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Biomedical subjects

K Carter

Publications and source records attributed to K Carter.

6 recordsLinked to original sources
PubMed1992

Role of electric stimulation in bladder evacuation following spinal cord transection.

Neural stimulation is potentially a valuable therapeutic tool in the treatment of neurogenic bladder with detrusor areflexia. We studied 20 dogs in different groups, up to eight months, and compared the effect of electric stimulation with intermittent catheterization, specially during spinal shock phase. We found that early stimulation hastened the return of detrusor activity. When stimulation was delayed, the bladder could still regain its activity, and when the pace-maker was turned off, the detrusor activity was gradually decreased. Neurostimulation can completely empty bladder up to eight months. The lowest A.Ch. content in detrusor muscle was found in intermittent catheterization group and in this group the detrusor strips showed marked supersensitivity to urecholine stimulation than the bladders managed by electric stimulation. Also, we found that electric stimulation reduced the complications caused by intermittent catheterization and protected kidney function.

Animals↗
PubMed1991

Impaired anal sensation and early diabetic faecal incontinence.

Faecal incontinence develops in up to 20% of diabetic patients. To try to determine the relative contributions of sensory and motor neuropathy in this troublesome complication, anorectal function was examined in 10 male diabetic patients with early faecal incontinence (mucus leakage or faecal staining without the need to wear a pad), 10 asymptomatic male diabetic patients, and 10 normal control subjects. Motor function was tested using anal manometry to determine the resting and maximum squeeze pressure, and the functional anal canal length. No significant differences were found between the groups. Sensory function was tested by measuring the mucosal sensitivity to electrical stimulation, and the response to inflation of a balloon in the rectum. In the mid-anal canal position the symptomatic patients had a significantly higher sensory threshold at 6.6 +/- 2.8 mA compared with 3.0 +/- 1.2 mA in the normal control subjects (p less than 0.002), and in the high anal zone symptomatic patients had a significantly elevated sensory threshold at 9.1 +/- 2.0 mA compared with 4.6 +/- 1.6 mA in asymptomatic patients and 3.6 +/- 1.3 mA in the normal control subjects (both p less than 0.001). There were no significant differences in the first sensation of fullness, maximum tolerated volume or percentage fall from resting pressure between the groups on inflation of the balloon. Elevation of the sensory threshold in the upper anal canal is an early abnormality in the development of diabetic faecal incontinence.

Anal Canal↗
PubMed1991

Porcine model for vascular graft studies.

Models for the study of prosthetic vascular graft infection have been studied frequently in the dog and rabbit. We have developed a reproducible swine model to study this problem and its treatment. The cardiovascular system, healing characteristics, and the bloodstream clearance of bacteria in swine more closely resembles those of humans than do other animal models. The low cost and availability of the swine is an additional attractive aspect. One hundred fifty-six farm-bred pigs have undergone infrarenal aortic replacement with a 3-cm segment of 6-mm prosthetic graft over the past two years. Graft infection was produced by (1) direct inoculation of 10(6) Staphylococcus aureus at the time of the surgery or (2) intravenous infusion of bacteria (10(2)-10(6) organisms/mL) immediately after surgery. All animals were sacrificed 1 to 4 weeks later, depending on the study design. Cultures, histology, and electron microscopy were performed on each graft. Anesthetic complications were rare (2.5%). Postoperative complications leading to animal death decreased with increasing experience (11.5%), but included graft thrombosis, bleeding, sepsis, intussusception, and colonic ischemia. Wound infection was the most common cause of morbidity. The swine model is an attractive alternative to that of other animals for the study of prosthetic vascular graft infections. Further details of the operative technique and the comparison to the human and other animal models is discussed.

Animals↗
PubMed1990

Effect of basolateral acidification on the frog oxynticopeptic cell.

The effects of intracellular acidosis induced by acidification of the basolateral (nutrient) perfusate on the structure and function of the oxynticopeptic cell were studied in in vitro frog gastric mucosa. Changing the pH of the unbuffered nutrient perfusate (UNB) from 7.2 to 3.5 acidified the oxynticopeptic cell with no change in potential difference (PD) or resistance (R). Intracellular pH (pHi), PD, and R were 7.05 +/- 0.01, 16 +/- 1 mV, 165 +/- 7 omega.cm2 before and 6.44 +/- 0.01, 16 +/- 2 mV, 170 +/- 9 omega.cm2 after nutrient acidification. Acid secretion (H+) increased from 0.86 +/- 0.07 to 1.88 +/- 0.18 mu eq.cm-2.h-1. Addition of forskolin to tissues perfused with nutrient pH (pHn) 3.5 decreased PD to 2 +/- 2 mV and further increased H+ to 3.07 +/- 0.19 mu eq.cm-2.h-1. By light and electron microscopy oxynticopeptic cells perfused with UNB, pHn 3.5, appeared normal. Oxynticopeptic cells in tissues pretreated with omeprazole and then exposed to UNB, pHn 3.5, had extensive morphological damage. On increasing the pH of the nutrient perfusate from 3.5 to 7.2 there was prompt recovery of pHi in untreated and forskolin-stimulated mucosae (pHi 6.87 +/- 0.06 and 6.85 +/- 0.04) but no recovery of pHi in tissues pretreated with omeprazole or cimetidine (pHi 6.26 +/- 0.04 and 6.44 +/- 0.06, n = 6, 30 min after reexposure to UNB, pHn 7.2). We conclude that in a secreting mucosa intracellular acidification of the oxynticopeptic cell to pHi 6.4 is associated with normal morphology, PD, R, and increased H+, and that intracellular acidosis is not de facto deleterious.

Animals↗