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Biomedical subjects

C P Stewart

Publications and source records attributed to C P Stewart.

16 recordsLinked to original sources

Lower limb amputee survival.

A total of 1710 primary amputees have been studied over a 25 year period and their survival time has been calculated. These were all consecutive primary lower limb amputees admitted to the Dundee Limb Fitting Centre during the period 1965-1989. Overall, the median survival was 4 yr 9 mth for the below-knee amputee (1019 patients) and 4 yr 3 mth for the above-knee amputee (586 patients). The vascular related amputees had an overall median survival of 4 yr. In the two decades 1970-1979 and 1980-1989 there were significant differences between the survival time of the below-knee and above-knee amputee. The survival of the amputee has increased during the two decades from 3 yr 6 mth to 6 yr 6 mth (p greater than 0.001). For the first decade male above-knee and male below-knee amputee median survival was 3 yr 1 mth and 3 yr 11 mth respectively and for the second the survival was 5 yr 9 mth and 6 yr 11 mth for these levels of amputation. For 1970-1979 no significant differences were found between male and female peripheral vascular disease (PVD) and diabetes mellitus related amputee survival. For 1980-1989 significant differences were found between PVD related male above-knee amputees (3 yr 10 mth) and male below-knee amputees (6 yr 7 mth) (p greater than 0.01). Similar results were found for the female patients. Operative mortality was found to be 5% over the period 1975-1989 which compared favorably with previous studies.

Age Factors

Cause of death of lower limb amputees.

A study was carried out on the cause of death of 100 lower limb amputees who had been admitted to the Dundee Limb Fitting Centre, Tayside, Scotland for prosthetic management or wheelchair training. A comprehensive database has been established in the Centre for 25 years and the database is updated regularly. The date of death was collected and recorded. One hundred sequential deaths were investigated to review the cause of their death and compare this with the recorded causes of death for the Tayside population for the year of study. Ninety three per cent had an amputation for vascular related causes, with 73% having a below-knee amputation and 17% above-knee. Heart disease was the most frequent recorded cause of death (51%) of the amputee whereas only 28.1% of the Tayside group died from this pathology (p less than 0.01). Carcinomatosis was reported as a cause of death in 14% of the amputees and 23.5% of the Tayside group. Cerebrovascular disease caused death in 6% of the amputees and in 12.3% of the Tayside group (both p less than 0.01). These findings confirm earlier suggestions that vascular amputees die from heart disease more often than the general population.

Amputation, Surgical

Physiological considerations in seating.

Physiological changes occur with change of posture. Seating imposes significant effect on the cardiovascular, respiratory, abdominal, renal and neurological systems. The presence of severe skeletal deformities can significantly alter the physiological responses of the individual to changes in posture. In the case of severe kyphoscoliosis profound haemodynamic changes may occur. Lung perfusion has been shown to be posture dependent and the imposition of a specific seated position may have profound effects. This may compound existing lung problems for example bronchiectasis, which is not uncommon in these individuals, leading to hypoventilation. Abdominal compression which can occur with the patient in a flexed position can exacerbate a hiatus hernia, which can be both uncomfortable for the patient and may lead to feeding difficulties. The flexion at the hips of the lower limbs may also lead to problems of renal drainage especially where there is a catheter or other drainage appliance. Seating significantly affects many neurological reflexes. For example the presence of an extensor pattern can be helped by the adoption of a flexed position. The presence of pain can also influence the neurological response to a specific position. Those providing seating systems must consider the physiological effects that occur and compromise between these and the other requirements.

Abdomen

Electrogenic bicarbonate secretion by guinea pig gallbladder epithelium: apical membrane exit.

Guinea pig gallbladder epithelium secretes HCO3- by electroneutral mechanisms, resulting in transepithelial Cl- -HCO3- exchange. Adenosine 3',5'-cyclic monophosphate (cAMP) converts HCO3- secretion into an electrogenic process. This transformation was examined using voltage-clamp, pH-stat, and microelectrode techniques. Prostaglandin E1 (PGE1; 10(-6) M) was used to raise intracellular cAMP levels. It increased short-circuit current (Isc) by approximately 1.8 mumol.cm-2.h-1, an effect dependent on serosal HCO3- and, partly, on mucosal Cl-. Mucosal 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS; 10(-3) M) halved Isc, but only in Cl- containing solutions. PGE1 increased the secretory HCO3- flux from approximately 2.0 to approximately 2.7 mumol.cm-2.h-1 and reduced the absorptive HCO3- flux from approximately 1.1 to approximately 0.5 mumol.cm-2.h-1, with net HCO3- secretion accounting for the increase in Isc. During single-cell impalements, PGE1 depolarized the apical membrane by greater than 10 mV (transiently in the absence of HCO3-) and decreased the apparent ratio of membrane resistances (Ra/Rb) from 5-8 to a value close to zero. These effects were largely reduced in magnitude and rapidity by removing Cl- and HCO3- from both sides of the epithelium. Ion substitutions in the luminal perfusate revealed substantial Cl- and HCO3- permeabilities at the apical membrane under PGE1 conditions. Our results indicate that, in the presence of PGE1 (cAMP), HCO3- crosses the apical membrane by two different routes. A SITS-sensitive fraction leaves the cell in exchange for luminal Cl-, which, in turn, recycles into the lumen by electrodiffusion. The remaining HCO3- exits through a HCO3- conductive pathway.

1-Methyl-3-isobutylxanthine

A microelectrode study of responses to secretagogues by epithelial cells on villus and crypt of rat small intestine.

The cellular origin of the response to secretagogues in small bowel epithelium was investigated by recording the effect of 5-hydroxytryptamine (5-HT, 10(-4) mol/l), acetylcholine (10(-4) mol/l), and prostaglandin E2 (PGE2, 10(-5) or 10(-4) mol/l) on apical membrane potentials (Va) of crypt and villus cells of rat ileum and jejunum in vitro using intracellular microelectrodes. Experiments were performed under visual control; addition of secretagogues and other manipulations were carried out during single impalements. Under basal conditions, apical membrane potential differences were consistently higher in jejunum than ileum (-72 +/- 1 vs. -47 +/- 2 mV, respectively, for villus impalements; -61 +/- 2 mV vs. -57 +/- 1 mV, respectively, for crypt impalements), and in jejunum villous membrane potentials exceeded those in the crypt. In the ileum, this crypt-villus gradient was reversed. The three secretagogues increased transmural potential difference and transiently reduced Va in cells in both crypt and villus regions by 8 mV or more. Fractional apical membrane resistance (FR) declined in ileum by approximately 30% in response to 5-HT and PGE2, whereas little change in FR was observed in jejunal recordings. PGE2 was ineffective in crypt and villus when Cl- was replaced by gluconate in both the luminal and serosal perfusates but depolarized the apical membrane in both regions after serosal restoration of Cl- from -76 +/- 4 to -56 +/- 8 mV in villus and from -58 +/- 4 to -45 +/- 6 mV in crypt. Rapid luminal Cl- substitution depolarized Va on the villus from -77 +/- 2 to -74 +/- 3 mV, but this effect was enhanced in the presence of PGE2, reducing Va from -65 +/- 8 to -43 +/- 12 mV. Prior to PGE2 addition, Va was -81 +/- 4 mV for this group of experiments. FR rose in the nominal absence of luminal Cl- from 0.69 +/- 0.09 to 0.77 +/- 0.06. It is concluded that because a Cl(-)-dependent depolarization of apical membrane potentials occurs in villi and crypts, net secretion in the small bowel is probably not confined to the crypts and may also occur from villous epithelium.

Acetylcholine

Tumour related lower limb amputation: a 23 year experience.

This paper records the Dundee experience over 23 years and reports on 42 cases of tumour related lower limb amputations. There were 27 males and 15 females with 37 malignant and 5 benign tumours. Four of the 'benign' tumours proved to be osteoclastoma which were locally malignant. Prosthetic rehabilitation was achieved in all but one case. All patients fitted were able to use their prostheses.

Adult

Development of a universal wheelchair narrower.

A wheelchair user's mobility may be hampered by narrow doorways and restricted turning spaces. Mobility may be improved by undertaking expensive building alterations in the wheelchair user's own home and work environment. However, other environments, including modes of public transport, may still present considerable difficulties. One way of improving mobility is to reduce the overall width of a wheelchair with the occupant still seated within it. This is achieved by using a clamp, known as a "wheelchair narrower" which can be fitted and operated either by the wheelchair user or an attendant. The narrower takes advantage of the inherent design of a wheelchair which permits folding for storage. A universal wheelchair narrower was manufactured and tested at Tayside Rehabilitation Engineering Services. It was designed to be used on 69% of wheelchairs issued through the National Health Service in Scotland. Tests revealed that wheelchairs could be narrowed by between 38 and 127 mm depending upon the type of wheelchair. Active wheelchair users reported that the device was particularly useful when travelling.

Equipment Design

Glucose depolarizes villous but not crypt cell apical membrane potential difference: a micropuncture study of crypt-villus heterogeneity in the rat.

Brush-border membrane potentials and fractional resistances have been recorded from enterocytes at different points along the crypt-villus axis of rat ileum in vitro. Microelectrode impalements were obtained under visual control and brush-border membrane potentials were higher in crypt than in villous cells (-57 +/- 1.6 against -50 +/- 1.6 mV referred to the mucosal side). Replacing mannitol with D-glucose in the mucosal perfusate resulted in a rise in transmural potential difference (0.5 +/- 0.17 to 1.0 +/- 0.21 mV (n = 37)) and apical membrane potential was depolarized. This occurred consistently only in the upper two-thirds of the villus (-54 +/- 1.7 to -47 +/- 2.3 mV (n = 17)) and not in crypt cells (-56 +/- 2.6 to -57 +/- 2.4 mV (n = 10) or at the crypt-villus junction. The glucose-induced apical membrane depolarization in villous enterocytes was blocked by phlorizin, a competitive inhibitor of sodium-dependent glucose uptake (-50 +/- 2.1 to -53 +/- 2.8 mV (n = 9) in the presence of phlorizin and glucose). Transmural resistance, Rt, and fractional resistance, FR, were unaltered by glucose (61 +/- 3.4 to 61 +/- 3.5 omega X cm2 (n = 50] and (0.60 +/- 0.06 to 0.57 +/- 0.06 (n = 17]. This micro-puncture technique provides direct evidence for functional differentiation along the crypt-villus axis and indicates that active electrogenic accumulation of glucose is confined to villous epithelium.

Animals

The influence of smoking on the level of lower limb amputation.

A review of smoking habits of 77 vascular related amputees demonstrated a high incidence of smoking significantly greater for men than in the general population. Male smoking amputees with atherosclerosis related peripheral vascular disease were found to have a high risk of having an above-knee amputation. Those with diabetes mellitus whether male or female, smokers or not, had a significantly greater chance of having a below-knee amputation. Overall, non-smokers were found more likely to have a below-knee amputation than an above-knee (p less than 0.05).

Aged

Electroneutral secretion of bicarbonate by guinea pig gallbladder epithelium.

Transepithelial HCO3- movement in guinea pig gallbladder was investigated in vitro. Absorptive (JHCO3ms) and secretory (JHCO3sm) HCO3- fluxes, determined by use of the pH-stat method were approximately 1.0 and 2.1 mumol X cm-2 X h-1, respectively. The resultant net secretion equaled in magnitude, and balanced electrically, the excess in net absorption of Cl- over that of Na+ X JHCO3sm was dependent on luminal Cl- and serosal Na+; it was inhibited by mucosal 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS; 10(-3) M) and serosal ouabain (3 X 10(-5) M) but not by serosal amiloride (10(-3) M) and scarcely by bilateral methazolamide (10(-4) M). JHCO3ms was reduced by mucosal Cl- but enhanced by serosal Cl-; it was dependent on mucosal Na+ and inhibited by mucosal amiloride and bilateral methazolamide. Our findings are consistent with a model in which 1) serosal HCO3- enters the cell in cotransport with Na+ and is then extruded into the lumen by Cl-(-)HCO3- exchange at the apical membrane; 2) mucosal HCO3- enters the cell secondary to apical membrane Na+-H+ exchange and recycles into the lumen via Cl-(-)HCO3- exchange or is, to a lesser extent, absorbed across the basolateral membrane.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo

Noradrenaline as a possible mediator of the actions of angiotensin on fluid transport by rat jejunum in vivo.

1. Net fluid absorption and transmural potential difference were measured in the rat jejunum in vivo.2. Increased rates of net fluid transport were observed following infusions of angiotensin or noradrenaline. There was a small, but significant, fall in transmural p.d. associated with noradrenaline but not with angiotensin infusions.3. The alpha-adrenergic antagonists phentolamine and dihydroergotamine abolished both the angiotensin and the noradrenaline stimulations of transport and the noradrenaline-induced fall in p.d., whereas the beta-adrenergic antagonist propranolol did not significantly affect these responses.4. Phentolamine did not alter the rise in p.d. following administration of the cholinergic agonist pilocarpine.5. The protein synthesis inhibitor cycloheximide abolished both the angiotensin and the noradrenaline-induced stimulation of fluid transport.6. Neither angiotensin nor noradrenaline significantly altered jejunal cyclic AMP levels.7. Bilateral nephrectomy had no apparent effect upon the increase in fluid transport following noradrenaline infusions.8. The noradrenaline-induced stimulation of transport was unaffected, and the fall in p.d. potentiated in rats pre-treated with reserpine, but a marked inhibition of transport was observed following angiotensin infusions.9. The results are consistent with the view that noradrenaline may mediate the actions of angiotensin upon intestinal fluid absorption in the rat.

Angiotensin II