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Biomedical subjects

P Harris

Publications and source records attributed to P Harris.

At least 145 records · Page 8Linked to original sources
PubMed1992

Plasma potassium and lactate concentrations in thoroughbred horses during exercise of varying intensity.

To investigate the effect of moderate to high intensity exercise of up to 6 min duration on plasma potassium and lactate concentrations, 6 Thoroughbred horses were studied using a treadmill at a 5 degree incline. Each test consisted of an 8-min standardised warm-up followed by an exercise bout at 8, 9, 10 or 12 m/sec. The horses were galloped at each speed for up to a maximum of 6 min or until signs of fatigue were present. The horses were then walked at 0 degree incline. Carotid arterial blood samples were taken during and after the exercise. At 8, 9 and 10 m/sec there was a general pattern of an initial rise in potassium to a peak around 1.5 min of exercise with the concentration then slowly decreasing. At 12 m/sec there was a continuous rise to a peak at the end of exercise in all horses. Immediately after exercise there was a rapid return (within 3-4 min) to the potassium concentrations recorded at the end of the warm-up period. Plasma lactate peaked around the end of exercise at all speeds. At the highest intensity of exercise the mechanisms for the re-uptake of potassium did not appear to be able to match the rate of efflux. In contrast, at less intense work loads, the rate of re-uptake appeared to be similar to or slightly greater than the rate of efflux. It is possible that a disturbance in this balance between efflux and re-uptake could result in a disturbance in normal neuromuscular function during exercise.

Acid-Base Equilibrium↗
PubMed1992

Isoproterenol induces release of atrial natriuretic peptide from rat atrium in vitro.

To investigate the mechanism underlying the release of atrial natriuretic peptide (ANP) in in vitro condition, isolated, superfused rat atria were subjected to adrenergic, chronotropic, and mechanical stimulation. First administration of isoproterenol (Iso; either 10(-9) or 10(-6) M) caused a release of ANP, which was transient. Subsequent increments in concentration of Iso always resulted in a much lower release of ANP, despite the increased effects on the mechanical function of the atria. Stretching of the atria resulted in a transient release of ANP. Subsequent increments in stretching were followed by decreasing release of ANP. The total score of ANP in atrial tissue after Iso and stretching was not measurably depleted. Pacing the atria with increasing frequency did not induce release of ANP. Depolarization with 40 mM KCl abolished the release of ANP in response to Iso but not the release induced by stretch. In the presence of low external Ca2+, which abolished mechanical activity, both Iso and stretch could still induce release of ANP. Propranolol abolished the release of ANP by Iso but not that induced by stretching. Prazosin did not affect the release by either stretch or Iso. Stretching the atria 20 min after administration of Iso did not cause any further release of ANP. On the other hand, adding Iso 20 min after stretching induced a release of ANP. It is concluded that Iso and stretch cause a transient release from isolated strips of atria. The amount of ANP released is not related to the dose of Iso or to the load applied. Mechanisms involved in the release mediated by the two stimuli are different.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Pathogenesis of congestive state in chronic obstructive pulmonary disease. Studies of body water and sodium, renal function, hemodynamics, and plasma hormones during edema and after recovery.

BACKGROUND: The pathogenesis of salt and water accumulation in patients with chronic obstructive pulmonary disease is unclear and may differ from that in patients with congestive heart failure due to myocardial disease. This study was undertaken to investigate some of the mechanisms involved. METHODS AND RESULTS: Hemodynamics, water and electrolyte spaces, renal function, and plasma hormone concentrations were measured in nine patients with edema due to chronic obstructive pulmonary disease and in six patients after recovery. Mean cardiac output (3.8 +/- 0.26 l/min.m2) was normal, but right atrial (11 +/- 1 mm Hg) and mean pulmonary arterial (41 +/- 3 mm Hg) pressures were increased. Mean pulmonary arterial wedge pressure (11 +/- 1 mm Hg) was normal. Pulmonary vascular resistance (8.6 +/- 1.3 mm Hg.min.m2/l) was increased, but systemic vascular resistance (19.3 +/- 1.3 mm Hg.min.m2/l) and mean arterial pressure (83 +/- 4 mm Hg) were low. All patients were hypoxemic (PaO2, 40 +/- 2 mm Hg) and hypercapnic (PaCO2, 60 +/- 2 mm Hg). There was a significant increase in total body water (+21%), extracellular volume (+45%), plasma volume (+45%), blood volume (+88%), and exchangeable sodium (+38.2%). Renal plasma flow was severely reduced (-63.2%), but glomerular filtration rate was only mildly decreased (-32%). Significant increases were seen in plasma norepinephrine (3.5-fold normal), renin activity (7.6-fold normal), vasopressin (twice normal), atrial natriuretic peptide (9.4-fold normal), growth hormone (10.7-fold normal), and cortisol (1.9-fold normal). After recovery, the PaO2 increased (50 +/- 3 mm Hg) and PaCO2 fell (45 +/- 4 mm Hg), and the patients became free from edema. All the body compartments returned toward normal, although they did not entirely reach normal values. Renal plasma flow increased significantly, and glomerular filtration became normal. Right atrial and pulmonary arterial pressures and pulmonary vascular resistance decreased (p less than 0.01). Cardiac output decreased but not significantly. Blood pressure increased but not significantly. However, systemic vascular resistance increased significantly to a normal value. CONCLUSIONS: We conclude that patients with edema due to chronic obstructive pulmonary disease have severe retention of salt and water, reduction in renal blood flow and glomerular filtration, and neurohormonal activation similar to that seen in patients with edema due to myocardial disease. However, unlike the latter, in chronic obstructive pulmonary disease cardiac output is normal, and systemic vascular resistance and arterial blood pressure are low. This probably is due to the vasodilator properties of hypercapnia. The consequent low arterial blood pressure may be the stimulus for the neurohormonal activation and retention of salt and water.

Adult↗
PubMed1992

Mental health care in Japan.

Long-term institutionalization has been the primary treatment for mentally ill patients in Japan since the early 1920s. The average length of stay in a Japanese mental hospital in 1989 was 496 days, 41 times the average stay of patients in the United States. Although the government has encouraged and supported the integration of mentally ill people in the community and the development of rehabilitation programs since enactment of the Mental Health Law of 1988, implementation of such programs has been slow. The authors summarize the history of mental health care in Japan, discuss the current availability of mental health care facilities and personnel, and recommend changes needed to improve care.

Cross-Cultural Comparison↗
PubMed1992

General practitioners' reported knowledge about depression and dementia in elderly patients.

Previous studies have shown that general practitioners often fail to detect dementia and depression in their elderly patients. The present study aimed to find out how much knowledge general practitioners have of these disorders. The knowledge of 36 general practitioners was assessed and it was found that they had a limited knowledge of the symptoms and signs of dementia and depression. Furthermore, almost 60% of the general practitioners did not know that Alzheimer's disease is the most common dementing disorder.

Aged↗
PubMed1992

Temporal relations of the endocrine response to hypotension with sodium nitroprusside.

Sodium nitroprusside was infused intravenously for 10 minutes in normal men, reclining at 45 degrees, in a dose sufficient to decrease the arterial pressure by 10 mmHg. The effect on a variety of plasma hormones was measured during the infusion and for 20 minutes afterwards. The heart rate increased to a maximum of 149%. Norepinephrine rose to a maximum of 196% in 5 minutes. Epinephrine reached a peak of 207% after 10 minutes. Plasma renin activity reached a peak of 449% at 10 minutes. Aldosterone did not change during the infusion, but increased to a maximum of 145% 10 minutes later. Vasopressin increased sharply at the end of the infusion to 893% and then rapidly decreased. Corticotropin, prolactin and growth hormone started to increase toward the end of the infusion, but reached their maxima during recovery. Corticotropin (225%) and prolactin (288%) peaked 10 minutes after the infusion, while growth hormone (414%) appeared still to be rising 20 minutes after the end of the infusion. Cortisol also rose progressively during recovery to a level of 138%. No significant changes were seen in the concentrations of insulin, glucagon, atrial natriuretic peptide, bombesin or neurotensin.

Adult↗
PubMed1991

In vitro studies of the effect of MAb NDA 4 linked to toxin on the proliferation of a human EBV-transformed lymphoblastoid B cell line and of gibbon MLA leukemia cell line.

The rejection of allografts is mediated by cytolytic T cells and antibody-secreting B cells. Selective ablation of these activated cells from peripheral blood lymphocytes may offer a a method of controlling allograft rejection. An immunotoxin was prepared from the monoclonal antibody (mAb) NDA 4, which recognizes a differentiation antigen (NDA 4) common to activated B and T cells. MAb NDA 4 was conjugated to the ribosome-inhibiting protein gelonin via a cleavable disulfide bond provided by a crosslinking reagent. The purified immunotoxin was evaluated for in vitro cytotoxicity on NDA 4 positive T and B cell lines. Conjugation of mAb NDA 4 to gelonin increased the in vitro cytotoxicity by a concentration factor of 1000, compared to gelonin alone. The specificity and saturability of mAb NDA 4 binding, as well as the number of antigenic sites per cell on resting versus activated T lymphocytes, were also evaluated. Resting T cells expressed 400-800 sites per cell. PHA-activated T cells and the MLA T cell leukemia expressed 10,000 to 80,000 sites per cell. Peripheral blood mononuclear cells obtained from allografted baboons in quiescence or undergoing rejection were compared for NDA 4 expression by flow cytometry. Lymphocytes obtained from baboons rejecting a heart allograft expressed NDA 4, whereas transplant recipients in quiescence showed no detectable NDA 4. These results suggest that mAb NDA 4-derived immunotoxins may be valuable for the selective depletion of activated lymphocytes while sparing the resting population.

Animals↗
PubMed1991

Assessing the affective component of chronic pain: development of the Pain Discomfort Scale.

Few methods exist to assess the affective or reactive dimension of chronic pain, and there are psychometric and practical limitations on the methods that do exist. The current paper reports on the development and validation of the Pain Discomfort Scale, a 10-item instrument designed to fill the need for a brief and psychometrically sound measure of pain affect. Preliminary evidence supports the reliability and validity of the measure. Its internal consistency and test-retest stability coefficients are high. In addition, the results of both correlational and factor analyses of the PDS with other measures support its distinctiveness (from measures of pain intensity) and construct validity (as indicated by its close association with other measures of pain affect). These results support the use of the PDS in situations where a measure of the affective response to chronic pain is needed.

Affect↗
PubMed1991

The role of anti-HLA antibodies in heart transplantation.

The major threat to long-term survival of heart allograft recipients is the development of graft atherosclerosis, which seems to be a manifestation of chronic rejection. To assess the role of anti-HLA antibodies in heart allograft rejection we studied 107 patients and compared the survival of recipients who formed anti-HLA antibodies with the survival of recipients who developed no antibodies. At 4 years the actuarial survival was 90% in the nonproducer group and 38% in antibody-producers (P = 0.038). We further explored the possibility that HLA antigens from the injured graft are released into the circulation and can be found in the serum either free or complexed with anti-HLA antibodies. This hypothesis was confirmed by the finding that the frequency of sera containing soluble HLA antigens from the graft or immune complexes of HLA alloantigens with anti-HLA antibodies was significantly higher in patients who rejected compared with patients with successful heart allografts (P less than 0.05). Following depletion of soluble HLA antigens, anti-HLA antibodies became detectable in 53% and 74% sera obtained during the first and second year posttransplantation, respectively, from patients undergoing chronic rejection. Long-term survivors showed a significantly lower (P less than 0.001) frequency of anti-HLA antibodies in sera depleted of HLA antigens. Lastly, studies of anti-anti-HLA-A2 and A3 antibodies in recipient sera suggest that quiescence is maintained by antiidiotypic antibodies.

Antigen-Antibody Complex↗
PubMed1991

Diuretics as initial and sole treatment in chronic cardiac failure.

Six patients with chronic congestive cardiac failure, who had never received any drug treatment, were studied before and after one month of therapy with frusemide alone at a dose of 40 mg a day. Measurements were made at rest of plasma epinephrine, norepinephrine, renin activity, aldosterone, atrial natriuretic peptide, cortisol, growth hormone and prolactin, together with central hemodynamics, body fluid volumes and renal function. The initial measurements of hemodynamics, body fluid compartments and renal function confirmed the presence of the physiopathology typical of congestive cardiac failure. Plasma concentrations of norepinephrine, atrial natriuretic peptide, aldosterone and growth hormone were significantly increased. The mean value of plasma renin activity, although high, was not significantly different from normal. After one month of treatment, body weight, body fluid volumes and exchangeable sodium were reduced. Hemodynamics and renal plasma flow and glomerular filtration were not significantly affected. Plasma norepinephrine fell to within normal limits; atrial natriuretic peptide increased significantly; plasma renin activity and cortisol increased to levels which were abnormally high; growth hormone increased to levels similar to those associated with acromegaly. Increased circulating concentrations of atrial natriuretic peptide during treatment by frusemide may have an important influence on the kidney, blood vessels and neuro-endocrine response.

Extracellular Space↗
PubMed1991

Does estrogen replacement therapy protect against rheumatoid arthritis?

The incidence of rheumatoid arthritis (RA) was compared in 2 cohorts of women aged 35-64. One consisted of 1,075 estrogen replacement therapy (ERT) users and the other was 3,251 women from general practice registers. Screening detected 32 cases; 8 postmenopausal control and 6 ERT women developed RA during the study period 1982-1986. This produced incidence rates of 19.7/10,000 and 12.3/10,000 years of observation for ERT and controls, respectively. The relative risks for ERT was 1.62 (95% CI 0.56-4.74) and reduced towards unity after adjustment for potential confounders. Despite the wide confidence interval, our data do not support the previous observation of a 4-fold reduction in RA incidence in ERT users. Indeed the incidence rate in the exposed group in this study exceeded current population estimates of RA incidence in postmenopausal women. We believe that the high incidence rates could be best explained by the self-selection for estrogen therapy at the menopause of those with undiagnosed joint symptoms. These findings underscore the difficulties in elucidating the relationship between ERT and RA.

Adult↗
PubMed1991

Pulmonary peptides, norepinephrine and endocrine cells in monocrotaline pulmonary hypertension.

The concentrations of norepinephrine and of the peptides bombesin, calcitonin gene-related peptide and neurotensin were measured in rats with monocrotaline pulmonary hypertension. The numbers of pulmonary endocrine cells showing positive immunoreactivity for calcitonin, calcitonin gene-related peptide, protein gene product 9.5 and bombesin were counted in a second group of rats with monocrotaline pulmonary hypertension. The concentration of norepinephrine in the lungs decreased significantly in the test rats but this could be attributed to dilution by an increased mass of tissue. The pulmonary concentration of all three peptides showed a decrease in the rats treated with monocrotaline but this was highly significant only in the case of bombesin. The pulmonary content of bombesin showed a substantial and significant decrease in the test rats. No neuroendocrine cells immunopositive for bombesin were identified in any of the control or test rats. There was no difference between the control and test rats with respect to the form or distribution of the cells immunoreactive for the other three The lack of pulmonary endocrine cells showing immunoreactivity for bombesin may be related to the absence of intimal proliferation in the pulmonary arteries in this species. This is in striking contrast to what occurs in plexogenic pulmonary arteriopathy in man and suggests that monocrotaline-induced pulmonary hypertension in rats is not a good animal model for this disease.

Animals↗
PubMed1991

Temporal relations of the endocrine response to exercise.

We have followed the hormonal response to exercise in twelve normal males cycling at a constant moderate load for ten minutes. Plasma concentrations of a variety of hormones were measured at set times before and during exercise and for twenty minutes afterward. The plasma concentration of norepinephrine and epinephrine and plasma activity of renin rose to a maximum at the end of exercise and then declined. The plasma concentrations of neurotensin and atrial natriuretic peptide followed a similar course. Plasma vasopressin rose to a peak at the end of exercise and then fell transiently below the initial value ten minutes after exercise. The plasma concentrations of aldosterone, prolactin and adrenocorticotropin increased during exercise but continued to do so, reaching a peak at ten minutes after exercise. Plasma growth hormone increased during exercise and continued to increase throughout the period of twenty minutes' recovery. Cortisol did not change during exercise but rose progressively during the recovery period. Plasma concentrations of glucagon did not change while that of insulin decreased during exercise. The plasma concentration of bombesin slowly increased during exercise and declined during recovery, reaching a basal value 10 minutes later.

Adult↗