Biomedical subjects

R M Moore

Publications and source records attributed to R M Moore.

At least 55 records · Page 3Linked to original sources

PubMed1996

Effect of high-molecular weight dextran macromolecules on low-flow ischemia and reperfusion of the large colon in horses.

OBJECTIVE: To evaluate the effect of high-molecular weight (MW) dextran macromolecules on low-flow ischemia and reperfusion of the large colon in horses. DESIGN: Horses subjected to low-flow ischemia and reperfusion of the large colon were treated with either 0.9 NaCl (group 1, n = 6) or high-MW dextran (group 2, n = 6) solutions. ANIMALS: 12 adults horses. PROCEDURE: Horses were subjected to 3 hours' low-flow ischemia followed by 3 hours' reperfusion. A dose of either 0.9% NaCl or a 6% solution of high-MW (250,000) dextran (10 ml/kg of body weight) was administered i.v., 30 minutes prior to reperfusion. Hemodynamic variables were recorded at 30-minute intervals. Systemic arterial and colonic venous blood were collected for determination of PCV, plasma total protein, and whole blood lactate concentrations, and for blood gas and oximetry analyses. Histologic examination of large-colon biopsy specimens was performed. RESULTS: Mean arterial pressure was greater in group-2 horses, compared with group-1 horses, from 3 to 3.25 hours, but there were no significant differences between groups for any of the other hemodynamic variables. Compared with baseline values, colonic blood flow was significantly lower from 0.5 to 3 hours and was significantly greater from 3.25 to 6 hours. Arterial and colonic venous PCV were significantly lower than baseline values from 3 to 3.25 hours, and at 3 hours, respectively, in group-2 horses. These values were significantly lower in group-2 horses, from 3 to 6 and 3 to 5 hours, respectively. There was significant mucosal necrosis, hemorrhage, edema, and neutrophil infiltration in horses of both groups; however, there were no significant differences between the 2 groups. CONCLUSIONS: High-MW dextran did not protect the colonic mucosa from low-flow ischemia and reperfusion; there were no deleterious effects on colonic mucosa or on systemic hemodynamic or metabolic variables. CLINICAL RELEVANCE: Reperfusion with high-MW dextran solution probably would not protect the large colon from ischemia-reperfusion injury associated with large-colon volvulus.

Animals↗

PubMed1996

Alterations in colonic arterial and venous plasma neuropeptide concentrations in horses during low-flow ischemia and reperfusion of the large colon.

OBJECTIVE: To measure colonic arterial (CA) and colonic venous (CV) plasma neuropeptide concentrations during low-flow ischemia and reperfusion of the large colon in horses. ANIMALS: 10 adult horses. PROCEDURE: CA and CV plasma samples collected from anesthetized horses during experimentally induced low-flow colonic ischemia and reperfusion were assayed for vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and substance P (SP), using radioimmunoassays. In 6 anesthetized horses, colonic ischemia (20% of baseline (BL]) was maintained for 3 hours, then blood flow was restored and monitored for 3 hours. Hemodynamic variables were monitored continuously and recorded at 30-minute intervals. CA resistance was calculated from colonic blood flow (Q(colon)) and mean CA pressure values at each time. Blood was obtained from CA and CV catheters at 0, 1, 2, 3, 3.25, 3.5, 4, 5, and 6 hours; plasma VIP, CGRP, and SP concentrations were quantified, using radioimmunoassays. In 4 additional horses, VIP and CGRP were measured in CA and CV blood at 0, 0.25, 0.5, 0.75, and 1 hour. RESULTS: Heart rate was significantly increased at 5.5 and 6 hours; other alterations in systemic hemodynamic variables were not significant. Decrease in Q(colon) during ischemia was significant; Q(colon) rebounded to a value significantly greater than BL value within 5 minutes of reperfusion and was maintained above the BL value during 3 hours of reperfusion. Mean CA pressure was significantly decreased during ischemia, but returned to a value not different from the BL value by 3.25 hours. Mean CV pressure remained unchanged from the BL value during ischemia, but increased to a value significantly greater than the BL value by 3.25 hours and remained increased through 6 hours. CA resistance began to decrease during early ischemia and was significantly less than the BL value by 3.25 hours; it remained less than the BL value through 4 hours. Increase in CV VIP concentration was significant by 0.25 hour of ischemia, but decreased to a value not different from BL value by 3.25 hours. Increase in CV CGRP was significant at 3.25 hours, but this variable returned to a value not different from BL value by 3.5 hours. CONCLUSIONS: CV VIP concentration increases during low-flow colonic ischemia, and CV and CA CGRP and CA SP concentrations increase during early reperfusion.

Animals↗

PubMed1995

Arthroscopic findings in the carpal joints of lame horses without radiographically visible abnormalities: 41 cases (1986-1991).

Arthroscopy was performed in 1 carpal joint unilaterally in 27 horses and either in 2 carpal joints unilaterally or 1 carpal joint bilaterally in 7 horses. All horses were lame, but the cause of lameness could not be determined from radiographs. Twenty-seven carpi did not have radiographically visible abnormalities; the remaining 14 had only mild to moderate lucency or sclerosis of the radial facet of the third carpal bone. The primary abnormalities identified during arthroscopy included a crush fracture of the third carpal bone (7 carpi), an incomplete fracture of the third carpal bone in the frontal plane (13 carpi), an incomplete fracture of the third carpal bone in the sagittal plane (1 carpus), a crush fracture of the radial carpal bone (1 carpus), a chip fracture of the intermediate carpal bone (1 carpus), damage to the articular cartilage of the third carpal bone (12 carpi), tearing or fraying of the medial palmar intercarpal ligament (4 carpi), and synovitis (2 carpi). All of the horses in this study were racehorses (29 Standardbreds and 5 Thoroughbreds), and race records were used to evaluate performance before and after surgery. Twenty-four of 34 horses raced preoperatively, and 25 of 34 raced postoperatively. Twenty-three of the 27 (85%) horses in which a single joint was examined raced postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Mural blood flow distribution in the large colon of horses during low-flow ischemia and reperfusion.

Six horses were subjected to 3 hours of low-flow ischemia and 3 hours of reperfusion of the large colon. After induction of anesthesia, the large colon was exteriorized through a ventral midline celiotomy. Colonic blood flow was measured continuously, using Doppler ultrasonic flow probes placed on the colonic arteries supplying the dorsal and ventral colons and was allowed to stabilize for 15 to 30 minutes after instrumentation. Low-flow ischemia was induced by reducing colonic arterial blood flow to 20% of baseline (BL) flow. Colonic mucosal, seromuscular, and full-thickness blood flow were determined on a tissue-weight basis by injecting colored microspheres proximally into the colonic artery supplying the ventral colon. Reference blood samples were obtained at a known flow rate from the colonic artery and vein at a site more distal to the site of injection. Left ventral colon biopsy specimens were harvested at BL, 3 hours of ischemia, and 15 minutes of reperfusion. Blood and tissue samples were digested and filtered to collect the microspheres, and dimethylformamide was added to release the colored dyes. Dye concentration in blood and tissue samples was measured by use of spectrophotometry, and tissue-blood flow was calculated. Data were analyzed, using two-way ANOVA for repeated measures; statistical significance was set at P < 0.05. Doppler blood flow decreased to approximately 20% of BL, whereas microsphere blood flow ranged between 13.7 and 15.5% of BL at 3 hours of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Systemic and colonic venous plasma eicosanoid and endotoxin concentrations, and colonic venous serum tumor necrosis factor and interleukin-6 activities in horses during low-flow ischemia and reperfusion of the large colon.

Twenty-four horses were randomly allocated to 3 groups. Horses were anesthetized, subjected to a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls. Group-2 horses were subjected to 6 hours of low-flow colonic arterial ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline (BL) samples were collected, then low-flow ischemia was induced by reducing ventral colonic arterial blood flow to 20% of BL. All horses were monitored for 6 hours after BL data were collected. Blood samples were collected from the colonic vein and main pulmonary artery (systemic venous [SV]) for measurement of plasma endotoxin, 6-keto prostaglandin F1 alpha (6-kPG), thromboxane B2 (TXB2), and prostaglandin E2 (PGE2) concentrations. Tumor necrosis factor and interleukin-6 activities were measured in colonic venous (CV) serum samples. Data were analyzed, using two-way ANOVA, and post-hoc comparisons were made, using Dunnett's and Tukey's tests. Statistical significance was set at P < 0.05. Endotoxin was not detected in CV or SV plasma at any time. There was no detectable tumor necrosis factor or interleukin-6 activity in CV samples at any time. There were no differences at BL among groups for CV or SV 6-kPG, PGE2, or TXB2 concentrations, nor were there any changes across time in group-1 horses.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1995

Systemic and colonic venous hemostatic alterations in horses during low-flow ischemia and reperfusion of the large colon.

Twenty-four horses were randomly allocated to 3 groups. All horses underwent a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls, group-2 horses underwent 6 hours of colonic ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline blood samples were collected, then low-flow colonic ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. All horses were monitored for 6 hours. Citrated systemic venous (SV) blood samples were collected from the main pulmonary artery, and colonic venous (CV) samples were collected from the colonic vein draining the ventral colon. Samples were collected at 0, and 2, 3, 3.25, 4, and 6 hours for determination of one-stage prothrombin time, activated partial thromboplastin time, antithrombin III activity, and fibrinogen concentration. Data were analyzed statistically, using two-way ANOVA for repeated measures, and post-hoc comparisons were made by use of Student Newman Keul's test. Statistical significance was set at P < 0.05. There were significant decreases in all hemostatic variables by 2 hours in SV and CV samples from horses of all 3 groups, but there were no differences among the 3 groups for any of these variables. These hemostatic alterations could have been secondary to a hypercoagulable state or to fluid therapy-induced hemodilution. Colonic ischemia-reperfusion was not the cause of these alterations because these alterations also were observed in the sham-operated control horses. Significant temporal alterations existed even after accounting for the hemodilution.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1995

Effects of dimethyl sulfoxide, allopurinol, 21-aminosteroid U-74389G, and manganese chloride on low-flow ischemia and reperfusion of the large colon in horses.

Thirty horses were randomly assigned to 1 of 5 groups. All horses were anesthetized and subjected to ventral midline celiotomy, then the large colon was exteriorized and instrumented. Colonic arterial blood flow was reduced to 20% of baseline (BL) and was maintained for 3 hours. Colonic blood flow was then restored, and the colon was reperfused for an additional 3 hours. One of 5 drug solutions was administered via the jugular vein 30 minutes prior to colonic reperfusion: group 1, 0.9% NaCl; group 2, dimethyl sulfoxide: 1 g/kg of body weight; group 3, allopurinol: 25 mg/kg; group 4, 21-aminosteroid U-74389G: 10 mg/kg; and group 5, manganese chloride (MnCl2): 10 mg/kg. Hemodynamic variables were monitored and recorded at 30-minutes intervals. Systemic arterial, systemic venous (SV), and colonic venous (CV) blood samples were collected for measurement of blood gas tensions, oximetry, lactate concentration, PCV, and plasma total protein concentration. The eicosanoids, 6-keto prostaglandin F1 alpha, prostaglandin E2, and thromboxane B2, were measured in CV blood, and endotoxin was measured in CV and SV blood. Full-thickness biopsy specimens were harvested from the left ventral colon for histologic evaluation and determination of wet weight-to-dry weight ratios (WW:DW). Data were analyzed, using two-way ANOVA for repeated measures, and statistical significance was set at P < 0.05. Heart rate, mean arterial pressure, and cardiac output increased with MnCl2 infusion; heart rate and cardiac output remained increased throughout the study, but mean arterial pressure returned to BL values within 30 minutes after completion of MnCl2 infusion. Other drug-induced changes were not significant. There were significant increases in mean pulmonary artery and mean right atrial pressures at 2 and 2.5 hours in horses of all groups, but other changes across time or differences among groups were not observed. Mean pulmonary artery pressure remained increased through 6 hours in all groups, but mean right atrial pressure had returned to BL values at 3 hours. Mean colonic arterial pressure was significantly decreased at 30 minutes of ischemia and remained decreased through 6 hours; however, by 3.25 hours it was significantly higher than the value at 3 hours of ischemia. Colonic arterial resistance decreased during ischemia and remained decreased throughout reperfusion in all groups; there were no differences among groups for colonic arterial resistance.(ABSTRACT TRUNCATED AT 400 WORDS)

Allopurinol↗

PubMed1994

Examination of the equine patient with gastrointestinal emergency.

Clinical examination of the equine patient with acute abdominal pain should identify the affected body system and yield a provisional diagnosis. Determination of signalment, history, physical examination, and basic laboratory tests should assist in classification of the gastrointestinal disorder and direct the therapeutic plan. Determination of the definitive diagnosis of abdominal pain based on clinical examination is not crucial. For a successful outcome, efforts should be directed toward early recognition of the need for surgery and treatment of cardiovascular compromise in horses with severe gastrointestinal disease.

Animals↗

PubMed1994

Histopathologic evidence of reperfusion injury in the large colon of horses after low-flow ischemia.

Effects of low-flow ischemia and reperfusion of the large colon on mucosal architecture were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline values. Systemic hemodynamic and metabolic variables were maintained constant and in a normal physiologic range. Full-thickness biopsy specimens were obtained from the left ventral colon for histomorphologic and morphometric examination at baseline and at 30-minute intervals for 6 hours; additional biopsy specimens were collected at 185, 190, and 195 minutes (corresponding to 5-, 10-, and 15-minute periods of reperfusion in group-3 horses). There were no differences among groups at baseline or across time in group-1 horses for any of the histopathologic variables. There were significant (P < 0.05) increases in percentage of surface mucosal disruption, estimated and measured percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, and cellular debris index during 0 hour to 3 hours, compared with baseline, and from 3 hours to 6 hours, compared with 3 hours in horses of groups 2 and 3. Estimated percentage depth of mucosal loss and cellular debris index were significantly (P < 0.05) greater in group-3 horses, compared with group-2 horses during the interval from 3 to 6 hours. There were trends toward greater percentage of surface mucosal disruption and mucosal edema during the early phase of reperfusion (3 to 4 hours) and greater mucosal hemorrhage, measured percentage depth of mucosal loss, and mucosal interstitial-to-crypt ratio during the late phase (4 to 6 hours) of reperfusion in group-3 horses vs group-2 horses. Reestablishment of colonic arterial blood flow after low-flow ischemia caused greater mucosal injury than did a comparable period of continued ischemia. Thus, reperfusion injury was detected in the large colon of horses after low-flow arterial ischemia. The serial mucosal alterations that developed in the colon were comparable in horses of groups 2 and 3; however, reperfusion exacerbated colonic mucosal injury.

Analysis of Variance↗

PubMed1994

Characterization of the hemodynamic and metabolic alterations in the large colon of horses during low-flow ischemia and reperfusion.

Effects of low-flow ischemia and reperfusion of the large colon on systemic and colonic hemodynamic and metabolic variables were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. Heart rate, arterial blood pressures, cardiac index, pulmonary artery pressure, right atrial pressure, and colonic blood flow were monitored. Arterial, mixed-venous, and colonic venous blood gas and oximetry analyses; PCV; and blood lactate and pyruvate and plasma total protein concentrations were measured. Data were recorded, and blood samples were collected at baseline and at 30-minute intervals for 6 hours; additionally, data were collected at 185, 190, and 195 minutes (corresponding to 5, 10, and 15 minutes of reperfusion in group-3 horses). There were no differences among groups at baseline or across time for any systemic hemodynamic or metabolic variable. Colonic blood flow did not change across time in group-1 horses. Colonic blood flow significantly (P < 0.05) decreased to 20% of baseline at induction of ischemia in horses of groups 2 and 3 and remained significantly decreased throughout the ischemic period in horses of groups 2 (6 hours) and 3 (3 hours). Colonic blood flow significantly (P < 0.05) increased above baseline by 5 minutes of reperfusion in group-3 horses. Colonic oxygen delivery and oxygen consumption, and colonic venous pH, PO2, percentage saturation of hemoglobin, and oxygen content were significantly (P < 0.05) decreased within 30 minutes after induction of ischemia in horses of groups 2 and 3; colonic venous PCO2, colonic oxygen extraction ratio, and lactate and pyruvate concentrations were significantly (P < 0.05) increased by 30 minutes of ischemia. These alterations continued throughout ischemia, but within 5 minutes of reperfusion in group-3 horses, these variables either returned to baseline (pH, PCO2, lactate, pyruvate), significantly (P < 0.05) increased above baseline (PO2, oxygen content, % saturation of hemoglobin), or significantly (P < 0.05) decreased below baseline (colonic oxygen extraction ratio). Colonic oxygen consumption remained decreased during reperfusion in group-3 horses. Colonic mucosal ischemia-reperfusion injury observed in this model of ischemia was associated with local colonic hemodynamic and metabolic alterations in the presence of systemic hemodynamic and metabolic stability.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Neutrophil accumulation in the large colon of horses during low-flow ischemia and reperfusion.

Histomorphologic/morphometric evaluation, leukocyte scintigraphy, and myeloperoxidase activity were used to determine whether neutrophils accumulate in the large colon of horses during low-flow ischemia and reperfusion. Twenty-four adult horses were assigned to 1 of 3 groups: group 1, sham-operated (n = 6); group 2, 6 hours of ischemia (n = 9); and group 3, 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia of the large colon was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. Radiolabeled (99mTc) autogenous neutrophils were injected at 175 minutes, which corresponded to 5 minutes prior to reperfusion in group-3 horses. Full-thickness biopsy specimens of the left ventral colon were collected at baseline and at 30-minute intervals for 6 hours; a portion of the biopsy specimen was placed in formalin for histologic examination, and the remainder was used to measure mucosal radioactivity and myeloperoxidase activity. There were no differences in baseline mucosal neutrophil index, mucosal neutrophil numbers, submucosal venular neutrophil numbers, mucosal radioactivity, or mucosal myeloperoxidase activity among groups, or over time in group-1 horses. Neutrophils accumulated in the colonic mucosa during ischemia and further increased at reperfusion, as indicated by neutrophil index (morphology) and mucosal neutrophil numbers (morphometry); mucosal neutrophil index was significantly (P < 0.05) greater in group-3 horses during reperfusion than at the corresponding periods of ischemia in group-2 horses. Neutrophil numbers were significantly (P < 0.05) increased in submucosal venules at 10 minutes of reperfusion in group-3 horses and were significantly (P < 0.05) greater in group-3 than in group-2 horses during the interval from 3 to 6 hours. Mucosal radioactivity significantly (P < 0.05) increased at reperfusion in group-3 horses; there was a trend (P = 0.076) toward greater mucosal radioactivity in group-3, compared with group-2 horses, throughout the 3- to 6-hour interval. There were no differences in mucosal myeloperoxidase activity among or within any of the 3 groups over time. Neutrophils accumulated in the large colon of horses during low-flow ischemia and reperfusion. Neutrophil infiltration was detected by histologic examination and leukocyte scintigraphy, but not by measurement of myeloperoxidase activity. The accumulation of neutrophils during ischemia and the further neutrophil infiltration during reperfusion indicate that neutrophils may contribute to reperfusion injury of the large colon.

Animals↗

PubMed1993

Protein kinase A activators inhibit agonist induced prostaglandin production in human amnion.

Prostaglandin (PG) production by human amnion has been postulated to have a role in the onset of labor. Previous work by ourselves and others has demonstrated that oxytocin, phorbol esters and epidermal growth factor (EGF) increase PGE2 production in human amnion cells by activation of the Phospholipase C/Protein Kinase C (PKC) cascade system. The present study was undertaken to determine the effect of prior activation of the Adenylate Cyclase cascade system upon subsequent stimulation of PGE2 production by oxytocin, phorbol 12-myristate-13-acetate (PMA) or EGF in amnion cells and membrane discs. Isoproterenol, forskolin and dibutyryl cyclic adenosine monophosphate (dbcAMP) were utilized to activate the Adenylate Cyclase system at the receptor, enzyme and second messenger level. In control amnion cells, oxytocin, PMA and EGF each provoked dose dependent increases in PGE2 production. In cells preincubated with dbcAMP, forskolin or isoproterenol, agonist stimulated PGE2 production was markedly (50-90%) inhibited (p < 0.01). Inhibition was dose dependent upon preincubator concentrations. Maximal inhibition by adenylate cyclase activators occurred with 2-4 h of preincubation. In membrane discs, forskolin preincubation also inhibited oxytocin, PMA and EGF stimulation of PGE2 production. Activation of the Adenylate Cyclase system in human amnion cells or membrane discs inhibits the subsequent action of potent stimulators of PGE2 production in human amnion.

Adenylyl Cyclases↗

PubMed1993

Ritodrine: a beta-adrenergic receptor antagonist in human amnion.

OBJECTIVE: Human amnion is important in the initiation of labor. Ritodrine, when administered as a tocolytic, is found unchanged in amniotic fluid. We characterized effects of ritodrine binding to beta-adrenergic receptors in amnion and amniocytes. STUDY DESIGN: Iodine 125-iodopindolol, beta-adrenergic receptor agonists, and beta-adrenergic receptor antagonists were used to describe binding characteristics. Experiments were designed with and without isoproterenol and ritodrine to study intracellular cyclic adenosine 3'5'-monophosphate and prostaglandin E2 release. RESULTS: Scatchard analysis revealed a single class of saturable binding sites, with maximum binding capacity of 70.0 +/- 17.2 fmol/mg protein (n = 12) and with high-affinity dissociation constant of 458.9 +/- 72.1 pmol/L. Agonists and antagonists competed for the 125I-iodopindolol binding site consistent with a beta 2-adrenergic receptor. Hill coefficients were 0.6 to 0.8 for agonist competition and 1.0 for antagonist competition and ritodrine. Stimulation with isoproterenol resulted in dose-dependent increases in cyclic adenosine 3'5'-monophosphate and prostaglandin E2. Ritodrine failed to stimulate cyclic adenosine 3'5'-monophosphate and inhibited isoproterenol-stimulated cyclic adenosine 3'5'-monophosphate and prostaglandin E2 production. CONCLUSION: In human amnion binding of ritodrine to beta 2-adrenergic receptors and lack of ritodrine-mediated postreceptor effects are characteristic of a beta 2-adrenergic antagonist.

Amnion↗

PubMed1993

An overview of occupational hazards among veterinarians, with particular reference to pregnant women.

Veterinarians are challenged by an imposing group of occupational hazards, including exposure to ionizing radiation, injury, infectious agents, and chemicals. In this paper, the health hazards in the typical veterinary practice are inventoried, and the risks of each are assessed. During the past few decades, there has been a significant increase in women entering the veterinary profession. Information is presented concerning the impact of various occupational hazards on the health of female practitioners and paraprofessionals, particularly in regard to the reproductive system. Many of the occupational hazards are exclusively, or more significantly, detrimental to females (particularly when pregnant) and to their unborn. Women must be aware of and avoid these hazards in their clinical environment. The purpose of this review is to assist practitioners in identifying and assessing the hazards in their practice and determining what steps must be taken to eliminate or reduce them.

Animals↗

PubMed1993

The prevalence of tympanostomy tubes in children in the United States, 1988.

Information from the 1988 National Health Interview Survey Medical Device Implant Supplement was used to obtain the first population estimates of the prevalence of implanted tympanostomy tubes, a common treatment for otitis media. The prevalence rate was estimated to be 13 per 1000 children aged younger than 18 years. Statistically significant differences in prevalence were found for sex (boys, 15/1000; girls, 10/1000), race (Whites, 15/1000; others, 4/1000), and activity level ("limited," 44/1000; others, 11/1000). Thirty percent of the tubes were replacements; infection was the reason for 75% of the original implants. The morbidity and costs associated with tympanostomy tubes are of public health importance.

Adolescent↗

PubMed1993

The prevalence of internal orthopedic fixation devices in children in the United States, 1988.

This study provides the first estimated prevalence of implanted orthopedic fixation devices (e.g., pins or wires) among children in the United States, based on the Medical Device Implant Supplement to the 1988 National Health Interview Survey. The overall prevalence was 27 per 10,000 children younger than 18 years; prevalence was highest (59/10,000) among those aged 12 to 17 years. The lower extremities were the most frequent body site (43%) and injury was the leading specific reason for implantation (37%). Some (10%) were replacement implants.

Adolescent↗

PubMed1993

National survey of self-reported breast implants: 1988 estimates.

This report provides the first population-based national estimates of the prevalence of adult women with breast implants in the U.S. These findings are based on the Medical Device Implant Supplement to the 1988 National Health Interview Survey. The overall prevalence was 33 implant recipients (95% confidence limits [CL]: 26 to 40) per 10,000 women. Almost three-fourths had two implants: prevalence peaked at 85 (59 to 100) per 10,000 for women aged 35 to 44 years. Implant prevalence was statistically significantly greater among women who were white, residents of the south and west, had higher family income, and had more education, who worked, or were slim. Among current implants, 87% were original. Complications were reported for 24% of the implants.

Adolescent↗

PubMed1992

Racial differences in the prevalence of intraocular lens implants in the United States.

We generated population-based estimates of the prevalence of intraocular lens implants by using the 1988 Medical Device Implant Supplement to the National Health Interview Survey. This national survey of a probability sample of the civilian noninstitutionalized United States population comprised 47,485 households and 122,310 persons. To produce national projections, we used survey respondent-reported data based on 1,941 reported intraocular lenses in 1,337 persons. Projected to the United States population, an estimated 2.6 million people had a total of 3.8 million lens implants. The predominant reason for the implant was cataract. The intraocular lens replacement rate was 0.9%. The use of intraocular lens implants was statistically significantly different from the general population in persons with the following socioeconomic characteristics: age (65 years or older), race (white), gender (female), annual family income (less than $20,000, although more commonly at or above the poverty threshold), and education (less than high school). The prevalence rates per 1,000 persons according to age were as follows: 0.3 for persons 44 years old or younger, 9.9 for persons 45 to 64 years old, 33.3 for persons aged 65 to 69 years, 63.5 for persons aged 70 to 74 years, and 113.5 for persons 75 years old or older.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗