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Biomedical subjects

M A Adams

Publications and source records attributed to M A Adams.

At least 19 recordsLinked to original sources
PubMed1992

Development and validation of a new transducer for intradiscal pressure measurement.

Potentially damaging tensile stresses in the annulus fibrosus are directly related to the hydrostatic pressure in the centre of an intervertebral disc: the design and development of a miniature strain gauge pressure transducer is described for measuring such pressures. Static calibration tests in bulk liquid demonstrated that measurements made with the transducer were of sufficient accuracy and stability for in vitro and in vivo investigations of spinal mechanics, and a study of the dynamic behaviour of the transducer demonstrated that it had a frequency response suitable for in vitro and in vivo investigations. Tests within loaded cadaveric discs showed that the transducer could be used to make repeatable measurements which were free from significant artefacts, when the disc was subjected to forces of up to 4000 N and when deformed in full flexion/extension.

Adult↗
PubMed1992

Internal intervertebral disc mechanics as revealed by stress profilometry.

A technique was developed for measuring the distribution of stress within loaded cadaveric intervertebral discs. A strain-gauged membrane mounted on the side of a 1.3-mm diameter needle was pulled through the disc at constant speed. The orientation of the membrane was changed by rotating the needle, so that profiles of vertical and horizontal components of compressive stress could be obtained. The measurements were reproducible and did not perturb the tissue to any significant extent. Stress profiles varied considerably between discs and were highly dependent on the severity of degenerative changes. They also showed that the mechanical behavior of individual disc tissues was dependent not only on their location, but also on the loading and loading history of the disc. The new insight into internal disc mechanics revealed by stress profilometry may lead to a greater understanding of the mechanisms of disc function and failure.

Aging↗
PubMed1992

Characterization of the baroreceptor heart rate reflex during development in spontaneously hypertensive rats.

1. We have examined the baroreceptor-heart rate (HR) reflex in weight-matched conscious spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats during development. 2. Graded steady-state changes in mean arterial pressure (MAP) and the corresponding HR responses before and after vagal blockade with methylatropine were fitted to an S-shaped logistic function. 3. At 6 weeks of age, SHR had a 17% higher MAP than WKY and an increased baroreflex gain (slope) compared with WKY due to an increased curvature of the MAP-HR relationship. The HR range (the difference between the upper and lower HR plateaus) was similar in the two strains at this time. 4. From 9-14 weeks of age, the baroreflex gain progressively increased in WKY and decreased in SHR due to corresponding alterations in HR range. 5. By 20 weeks the baroreflex gain was 23% lower in SHR than WKY due to a 37% lower HR range. 6. There were no differences between the two strains in the sympathetic component of the baroreflex at any age, suggesting that the changes to baroreflex properties were confined to the cardiac vagus. 7. Pretreatment with enalapril from 4-9 weeks reduced the hypertension of SHR at 14 and 20 weeks by 38% and abolished all baroreceptor-HR reflex differences between the two strains. 8. These studies suggest that the major alteration to the baroreceptor-heart rate reflex in the SHR during development was a reduction in the maximum vagal capacity to respond to changes in blood pressure. This effect developed after the onset of hypertension and was prevented by antihypertensive treatment early in life. The lack of effect on the cardiac sympathetic component suggests that altered arterial baroreceptor afferents are not unlikely to be responsible.

Animals↗
PubMed1992

Vasodilators inhibit acute alpha 1-adrenergic receptor-induced trophic responses in the vasculature.

Cardiovascular hypertrophy plays an important role in the development and maintenance of hypertension. Hyperactivity of the sympathetic nervous system may be one of the initiating factors responsible for the stimulation of growth processes involved in these structural alterations. We have used a well-established early biochemical marker of cellular growth processes, induction of ornithine decarboxylase (ODC), to determine whether alpha 1-adrenergic receptor-induced vascular trophic responses are dependent on arterial pressure elevation. Hydralazine or felodipine were coadministered to control the alpha 1-adrenergic receptor agonist-induced rise in mean arterial pressure (MAP). Methoxamine (2, 5, or 10 mg/kg s.c.) increased the average MAP (up to 20 mm Hg) and vascular ODC activity (up to ninefold) above control rats over 4 hours. Concomitant administration of hydralazine (0.5, 1.25, or 5 mg/kg s.c.) or felodipine (100 or 250 micrograms/kg s.c.) with methoxamine (10 mg/kg) attenuated the alpha 1-adrenergic receptor-induced activation of ODC in the aorta and mesenteric resistance vasculature, as well as the MAP increases. Vasodilators alone did not lower basal vascular ODC activity. The major findings include: 1) alpha 1-adrenergic receptor activation dose-dependently induces vascular ODC activity concomitantly with MAP elevation, 2) vasodilators inhibited both the alpha 1-adrenergic receptor-induced MAP increases and the activation of mesenteric vascular and aortic ODC, and 3) the stimulus-response correlation between MAP elevation and mesenteric (r = 0.78) and aortic (r = 0.92) ODC activation was characterized by a logistic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1992

Bioequivalence of verapamil hydrochloride extended-release pellet-filled capsules when opened and sprinkled on food and when swallowed intact.

A study was performed to determine whether verapamil hydrochloride administered in extended-release pellet-filled capsules is bioequivalent to the same formulation administered by sprinkling the contents of the capsules onto food. Thirty-two healthy subjects participated in the randomized, two-way crossover study. In treatment A, the subjects swallowed the contents of a verapamil hydrochloride extended-release pellet-filled capsule, 240 mg, that had been sprinkled on applesauce. In treatment B, the subjects swallowed the same type of capsule intact. Blood samples were drawn at baseline, every hour for 10 hours, and at 12, 15, 24, 30, 36, and 48 hours after each dose administration. The plasma was analyzed for verapamil and norverapamil by high-performance liquid chromatography. The following calculations were performed: AUC0-48, AUC0-infinity, Cmax, tmax, and k. Results for the two treatments were compared by analysis of variance. There were no significant differences between the AUC0-48, AUC0-infinity, Cmax, tmax, and k for the two methods of dose administration. For verapamil the differences for all variables were less than 5%, and for norverapamil the differences were less than 4% for all variables except tmax (9.5%). The 90% confidence intervals were within acceptable limits for all variables except the norverapamil tmax comparison. Sprinkling the contents of extended-release pellet-filled capsules onto food provides verapamil hydrochloride that is bioequivalent to that obtained from the intact capsules.

Administration, Oral↗
PubMed1991

A technique for quantifying the bending moment acting on the lumbar spine in vivo.

The bending properties of cadaveric lumbar spines were measured and used to convert in vivo measurements of lumbar flexion into bending moments ('stresses'). Forty-two lumbar motion segments were subjected to complex physiological loading and graphs were obtained of bending moment vs flexion angle. Variability was reduced by expressing both variables as a percentage of their values at the elastic limit. Data were averaged for each lumbar level, and a composite bending curve was compiled for the lumbar spine, L1-S1. A linear relationship was established between lumbar flexion measured in vitro and in vivo. This enabled values of 'per cent lumbar flexion' measured in vivo to be converted into 'per cent maximum bending moment' with a maximum likely error of about +/- 8%, which is equivalent to about +/- 5 Nm at L5-S1 for an average person. The technique was applied to 28 subjects, using dynamic measurements of lumbar flexion obtained with the '3-Space Isotrack' system. The bending moment at L5-S1 was 12 Nm on average when picking a pen up off the floor. Highly significant increases in bending moment were observed when heavier and bulkier objects were lifted.

Adult↗
PubMed1991

Axial movement and tibial fractures. A controlled randomised trial of treatment.

Diaphyseal fractures of the tibia in 80 patients were treated by external skeletal fixation using a unilateral frame, either in a fixed mode or in a mode which allowed the application of a small amount of predominantly axial micromovement. Patients were allocated to each regime by random selection. Fracture healing was assessed clinically, radiologically and by measurement of the mechanical stiffness of the fracture. Both clinical and mechanical healing were enhanced in the group subjected to micromovement, compared to those treated with frames in a fixed mode possessing an overall stiffness similar to that of others in common clinical use. The differences in healing time were statistically significant and independently related to the treatment method. There was no difference in complication rates between treatment groups.

Adolescent↗
PubMed1991

Depression associated with antihypertensive drugs.

BACKGROUND: Depression is a potential side effect of antihypertensive drug therapy. Consideration of this side effect is a reason often cited by physicians for not choosing certain drugs. METHODS: In this prospective study the relative rates of depression were measured by the Zung Self-Rating Depression Scale (SDS) in patients from four hypertension treatment groups. Treatment groups consisted of 466 patients receiving: (1) no drug therapy, (2) diuretics only, (3) diuretics plus reserpine, and (4) diuretics plus beta-blockers. Demographic data including age, sex, and race were collected. Analysis of variance was used to compare the rate of depression among the treatment groups, as well as among age, sex, and racial groups. RESULTS: Using a Zung SDS index of greater than or equal to 50, 35.4% of the hypertensive population was depressed. Age and sex were not significant factors in the frequency of depression. Blacks scored higher than whites in all drug treatment groups except those treated with high lipophilic beta-blockers, but the rate of depression was not higher. Whites on the lowest dose of reserpine had the lowest rate of depression. The rate of depression among those taking reserpine or beta-blockers was no different than that among those receiving either no treatment or diuretics. CONCLUSIONS: Reserpine or beta-blocker therapy did not cause any more depression than any other antihypertensive treatment.

Adolescent↗
PubMed1990

Cardiac and vascular structural adaptation in experimental hypertension.

Various colonies of the spontaneously hypertensive rat (SHR) of the same age demonstrate different forms of the left ventricle (LV) in end-diastole. SHR from breeders in Australia and Switzerland exhibit concentrically hypertrophied LV, evident from an increased wall thickness to internal radius ratio (w/ri), while SHR from a Danish colony show an unchanged w/ri ratio, indicating eccentrically hypertrophied LV. These differences may be related to changes in arterial blood pressure and/or altered cardiac filling patterns. A more favourable situation seems to prevail for the eccentrically hypertrophied SHR heart compared with the concentrically hypertrophied heart, the former demonstrating enhanced cardiac function. Thus, an LV with increased diastolic diameter, as in the eccentrically hypertrophied SHR heart, can produce an elevated stroke volume for a given degree of myocardial shortening. In renal hypertension, however, LV function was depressed, probably due to a factor, possibly released upon clipping of the renal artery, that has inherent negative inotropic properties. Here, the reduction of LV performance could be explained neither by the changed LV geometrical design nor by the altered myocardial myosin isoenzyme pattern. At low aortic pressures and hence limited coronary perfusion, LV performance is attenuated in SHR and renal hypertensive rats, most likely due to the vascular structural changes within the coronary vascular bed.

Animals↗
PubMed1990

Metoprolol suppresses the development of ethanol-induced cardiac hypertrophy in the rat.

Subacute, severe intoxication with ethanol stimulates the peripheral sympathetic nervous system in the rat and enhances the excretion of adrenaline and noradrenaline. In association with this effect there is a rapid development of cardiac hypertrophy, with proportional heart weight increasing by 12% within 48 h. At this time adrenal medullary adrenaline content was depressed by more than 35%, whereas nonadrenaline content of the adrenal and heart were not affected. Metoprolol (20 mg/kg, t.i.d.) was without effect when used alone and had little if any impact on the ethanol-induced changes. Metoprolol (100 mg/kg, t.i.d.) reduced adrenal catecholamine content, but not cardiac noradrenaline content, and diminished cardiac weight in control animals. The combination of ethanol with the high dose of methoprolol enhanced the loss of medullary catecholamine and reduced cardiac noradrenaline content, whereas cardiac weight was the same as in control animals. A correlation between sympathetic activation and increasing cardiac mass and its antagonism by metoprolol implies a beta-adrenoceptor mediated link in the cardiac hypertrophy induced by ethanol.

Adrenal Glands↗
PubMed1990

Enalapril can prevent vascular amplifier development in spontaneously hypertensive rats.

Three groups of spontaneously hypertensive rats (SHR) were given enalapril (25 mg/kg/day) from 4 to 9 weeks, 4 to 14 weeks, and 14 to 20 weeks of age. The drug was stopped and observations continued for another 16-21 weeks. At selected times, we measured blood pressure, in vitro hindquarter vascular resistance properties, left ventricular weight/body weight ratio, and skeletal muscle vessel norepinephrine kinetics in treated and untreated SHR and in Wistar-Kyoto (WKY) rats. At the end of each treatment period, all cardiovascular variables were close to values of WKY rats and well below those of untreated SHR, and the norepinephrine or fractional rate constant was about 25% below those levels. After enalapril was stopped, blood pressure and left ventricular weight/body weight ratio increased in parallel to levels ranging from 30% to 50% of the normal difference between untreated SHR and WKY rats. However, in SHR treated from 4 to 9 weeks and from 4 to 14 weeks of age, hindquarter resistance properties remained close to WKY rat levels for the entire observation period of 16-21 weeks after treatment, suggesting suppression of the enhanced resistance responses of SHR (amplifier properties). In SHR treated from 14 to 20 weeks of age, suppression of amplifier properties was more transient, and they redeveloped partially 5-6 weeks after cessation of therapy. When enalapril was given up to 14 weeks of age, the long-term suppression of amplifier properties was probably mainly through prevention of smooth muscle hypertrophy in resistance vessels and possibly through other mechanisms (e.g., "rarefaction").(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Regression of cardiac hypertrophy in spontaneously hypertensive rats by enalapril and the expression of contractile proteins.

Several experimental models involving the development of cardiac hypertrophy in adult rats are characterized by the reexpression of the fetal isoform of myosin heavy chain (V3). To determine whether a similar adult-to-fetal shift in the expression of the thin-filament proteins occurs during cardiac hypertrophy, we have examined the expression of the isoforms of myosin, tropomyosin, and troponin T in the left ventricle of young spontaneously hypertensive rats (SHR) with and without treatment using enalapril, an angiotensin converting enzyme inhibitor. Phosphorylation of tropomyosin, which is predominant in the fetal state, was also analyzed. Twelve-week-old SHR were treated with enalapril for 2, 5, 8, and 9 weeks followed by withdrawal of treatment for 9 weeks. Control SHR, without drug treatment, were weight- and age-matched. After 9 weeks of enalapril treatment, mean arterial blood pressure was reduced (from 166 +/- 11 to 89 +/- 5 mm Hg), and left ventricular weight/body weight ratio was regressed (from 2.53 +/- 0.14 to 1.96 +/- 0.05 g/kg) to normotensive levels. During the 9-week treatment period, the percent V3 decreased in SHR substantially from 35 +/- 3% to 13 +/- 1%. There was a significant correlation between the left ventricular hypertrophy and the percent V3 myosin expression in the SHR during regression (r = 0.697, p less than 0.001). However, only the adult isoforms of tropomyosin and troponin T were detected in the SHR with or without enalapril treatment, and the level of tropomyosin phosphorylation remained constant irrespective of the degree of left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Diurnal changes in spinal mechanics and their clinical significance.

Diurnal changes in the loads acting on the spine affect the water content and height of the intervertebral discs. We have reviewed the effects of these changes on spinal mechanics, and their possible clinical significance. Cadaveric lumbar spines subjected to periods of creep loading show a disc height change similar to the physiological change. As a result intervertebral discs bulge more, become stiffer in compression and more flexible in bending. Disc tissue becomes more elastic as its water content falls, and its affinity for water increases. Disc prolapse becomes more difficult. The neural arch and associated ligaments resist an increasing proportion of the compressive and bending stresses acting on the spine. Observations on living people show that these changes are not fully compensated for by modified muscle activity. We conclude that different spinal structures are more heavily loaded at different times of the day. Therefore, the time of onset of symptoms and signs, and any diurnal variation in their severity, may help us understand more about the pathophysiology of low back pain and sciatica.

Back Pain↗
PubMed1990

Unconstrained shoulder arthroplasty. A five-year average follow-up study.

A series of 42 total shoulder arthroplasties and four humeral hemiarthroplasties were performed with either the English-McNab or Neer prosthesis. Retrospective follow-up study averaged five years with a three-year minimum. Preoperative diagnoses included rheumatoid arthritis, osteoarthritis, posttraumatic arthritis, rotator cuff arthropathy, avascular necrosis, failed prosthesis, and congenital dislocation. Postoperatively, pain improved in 94% of shoulders, and active range of motion improved an average of 42 degrees in abduction and 47 degrees in forward flexion. Rotator cuff lesions were correlated with poorer postoperative function. Complications developed in four shoulders (9%) and consisted of humeral component protrusions (two shoulders), loosened prosthesis (one shoulder), and unrecognized, preoperative tuberculous infection (one shoulder). Fifteen glenoid components (36%) and six humeral components (13%) developed lucent lines roentgenographically, but only one glenoid component developed migration.

Adult↗
PubMed1989

Effect of enalapril on aortic smooth muscle cell polyploidy in the spontaneously hypertensive rat.

The angiotensin converting enzyme (ACE) inhibitor enalapril was used to examine the effects of inhibition, regression and redevelopment of hypertension on the ploidy of aortic smooth muscle cells in spontaneously hypertensive rats (SHR). The incidence of polyploidy cells, as determined by flow cytometric DNA analysis, directly paralleled changes in systolic blood pressure. When the development of hypertension was inhibited by treatment with enalapril, the incidence of polyploid cells remained low compared with untreated age-matched SHR. Likewise, when the blood pressure of hypertensive animals was lowered by enalapril treatment, the incidence of polyploid cells decreased. Addition of enalapril to primary cultures of smooth muscle had no direct effect on proliferation or the incidence of polyploidy. These results suggest that angiotensin II may be involved in the development of vascular smooth muscle polyploidy in vivo, either by a direct effect on the cells or indirectly by elevating blood pressure or by potentiation of sympathetic discharge.

Angiotensin II↗
PubMed1989

Lack of cardiac alpha 1-adrenoceptor involvement in ethanol-induced cardiac hypertrophy.

The development of cardiac hypertrophy was examined in rats given ethanol in a nutritionally adequate, liquid diet mixture, by intubation, in severely intoxicating doses at 8-h intervals for up to 96 h, alone or in combination with prazosin. Other groups of rats received isocalorically paired quantities of maltose-dextrin. Adrenal glands of rats receiving ethanol were larger than those from control animals. Prazosin did not affect this measure. In contrast, concurrent treatment with prazosin enhanced the loss of medullary catecholamines and noradrenaline from hearts of rats given ethanol, while it had no such effects in controls. Reflecting these changes, excreted quantities of catecholamines were markedly increased in rats given ethanol and prazosin. Hearts of animals given the combined treatment of ethanol and prazosin showed cardiomegaly at 24 h, when there was an increase of about 20% in proportional heart weight, an increase that persisted through the remaining 3 days of the study. At 48 h, hearts of animals given prazosin and ethanol were heavier than those given ethanol alone. A significant correlation between catecholamine excretion and the development of cardiac hypertrophy was identified. The results of the study show that prazosin can enhance effects of ethanol on the peripheral sympathetic nervous system. Moreover, the results suggest that postsynaptic alpha 1-adrenoceptor stimulation in the heart is not an important contributor to ethanol-induced cardiomegaly.

Adrenal Glands↗