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Biomedical subjects

M M Henry

Publications and source records attributed to M M Henry.

At least 73 records · Page 4Linked to original sources

Effect of dietary linolenic acid on endotoxin-induced thromboxane and prostacyclin production by equine peritoneal macrophages.

In laboratory animals, the incorporation of alpha linolenic acid or other n-3 series fatty acids into the diet results in marked changes in cell membrane composition as well as arachidonic acid metabolism. The purpose of the present study was to determine whether endotoxin-induced thromboxane A2 (TxA2) and/or prostacyclin (PGI2) production by equine peritoneal macrophages was altered by feeding horses a diet containing 8% linseed oil as a source of alpha linolenic acid for 8 weeks. Peritoneal macrophages were cultured in vitro in the presence of endotoxin (LPS) (0.5-500 ng/ml) or calcium ionophore for 6 and 24 hours. After horses were fed the alpha linolenic acid-enriched diet, their peritoneal macrophage production of TxA2 was reduced in response to 0.5 ng/ml and 5 ng/ml LPS. compared to that before the diet (P less than .05). The production of PGI2 during 6 hour incubation with 5 ng/ml and 50 ng/ml LPS and during 24 hour incubation with 5 ng/ml LPS were reduced, compared to that before the diet (P less than .05). Peritoneal macrophage production of PGI2 during 24 hour incubation with nothing, LPS (0.5 ng/ml, 5 ng/ml and 500 ng/ml), and calcium ionophore was greater than during 6 hour incubation, after horses were fed the ALA-rich diet (P less than .05). Results suggest that linseed oil supplementation may be an aid in prophylaxis of endotoxemia in horses.

Animals↗

Neurologic cause of idiopathic incontinence.

The relationship between the pudendal and perineal nerve terminal motor latencies and descent (weakness) of the perineum on straining was investigated in 31 patients with idiopathic fecal incontinence, and in 30 patients with double incontinence. Pelvic floor descent was correlated with increased pudendal nerve terminal motor latency in both groups of patients. In the patients with double incontinence, there was a less significant correlation between perineal descent and increased perineal nerve terminal motor latency. In the patients with fecal incontinence, but without urinary incontinence, there was no correlation between perineal descent and perineal nerve terminal motor latency. These data support the concept that pelvic floor weakness can result in damage to the pudendal and perineal nerves, leading to fecal and urinary incontinence. In patients with isolated fecal incontinence the perineal nerves are relatively spared. Thus these common types of incontinence probably have a neurologic cause, and neurophysiologic methods can be used in their assessment.

Adult↗

Delayed external sphincter repair for obstetric tear.

In some patients with faecal incontinence due to an obstetric tear of the external and sphincter there is additional weakness of the anal sphincter muscles from damage to the innervation of these muscles during delivery. Of 19 patients who required surgical repair of an obstetric sphincter tear some months or years after injury, 9 (47 per cent) had evidence of pudendal nerve damage at pre-operative anorectal physiological investigation. The result of surgical repair was excellent or good in eight of the ten patients in whom there was no evidence of nerve damage, while this was the case in only one of the nine patients with nerve damage. These results are significantly different (P = 0.018). Thus the functional result of delayed anal sphincter repair after obstetric lesions is partly dependent upon whether the nerve supply is intact. Pre-operative physiological evaluation can give information on the probability of a successful surgical result.

Adult↗

Temperature gradient between the rectum and the anal canal: evidence against the role of temperature sensation as a sensory modality in the anal canal of normal subjects.

Temperature difference between the rectum and anal canal is a fundamental requirement for the hypothesis that temperature sensation is of physiological importance in discrimination of anorectal contents occurring during the 'sampling reflex'. The temperature gradient between the rectum and the anal canal was measured in 47 normal subjects (mean age 51.6 years +/- 16.8 s.d., 24 men). The maximum mean difference in temperature between the rectum and the anal canal was 0.13 degrees C (0.06-0.19, 95 per cent confidence intervals) and occurred 4 cm from the anal verge. This difference is too small to be detected by the anal canal mucosa. Under normal physiological circumstances the conscious appreciation of temperature of faeces passing from the rectum to the anal canal is impossible during the anorectal sampling reflex.

Adult↗

Increase in pudendal nerve terminal motor latency with defaecation straining.

The relationship between perineal descent and pudendal nerve damage was tested in 57 consecutive patients by measuring the left and right pudendal nerve terminal motor latency (PNTML) before and after a maximal defaecation straining effort. In 13 patients the PNTML was also measured 1 and 4 min later. The difference between the mean PNTML before and after straining (delta PNTML) was correlated with the amount of descent (r = 0.40, P less than 0.005), and with the perineal position during straining (r = -0.46, P less than 0.001). Four minutes after the straining effort the PNTML again approached the resting value in each subject. These findings support the concept that perineal descent causes pudendal nerve damage.

Adult↗

Asymmetrical pudendal nerve damage in pelvic floor disorders.

Differences in the left and right pudendal nerve terminal motor latencies have been observed in patients with pelvic floor disorders. Until now the mean value of the left and right pudendal latencies has been used as the index of pudendal neuropathy. In 22 patients of a group of 156 patients studied the pudendal nerve terminal motor latency was abnormally raised on one side only. These patients are thought to have pudendal neuropathy whether or not the mean value of the left and right pudendal latencies is also raised. This observation may have therapeutic implications.

Adult↗

Fecal incontinence and rectal prolapse.

The majority of patients who suffer from full-thickness prolapse can be treated successfully and safely. The small proportion who remain incontinent of feces after correction of prolapse may at a later date be helped by postanal repair. If dietary indiscretion and abnormal patterns of defecation are major etiologic factors in this condition, then measures to improve dietary and defectory habits must be instituted mainly to prevent further problems after the deformity has been cured surgically. There seems no doubt that following rectopexy there is an increased tendency to constipation.

Fecal Incontinence↗

Combined sensory and motor deficit in primary neuropathic faecal incontinence.

Eleven patients with idiopathic faecal incontinence (IFI) and nine normal controls were studied with techniques of mucosal electrosensitivity and rectal distention for the quantitative assessment of anal and rectal sensation and with manometric and electromyographic tests for the assessment of anorectal motor function. The tests of motor function showed pelvic floor motor neuropathy in the patients with IFI, compared with controls, anal canal resting and voluntary contraction pressures were significantly (p less than 0.05, p less than 0.002) lower, pudendal nerve terminal motor latency and external anal sphincter fibre density were significantly (p less than 0.05, p less than 0.05) raised. The results of mucosal electrosensitivity (MES) disclosed a sensory deficit in the anal canal in patients with IFI, compared with controls, MES threshold was significantly (p less than 0.002) higher. Sensory thresholds to rectal distension were similar in the two groups. This study shows that sensory deficit of the anal canal occurs in combination with the motor neuropathy of the anal canal musculature in primary neuropathic faecal incontinence.

Adult↗

Pelvic floor neuropathy: a comparative study of diabetes mellitus and idiopathic faecal incontinence.

Twenty one patients with diabetic peripheral neuropathy, 18 with idiopathic faecal incontinence and 11 normal controls were studied with techniques of mucosal electrosensitivity, rectal distension for the quantitative assessment of anorectal sensation, and manometric and electromyographic tests for the assessment of anorectal motor function. An asymptomatic sensorimotor deficit was found in the anal canal of patients with diabetic peripheral neuropathy. Mucosal electrosensitivity thresholds in the anal canal were significantly higher (p less than 0.01 v controls) and fibre density of the external anal sphincter significantly raised (p less than 0.0001 v controls). Anal manometry and pudendal nerve terminal motor latencies were similar to controls. In patients with idiopathic faecal incontinence the tests of sensory and motor function also showed a sensorimotor neuropathy; compared with controls, mucosal electrosensitivity thresholds were significantly higher (p less than 0.002), anal canal resting and maximum squeeze pressures were significantly lower (p less than 0.05 and p less than 0.002 respectively), and pudendal nerve terminal motor latencies and fibre density of the external anal sphincter were significantly raised (both p less than 0.05). Sensory thresholds to rectal distension were similar in all groups. Pelvic floor sensorimotor neuropathy in diabetic patients has several features in common with that of patients with idiopathic faecal incontinence but its functional significance remains uncertain.

Adult↗

Lower respiratory illness in early childhood and lung function and bronchial reactivity in adolescent males.

We examined the relationship between lower respiratory illness (LRI) experience in early childhood and lung function and bronchial reactivity in 57 boys, 11 to 22 yr of age, whose histories of outpatient physician visits for wheezing and nonwheezing LRI had been documented prospectively during their first 6 yr of life. These boys were a subpopulation of 159 children whose early childhood LRI experience and spirometric performance had been studied an average of 4 yr previously. The majority of boys had been free of chronic respiratory symptoms in the 2 yr before evaluation. Boys with histories of 2 or more preschool wheezing illnesses had lower mean levels of performance for FEV1, FEF25-75, FEF50, FEF75, and FEV1/FVC than did boys who had zero or 1 preschool wheezing illness, replicating observations that had been made when the boys had been studied 4 yr previously. Boys with lower spirometric performance relative to the study population on initial testing continued to have lower relative levels of spirometric performance 4 yr later. Neither preschool wheezing nor nonwheezing illness experience was associated with the degree of methacholine sensitivity measured in adolescence. Increasing degrees of methacholine sensitivity were associated with lower levels of spirometric performance; however, preschool wheezing illness experience remained a significant correlate of spirometric performance after adjustment for level of methacholine sensitivity. We conclude that recurrent preschool wheezing illness in these adolescent boys was associated with persistently lower lung function, but not enhanced methacholine sensitivity, during the middle to late school years.

Adolescent↗

Combined sphincter repair and postanal repair for the treatment of complicated injuries to the anal sphincters.

The management of seven patients with multiple injuries to the anal sphincter musculature and its nerve supply, from major pelvic trauma, anal fistula surgery, or obstetric trauma, was reviewed. All were either incontinent of solid stools or had defunctioning colostomies. Anal manometry was abnormal in all patients. Concentric needle electromyography (EMG) showed anterior division of the external sphincter in all the patients; five also had posterior division of both the external sphincter and puborectalis. EMG abnormalities were found in the lateral quadrants of these muscles, particularly the external sphincter. Single fibre needle EMG showed evidence of reinnervation in the external sphincter in six patients, and in the puborectalis in two, indicating partial denervation of the muscles. Treatment was by anterior sphincter repair using an overlapping technique, combined with postanal repair; the repairs were protected by a defunctioning colostomy. When assessed 4-60 months (mean 17 months) after colostomy closure all seven patients were continent of solid and semi-formed stools, but had urgency of defaecation. None could control liquid stool or flatus. After complicated sphincter injuries planned surgical reconstruction, based on EMG assessment of the sphincter muscles, can restore acceptable continence.

Adolescent↗

Endotoxin-induced procoagulant activity in equine peripheral blood monocytes.

Increasing evidence has demonstrated the importance of monocyte procoagulant activity (PCA) in the pathogenesis of coagulopathies in a variety of diseases. Because endotoxin precipitated coagulopathies are common sequelae to intestinal ischemia/endotoxemia in the equine species, we investigated the ability of equine peripheral blood monocytes to express PCA. Monocytes isolated from five healthy adult horses were incubated in vitro with Escherichia coli endotoxin (10 micrograms), and the PCA was measured by the ability of cellular lysates to accelerate the clotting times of equine plasma in a modified one-stage recalcification assay. Equine monocyte PCA was identified as thromboplastin based on lack of clot formation in factor VII-deficient plasma. The induction of PCA occurred as early as 2 hr after endotoxin exposure, peaked at 6 hr (396% increase), and then gradually declined. The amount of PCA was proportional to the dose of endotoxin (0.01 to 100 micrograms) and the number of monocytes. Neither platelets nor neutrophils produced PCA, either in the absence or presence of endotoxin (1 microgram). Lymphocytes at a concentration of 4 x 10(6)/ml RPMI did produce a significant amount of PCA, compared to the time-matched controls. Co-incubation of neutrophils or lymphocytes with monocytes did not alter the PCA, whereas coincubation of platelets and monocytes significantly enhanced the expression of PCA. This effect was further augmented by the addition of endotoxin (1 microgram).

Animals↗

Natural history of anterior mucosal prolapse.

Case notes of 250 patients (M:F, 1:2.7; age 48.7 +/- 16.5 years) in whom anterior mucosal prolapse had been diagnosed, at one hospital between 1974 and 1976, were reviewed. The commonest symptoms were bleeding (56 per cent), pain (32 per cent) and a sense of prolapse (32 per cent). The prevalence of constipation was significantly higher among women (47 per cent) than men (29 per cent). Perineal descent was present in 20 per cent of cases and was significantly more frequently associated with excessive straining at defaecation (28 per cent) compared with patients in whom there was no history of excessive straining (12 per cent). Sixty-six patients (26 per cent) experienced recurring symptoms over the 10 year period following presentation but did not deteriorate, while 28 patients (11 per cent) deteriorated. Deterioration was associated with a history of symptoms for longer than 1 year at the time of presentation, female sex, and the presence of perineal descent on clinical examination. The risk of developing perineal descent was less than 10 per cent over the 5 years after presentation while that of developing sphincter laxity among patients who had already developed perineal descent was 30 per cent over this period. Complete rectal prolapse occurred in 20 per cent (3/15) of patients with clinical perineal descent and sphincter laxity but was not seen in the absence of these signs. The results of treatment by submucosal phenol injection, mucosal rubber banding, or glycerine suppositories were the same.

Adult↗

Relation between perineal descent and pudendal nerve damage in idiopathic faecal incontinence.

In 60 patients with idiopathic anorectal incontinence, without neurological disease, there was a significant relationship, shown by regression analysis, between the pudendal nerve terminal motor latency and the extent of perineal descent during straining (r 0.59; p less than 0.001), and the plane of the perineum on straining (r -0.61; p less than 0.001). These data are consistent with the suggestion that perineal descent can lead to stretch-induced damage to the perineal nerves in this condition.

Action Potentials↗