of established hypertension in adult stroke-prone spontaneously hypertensive rats (SHRSP). The ACE inhibitor, enalaprilat, was infused i.c.v. for two weeks at a rate of 5 micrograms/h via osmotic minipumps. Control rats were either untreated or infused with saline. Mean arterial pressure (MAP), measured via an indwelling catheter, fell within 24 h in the enalaprilat-treated rats and remained at least 30 mmHg lower than in controls. This difference persisted after intravenous (i.v.) administration of a vasopressin (AVP) antagonist but was eliminated by subsequent ganglion blockade with i.v. pentolinium. Without prior administration of the AVP antagonist, however, the reductions of MAP after pentolinium were smaller. The reduction was still attenuated in treated rats compared with controls but there was a significant difference in the residual MAP. Circulating catecholamine levels were reduced by central ACE inhibition. However, pressor responsiveness to i.v. phenylephrine was unaffected. The results suggest that, in SHRSP, central ACE inhibition lowers blood pressure by reducing sympathetic outflow, implying that central AII has a tonic sympathoexcitatory effect in this strain.

Animals↗
PubMed1991

Effects of depleting central and peripheral adrenaline stores on blood pressure in stroke-prone spontaneously hypertensive rats.

The potential role of adrenaline, both circulating and in the central nervous system, in the maintenance of high blood pressure was examined in stroke-prone spontaneously hypertensive rats (SHRSP). alpha-Monofluoromethyldopa, a long-lasting inhibitor of dopa decarboxylase, was used to induce rapid depletion of central and peripheral catecholamine stores. Subsequent inhibition of phenylethanolamine-N-methyltransferase (PNMT) allowed the gradual restoration of dopamine and noradrenaline but not adrenaline, resulting in a greater relative depletion of adrenaline. Adrenaline was almost totally depleted in the circulation and peripheral tissues. The resting level of blood pressure, however, was unaffected, excepting after administration of a vasopressin (AVP) antagonist. Moreover, there was no reduction in the magnitude of acute pressor responses to electrical stimulation of the rostral ventrolateral medulla oblongata (C1 area), despite extensive loss of adrenaline from the brainstem and spinal cord. The results suggest that adrenaline contributes to the resting level of blood pressure but that its loss can be offset by the pressor activity of AVP. Thus neither central nor peripheral adrenaline stores appear to be essential for the maintenance of hypertension or for centrally-evoked vasoconstriction in adult SHRSP.

Analysis of Variance↗
PubMed1991

Blood pressure reduction by fish oil in adult rats with established hypertension--dependence on sodium intake.

The effects of fish oil combined with dietary sodium restriction on blood pressure and mesenteric vascular resistance were examined in a series of experiments with adult normotensive (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). Rats were fed normal or low sodium diets containing fish oil, olive oil or safflower oil. Small but significant reductions of blood pressure (measured directly in conscious rats) were seen in SHRSP but not in WKY after 8 weeks on a fish oil/low sodium diet, compared with rats fed olive or safflower oil diets with normal sodium content. This antihypertensive effect was not dependent on neurally mediated vasoconstriction but was associated with a reduction of basal resistance in the blood-perfused mesenteric artery. Subcutaneous injection of fish oil reduced blood pressure in adult SHRSP on a normal sodium diet. However, there was a further fall in blood pressure when sodium intake was reduced. The results indicate the antihypertensive effect of fish oil can be enhanced by restricting sodium intake.

Animals↗
PubMed1991

Effects of dietary sodium and fish oil on blood pressure development in stroke-prone spontaneously hypertensive rats.

The postulated antihypertensive effect of dietary fish oil and the influence of dietary sodium on this effect were evaluated in young stroke-prone spontaneously hypertensive rats (SHRSP) by direct intra-arterial measurement of blood pressure. Weaning rats were fed synthetic diets containing olive oil or eicosapentaenoic acid-enriched fish oil (5% of dry weight) with normal (0.23%) or high (2.8%) sodium content. Catheters were implanted after 3 months for blood pressure measurement under resting conditions and to sample blood for catecholamine determinations. Effects of fish oil on vascular reactivity were assessed in the in situ blood-perfused mesentery. The overall observation, from a series of experiments, was that feeding diets containing 5% fish oil to young SHRSP resulted in a small but consistent suppression of the development of hypertension. This effect could be counteracted, however, by increasing dietary sodium intake. Observations after ganglion blockade indicate that the antihypertensive effect of fish oil is unlikely to result from a reduction in sympathetic vascular tone.

Animals↗
PubMed1990

Dietary sodium loading elevates blood pressure in baroreceptor denervated rats.

We have examined the possibility that defective baroreflex function may contribute to the hypertensive effect of a high dietary sodium intake. In a preliminary study we found that, after interrupting the baroreflex by sino-aortic denervation (SAD), feeding a high-sodium diet to normotensive Wistar/Kyoto rats (WKY) caused their tail-cuff blood pressure to rise to hypertensive levels. In the present study, SAD and sham-operated WKY were fed diets with either a low or a high sodium content. An increase in the sensitivity of blood pressure to sodium after baroreceptor denervation was confirmed by direct measurement of mean arterial pressure (MAP) in conscious rats via indwelling aortic catheters. After 8 weeks the MAP in SAD rats on the high sodium diet was 35 mm Hg higher than in SAD rats on the low sodium diet. Ganglion blockade reduced MAP to a similar level in all treatment groups, but pressor responses to phenylephrine were greater in SAD rats on the high sodium diet, suggesting that the hypertensive effect of sodium in this group might have been due to increased sympathetic vasoconstriction.

Animals↗
PubMed1989

Limited baroreflex control of heart rate in young stroke-prone spontaneously hypertensive rats.

Controversy regarding possible differences of baroreflex gain in spontaneously hypertensive rats (SHR) and their relationship to the rise in blood pressure may be due in part to variations in the methods used to assess baroreflex function. In this study, we have compared the baroreflex control of heart rate in normotensive (Wistar-Kyoto, WKY) and stroke-prone spontaneously hypertensive (SHRSP) rats at 1 and at 7 months of age. Mean arterial pressure and heart rate were monitored in conscious rats following implantation of arterial and venous catheters. Phenylephrine and nitroprusside were given intravenously and the peak responses of mean arterial pressure and heart rate were recorded. In the young rats, these recordings were repeated under anaesthesia. Individual slopes for responses to phenylephrine or nitroprusside were obtained by linear regression. A single relationship covering both sets of responses was also obtained by fitting the data to a sigmoidal curve. The latter approach enabled the baroreflex to be represented as a single function which has a single determinant of gain, operates within defined limits and can be readily related to resting mean arterial pressure and heart rate. This approach demonstrated that: (1) in adult SHRSP, the baroreflex had reset to operate at higher resting levels of mean arterial pressure; (2) the range of heart rate control was smaller in both young and adult SHRSP compared with WKY; (3) average gain was slightly, but not significantly lower in adult SHRSP; (4) anaesthesia reduced heart rate range and average gain in both strains of rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1989

Effects of chronic alcohol consumption and alcohol withdrawal on blood pressure in stroke-prone spontaneously hypertensive rats.

The development of blood pressure was monitored by the tail-cuff method in normotensive (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) receiving ethanol (alcohol) in drinking water from weaning (approximately 1 month of age). Alcohol administration over a 3-month period attenuated the development of hypertension in SHRSP and also caused a small reduction of the initial blood pressure rise in WKY. This was accompanied by a reduction of fluid intake and an increase of circulating antidiuretic hormone (arginine vasopressin; AVP). Circulatory volume remained constant. Direct measurement of arterial blood pressure in conscious rats before and after autonomic blockade confirmed the antihypertensive effect of alcohol in SHRSP and indicated that it is at least partly dependent on altered activity of neural mechanisms. Sudden withdrawal of alcohol caused an immediate increase of fluid intake followed by a rise of blood pressure lasting several days in both WKY and SHRSP. This withdrawal hypertension could not be attributed to changes in plasma catecholamines or AVP.

Animals↗
PubMed1989

Antihypertensive effect of alcohol in spontaneously hypertensive rats.

The influence of ethanol (alcohol) consumption on blood pressure during and after the development of hypertension was examined by using spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP). Normotensive Wistar-Kyoto (WKY) rats were also used for comparison. Substituting alcohol (5-20%) for drinking water at 1 month of age retarded the age-dependent rise of blood pressure in all three strains so that, at 7 months, blood pressure measured by a tail-cuff method was 24 mm Hg, 26 mm Hg, and 41 mm Hg lower in the alcohol-treated WKY rats, SHR, and SHRSP, respectively, than in untreated rats. Significant differences in blood pressure were seen in each strain after only 3 months. Withdrawal of alcohol at this stage caused an acute rise of blood pressure then a return to subnormal levels, which persisted for a further 3 months. Administration of 15% alcohol to adult WKY rats and SHR for 2 months had no significant effect on blood pressure. Increasing alcohol content to 20% for a further 2 months prevented rises of blood pressure in both strains. Thus, although continuous drinking of alcohol does not lower blood pressure, it appears to counteract the development of hypertension in rats.

Aging↗
PubMed1989

The demand and intensity of home health services following prospective payment.

The purpose of this study was to determine if there was an increase in both the number and the intensity of home health referrals following the implementation of the Medicare Prospective Payment System (PPS). The study involved a retrospective review of one home health agency's activity logs and client records from a six-month period before the implementation of the PPS and a six-month period after the implementation of the PPS. Data gathered revealed a 22 percent increase in the number of referrals after the implementation of the PPS, as well as statistically significant increases in several of the intensity indicators used in this study.

Aged↗
PubMed1988

Pressor responsiveness of the sub-retrofacial nucleus and the midbrain reticular formation in the rat after 6-hydroxydopamine-induced lesions of ascending and descending catecholamine pathways.

We have recently shown that intracerebroventricular (icvt) administration of 6-hydroxydopamine (6-OHDA) inhibits centrally-evoked pressor activity. To see whether this effect is attributable to the disruption of descending bulbospinal or, alternatively, ascending suprabulbar catecholamine (CA) pathways, spontaneously hypertensive rats (SHR) were given localized intracerebral injections of 6-OHDA. One month later, pressor responses evoked by electrical or chemical stimulation in the rostral ventrolateral medulla or midbrain were examined under urethane anaesthesia. Injections of 6-OHDA into the medial forebrain bundle, which depleted noradrenaline and adrenaline in the hypothalamus, lowered basal blood pressure but potentiated the pressor responses to stimulation. In contrast, intraspinal injection of 6-OHDA raised basal blood pressure and attenuated pressor responses. This was accompanied by a partial depletion of adrenaline and the almost complete disappearance of noradrenaline in the spinal cord. Thus, the attenuation of pressor responses observed previously following icvt 6-OHDA can be attributed to an effect on spinal CA pathways. The effects on basal blood pressure suggest that, in SHR, ascending CA pathways are tonically pressor, while spinal CA pathways are depressor. Whilst it is unlikely, therefore, that spinal CAs mediate vasomotor outflow, the altered responses to stimulation after 6-OHDA suggest that central CA pathways can modulate the sensitivity of vasomotor neurones.

Animals↗
PubMed1987

Haemophilus influenzae type b vaccine: use in the pediatric population.

To assess the use of the Haemophilus influenzae type b vaccine and the attitudes of health professionals regarding its use in the pediatric population, we conducted a study of community clinics, health department clinics, university-based teaching clinics, and private practice groups in the state of Texas. Whereas 59.6% of the private practice groups and 57.1% of the university-based teaching clinics administered the vaccine to more than 75% of their eligible children, 72.7% of community clinics and 81.7% of health department clinics never administered the vaccine to their eligible children. Likewise, whereas 100% of the university-based teaching clinics and 95.7% of the private practice groups had the vaccine available to their patients, only 22.7% of the community clinics and 15.5% of the health department clinics did so. The two most common reasons given by health professionals concerning the nonuse of the vaccine were nonavailability and high cost of the vaccine. Our findings suggest that a large segment of eligible children do not have access to this important vaccine and that children who depend on community and health department clinics for their routine health care are particularly affected in this regard. Strategies identified to increase the use of the vaccine include providing vaccine free of charge, increasing patient awareness of the vaccine benefits, and passing mandatory state laws requiring vaccine administration before day-care enrollment.

Attitude of Health Personnel↗
PubMed1986

Effects of short-term modification of dietary sodium intake on plasma catecholamines and blood pressure in prehypertensive children.

The influence of dietary sodium intake on plasma catecholamines was examined as part of a dietary intervention study in 21 prehypertensive school children. Diastolic blood pressure was significantly elevated in girls after 3 weeks on a high sodium diet compared with a low sodium diet. Plasma adrenaline levels were raised slightly by the high sodium intake but plasma noradrenaline was significantly reduced. Increases of plasma catecholamines in response to standing or cold stress were unaffected by changes in sodium intake. The results indicate that the pressor effect of dietary sodium in children is not attributable to increased sympathetic nerve activity.

Adolescent↗
PubMed1985

Influence of dietary sodium on blood pressure in baroreceptor-denervated rats.

One possible explanation for the salt sensitivity of blood pressure (BP) in certain hypertensive individuals is that neural mechanisms which normally counteract the pressor effect of a high dietary sodium intake are defective. We have tested this possibility in normotensive Wistar-Kyoto rats (WKY) by surgically ablating the arterial baroreflex mechanism. This manoeuvre, by itself, conferred substantial salt-sensitivity on the WKY rats whose BP is normally relatively insensitive to dietary sodium intake. The treated rats responded to a high sodium diet with a significant rise in systolic BP which was reversed by substituting a low sodium diet. Thus, impaired baroreflex function which has been observed in essential hypertension and in hypertensive animals, may be responsible for the hypertensive effect of sodium.

Animals↗
PubMed1984

Visualisation of catecholamine-fluorescent nerve cell bodies in the rat brain after colchicine treatment.

Central administration of colchicine causes accumulation of catecholamines in nerve cell bodies and enhances their visualisation in the rat brain by the formaldehyde-glutaraldehyde (FAGLU) histofluorescence method. The detection of catecholamine-containing nerve cells by the FAGLU method was considerably improved in rats pretreated with colchicine, and adrenaline-synthesising nerve cells, which are not normally detected by the FAGLU method, could be readily localized after colchicine. The identity of the FAGLU-fluorescent nerve cells was confirmed by simultaneous immunofluorescent detection of catecholamine-synthesising enzymes in sections of the medulla oblongata. The FAGLU method applied to colchicine-treated animals could provide a simple means of detecting central adrenaline nerve cells in other species.

Animals↗
PubMed1983

A biochemical and immunohistochemical study of central serotonin nerves in rats with chronic thiamine deficiency.

An immunohistochemical and neurochemical investigation of central serotonin (5-HT) nerves was made in rats deprived of dietary thiamine at various stages of development. The classical symptoms of severe thiamine deficiency were produced in adult rats which had been maintained on a synthetic thiamine-free diet for 5-8 weeks and in young rats reared from birth to weaning by thiamine-deficient mothers. Offspring of rats which had been thiamine-deficient throughout pregnancy were also studied; there were no visible symptoms of thiamine deficiency in these rats after weaning. The number and distribution of 5-HT nerve cell bodies in the brainstem were compared in control and thiamine-deficient rats after visualizing the cells by immunofluorescence of endogenous 5-HT. 5-HT nerve terminals and axons were also compared in normal and deficient rats by immunofluorescence after loading with 5,7-dihydroxytryptamine. The immunohistochemical examination showed that central 5-HT nerves were not affected in any of the groups of thiamine-deficient rats studied. This was confirmed by measurements of tryptophan hydroxylase activity and 5-HT concentration in several brain regions. These results do not support earlier reports of a selective impairment of central 5-HT nerves in chronic diet-induced thiamine deficiency.

Aging↗