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Biomedical subjects

J N Moore

Publications and source records attributed to J N Moore.

At least 55 records · Page 3Linked to original sources
PubMed1991

Tumor necrosis factor activity in serum from neonatal foals with presumed septicemia.

A study was performed to determine prevalence of tumor necrosis factor (TNF) activity in serum of equine neonates with presumed sepsis and to determine correlation between serum TNF activity and severity and outcome of disease. Twenty foals less than 21 days old were considered suitable for inclusion in this study by satisfying clinical and laboratory criteria suggestive of septicemia. At admission, blood samples were collected from all foals for determination of serum TNF activity, then clinical course and outcome of disease were recorded. Thirty-one clinically normal foals less than 21 days old served as controls for serum TNF activity. Serum TNF activity was estimated by use of an in vitro cytotoxicity bioassay and WEHI 164 clone-13 murine fibrosarcoma cells. Of the 20 foals with presumed sepsis, 5 had high serum TNF activity. Mean heart rate (P less than 0.005), mucosal petechial hemorrhages (P = 0.06), and death rate (P = 0.06) were greater in the group of foals with high serum TNF activity. These foals also had a lower mean neutrophil count (P less than 0.001), greater band-to-segmented neutrophil ratio (P less than 0.0001), and more prevalent neutrophil toxic changes (P = 0.07) than did foals without serum TNF activity (P = 0.02). Joint swelling was more prevalent in foals without serum TNF activity. Results of the study indicate that serum TNF activity is correlated with clinical criteria of sepsis in equine neonates. An association was apparent between disease severity and serum TNF activity in this group of foals with presumed septicemia.

Animals↗
PubMed1991

Repair of an open radial fracture in an adult horse.

An open radial fracture in an adult horse (450 kg) was repaired by internal fixation, using two 18-hole 4.5-mm broad dynamic compression plates and 5.5- and 4.5-mm bone screws. The fracture healed completely, but when evaluated 9 months after surgery, the horse was lame on the fractured limb at a trot. Local infiltration of anesthesia along the distal half of the bone plates greatly ameliorated the lameness, suggesting that the plates were irritating the soft tissues and extensor tendons along the cranial and lateral aspects of the antebrachium. Both bone plates were removed simultaneously with no complications, and the horse became sound.

Animals↗
PubMed1991

Clinical relevance of monocyte procoagulant activity in horses with colic.

Endotoxin-activated monocytes express a thromboplastin-like procoagulant activity on the cell surface that may serve as a focal point for formation of microvascular thrombi. Because coagulopathy is a common sequela to endotoxemia in the equine species, we investigated the ability of monocytes, isolated from horses with colic, to express procoagulant activity. On the day of admission, and on the third and fifth day of hospitalization, monocytes were isolated from 30 adult horses with colic. A coagulation profile, including prothrombin time, activated partial thromboplastin time, thrombin time, and plasma fibrinogen and serum fibrin degradation products concentrations, was determined at each sample collection. The concentration of endotoxin in the plasma was quantitated at the time of admission. Ten clinically normal adult horses served as controls. The procoagulant activity of monocytes isolated from horses with colic was significantly (P less than 0.05) greater than that of the monocytes isolated from clinically normal horses. On the first and third day of hospitalization, the mean prothrombin time was significantly (P less than 0.05) longer in horses with colic, compared with clinically normal horses, and was the most common abnormality in the coagulation profile on the day of admission (25/30; 83%). Mean fibrin degradation products concentration was significantly (P less than 0.05) greater in horses with colic on the day of admission and was the second most common abnormality in the coagulation profile on day 1 (23/30; 77%). In horses with colic, the mean prothrombin and activated partial thromboplastin times were significantly (P less than 0.05) longer in horses that did not survive, compared with horses that survived.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of an infusion of dopamine on the cardiopulmonary effects of Escherichia coli endotoxin in anaesthetised horses.

Horses with colic may be endotoxaemic and subsequently develop hypotension during anaesthesia for surgical operation. The aim of this study was to evaluate the efficacy of dopamine as a means to improve cardiovascular function in anaesthetised endotoxaemic horses. Nine horses (five in group 1 and four in group 2) were anaesthetised with thiopentone and guaifenesin and anaesthesia was maintained with halothane. After approximately one hour, facial artery pressure, heart rate, pulmonary artery pressure, cardiac output, temperature, pHa, PaCO2, PaO2, base excess, packed cell volume, plasma protein concentration and white cell count were measured (time 0). Escherichia coli endotoxin was infused intravenously over 15 minutes in both groups. Group 2 horses were given an intravenous infusion of dopamine (5 micrograms kg-1 min-1) starting five minutes after the start of the endotoxin infusion and continuing for 60 minutes. Measurements were made at 15 minute intervals for 120 minutes. In group 1, one horse died during the endotoxin infusion and in two other horses mean facial artery pressures decreased to 50 mm Hg. Total pulmonary vascular resistance and packed cell volume were significantly increased. Cardiac output, cardiac index and change in mean arterial pressure were significantly greater in group 2 horses than in group 1 horses. Conversely, diastolic pulmonary artery pressure, total vascular resistance and total pulmonary resistance were significantly less in group 2 than in group 1. PaO2, base excess and white blood cell count were significantly decreased in both groups. It was concluded that dopamine improved cardiovascular function in the presence of endotoxaemia and attenuated the rate of haemoconcentration, but had no effect on the development of decreased PaO2 or metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1991

Effects of slow infusion of a low dosage of endotoxin on systemic haemodynamics in conscious horses.

The effects of intravenous (iv) infusion of endotoxin for 60 mins at a cumulative dosage of 0.03 micrograms/kg bodyweight on systemic arterial, right atrial and pulmonary arterial pressures, heart rate, cardiac output, and derived pulmonary vascular resistance and total peripheral vascular resistance were compared to the effects of iv infusion of saline solution in four healthy horses. Heart rate was increased significantly after endotoxin infusion, although diastolic arterial pressure, systolic arterial pressure, electronically averaged arterial pressure, cardiac output, total peripheral resistance, and right atrial pressure did not change significantly. Average pulmonary arterial pressure was increased significantly by endotoxin infusion. This was accompanied by a trend toward increased diastolic pulmonary arterial pressure (P = 0.1), systolic pulmonary arterial pressure (P = 0.08) and pulmonary vascular resistance (P = 0.07). These results suggest that low dosages of endotoxin produce pulmonary hypertension without causing hypotensive, hypodynamic shock.

Animals↗
PubMed1991

In vitro responses of equine digital vessels to dopamine and fenoldopam.

The in vitro responses of isolated vascular preparations of digital arteries and veins obtained from healthy anaesthetised horses were determined for dopamine and fenoldopam. The digital vessels were harvested, cut into 4 mm vascular segments, suspended in tissue baths and attached to force-displacement transducers. Dose-response studies between 10(-8) and 10(-4)M concentrations were performed for all drugs. The change in tension of each vascular ring was measured in grams of force. The reactivity between palmar and plantar digital vessels and baseline vascular responses were determined for dopamine. The vascular responses of dopamine were compared to in vitro data for other known vasoconstrictor agents. The mechanism of vasoconstriction induced by dopamine was further defined using prazosin, a specific competitive alpha-1 adrenoceptor antagonist. The vasodilating ability of fenoldopam, a dopamine-1 (DA-1) receptor agonist, was also determined using noradrenaline- preconstricted vascular segments from palmar digital vessels. The effective concentration to produce 50 per cent of the maximal response (EC50) and the maximal contraction in grams of force per milligram of the vascular ring (g/mg) were calculated. There were no differences in the reactivity between the palmar and plantar digital vessels. Dopamine produced intense constriction in arteries and veins but only at very high molar concentrations. Prazosin decreased significantly the sensitivity of the veins to dopamine (increased the mean EC50 values) but not the arteries. Prazosin had no effect on the maximal contractions of the vessels. Fenoldopam produced very little relaxation of either the arteries or veins. These results suggest that dopamine produces constriction in equine digital arteries and veins and that the constriction is only partially mediated by alpha-1 adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1991

Antithrombin III activity in horses with colic: an analysis of 46 cases.

Antithrombin-III (AT-III) activity was measured at the time of admission in 46 horses referred with colic. Differences in AT-III activities between animals treated medically or surgically and survivors or non-survivors were compared. The mean AT-III values for the horses treated medically (76.2 per cent), surgical survivors (69.5 per cent) and surgical non-survivors (55.9 per cent) were significantly different from the reference value for healthy adults (92 to 108 per cent). The mean AT-III activity of the survivors was significantly (P less than 0.01) greater than that of the nonsurvivors. The majority of the survivors (11 to 13 horses) had AT-III activities exceeding 60 per cent of normal, whereas that of 10 of the 14 non-survivors was less than 60 per cent of normal. There was an apparent distinction between the survivors and non-survivors at approximately 60 per cent of normal AT-III activity.

Animals↗
PubMed1991

Whole blood re-calcification time in equine colic.

Whole blood re-calcification times were evaluated as a measure of endotoxin-associated coagulopathy in horses. First, the effects of endotoxin concentration and duration of in vitro incubation of citrated whole blood with endotoxin on the whole blood re-calcification time of blood collected from healthy horses were determined. Increasing concentrations or incubation times of endotoxin accelerated the whole blood re-calcification time. This effect was attributed mainly to increased monocyte thromboplastin activity. Second, whole blood re-calcification time, a clotting profile, plasma factor VII activity and plasma endotoxin concentration on blood samples obtained from 35 equine colic patients and 10 healthy horses were determined. Compared with healthy horses, colic patients had a longer mean whole blood re-calcification and prothrombin time, lower per cent factor VII activity and higher mean fibrin degradation products concentration. Within the colic patient group, horses that did not survive had detectable endotoxin in plasma, longer whole blood re-calcification and prothrombin times, and lower plasma factor VII activity, compared with colic patients that survived. These data indicate that colic patients with endotoxaemia experience hypercoagulable states, followed by consumptive coagulopathy. Although the cause of endotoxin-associated coagulopathy is likely multi-factorial, increased expression of monocyte thromboplastin activity may be involved in the pathogenesis of coagulopathy. The whole blood recalcification time is a simple, fast and inexpensive way to detect coagulopathy during endotoxaemia and determine the prognosis for survival.

Animals↗
PubMed1991

Influence of an omega-3 fatty acid-enriched ration on in vivo responses of horses to endotoxin.

Because certain inflammatory processes are dependent on the fatty acid composition of the cellular membrane, dietary manipulations that replace omega-6 fatty acids with omega-3 fatty acids may modify inflammatory responses. We investigated the effect of supplemental dietary linseed oil, containing the omega-3 fatty acid, alpha-linolenic acid, on in vivo responses of horses to endotoxin. One group of horses (n = 6) was fed a control pelleted ration (0% linseed oil), and another group of horses (n = 6) was fed an 8% linseed oil pelleted ration. After 8 weeks of consuming these rations, all horses were given 0.03 micrograms of Escherichia coli 055:B5 endotoxin/kg of body weight, infused over 30 minutes. Horses were monitored over 24 hours. Compared with baseline values within each ration group, endotoxin infusion caused significant (P less than 0.05) increase in rectal temperature, heart rate, and plasma concentration of thromboxane B2, 6-keto-prostaglandin F1 alpha, and fibrinogen and significant (P less than 0.05) decrease in total WBC count. Compared with baseline values within each ration group, endotoxin infusion failed to cause significant changes in prothrombin, activated partial thromboplastin, thrombin, or whole blood recalcification times, serum concentration of fibrin degradation products, PCV, or plasma total protein concentration. Before and after endotoxin infusion, horses given the linseed oil ration had longer mean whole blood recalcification time and activated partial thromboplastin time than did horses fed the control ration.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Effect of dietary alpha-linolenic acid on endotoxin-induced production of tumor necrosis factor by peritoneal macrophages in horses.

A study was conducted to determine whether dietary supplements with alpha-linolenic acid altered the ability of equine peritoneal macrophages to produce tumor necrosis factor (TNF) in response to endotoxin. Peritoneal macrophages were harvested from 6 healthy adult horses before and after the horses were fed a nutritionally balanced ration that contained 8% linseed oil as a source of alpha-linolenic acid. The macrophages were cultured in media containing no additives (control), endotoxin (0.5 to 50 ng/ml), or the calcium ionophore, A23187. Macrophage supernatants were collected after 6 and 24 hours' incubation and stored at -70 C. Tumor necrosis factor activity was estimated by a modified in vitro cytotoxicity bioassay, using the murine fibrosarcoma cell line, WEHI 164 clone 13. The TNF activity after 6 and 24 hours' incubation was greater in culture media of macrophages exposed to endotoxin than in media from control macrophages. For macrophages cultured in media that contained endotoxin, neither the concentration of endotoxin nor incubation time had any effect on TNF activity. Endotoxin-induced macrophage production of TNF, as determined by measurement of TNF activity, was significantly less after horses were fed the alpha-linolenic acid-rich ration for 8 weeks.

Animals↗
PubMed1991

Serum tumor necrosis factor activity in horses with colic attributable to gastrointestinal tract disease.

Over a 24-month period, serum tumor necrosis factor (TNF) activity was determined in 289 horses with colic attributable to gastrointestinal tract disease. Serum TNF activity was quantitated by use of a modified in vitro cytotoxicity bioassay, using WEHI 164 clone-13 murine fibrosarcoma cells. Causes for colic, determined by clinical and laboratory evaluation, exploratory celiotomy, or necropsy included: gastrointestinal tract rupture (GTR); ileal impaction; small intestinal strangulating obstruction (SIO); proximal enteritis (PE); transient small intestinal distention; large-colon displacement; large-colon volvulus; large-colon impaction; colitis; small-colon obstruction; peritonitis; and unknown. Each diagnosis was placed into 1 of 3 lesion categories: inflammatory disorders (GTR, PE, colitis, peritonitis); strangulating intestinal obstruction (SIO, large-colon volvulus); and nonstrangulating intestinal obstruction (ileal impaction, transient small intestinal distension, large-colon displacement, large-colon impaction, small-colon obstruction, unknown). The prevalence of high serum TNF activity and/or mortality were evaluated. Differences were tested at significance level of P less than 0.05. Approximately 20% of the 289 horses has serum TNF activity greater than that found in clinically normal horses (greater than 2.5 U/ml). Twenty-three horses (8%) had marked increase in serum TNF activity (greater than or equal to 10 U/ml) which was more prevalent among horses with SIO and PE than in horses of other diagnostic groups, except those with GTR. Mortality and marked increase in serum TNF activity were greater in horses with intestinal inflammatory disorders or strangulating intestinal obstruction than in horses with nonstrangulating intestinal obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Dexamethasone reduces endotoxin-induced tumor necrosis factor activity production in vitro by equine peritoneal macrophages.

This study evaluated the effect of dexamethasone on endotoxin-induced production of tumor necrosis factor (TNF) activity in vitro by equine peritoneal macrophages. Peritoneal macrophages from adult horses were cultured in the presence of dexamethasone (1-100 microM) for various time periods (2 hour, 0.5 hour, 0 hour) prior to the addition of endotoxin (5 ng/ml), then the secretion of TNF activity was evaluated. Macrophage supernatant concentrations of TNF activity were estimated by a modified in vitro cytotoxicity bioassay using the murine fibrosarcoma cell line, WEHI 164 clone 13. An experiment was performed to determine whether dexamethasone interfered with the cytolytic bioassay's ability to detect TNF activity. The endotoxin-induced TNF activity production by equine peritoneal macrophages was significantly reduced by co-incubation with 100 microM dexamethasone, but not by tested concentrations of dexamethasone less than 100 microM. This concentration of dexamethasone greatly exceeds those generally attained by therapeutic use of dexamethasone in horses. Preincubation time did not affect the ability of 100 microM dexamethasone to reduce TNF production by equine macrophages. The quantitation of equine TNF activity by its cytolytic bioassay was not altered by dexamethasone.

Analysis of Variance↗
PubMed1991

Effects of xylazine butorphanol on cecal arterial blood flow, cecal mechanical activity, and systemic hemodynamics in horses.

A chronic model with an ultrasonic transit time blood flow probe and strain gauge force transducers implanted on the cecum was used to evaluate cecal mechanical activity and cecal arterial blood flow in 4 conscious adult horses. Intravenous administration of xylazine (1.1 mg/kg of body weight) significantly decreased heart rate and cardiac output, but significantly increased diastolic pulmonary arterial pressure, mean pulmonary arterial pressure, carotid arterial pressure, and central venous pressure. Lateral cecal arterial blood flow after xylazine administration was decreased substantially more than was cardiac output, suggesting that xylazine caused constriction of the cecal vasculature. This effect of xylazine may have resulted from either a direct effect of xylazine on the cecal vasculature or from reflex vasoconstriction attributable to reduced cardiac output. Intravenous administration of butorphanol tartrate (0.1 mg/kg) did not significantly alter the hemodynamic responses to xylazine. Cecal mechanical activity, as measured by the motility index, was decreased for 120 minutes after administration of xylazine and for 150 minutes after administration of xylazine/butorphanol.

Animals↗
PubMed1991

Use of newly developed assays for protein C and plasminogen in horses with signs of colic.

Protein C content and plasminogen activity were measured in plasma from 100 horses with signs of colic. Data were analyzed by grouping horses 4 ways. Each horse was allotted to 1 of 2 outcome groups (survivors and nonsurvivors), 1 of 3 broad-category diagnosis groups (inflammatory disorders, strangulating obstructions, and all other gastrointestinal disorders), and 1 of 2 clinical management groups (medical and surgical). In a fourth grouping, all horses (although numbers of horses included in each subgroup were small) were assigned either to specific diagnostic groups that had high expectation for activated hemostasis (intestinal ischemia, endotoxemia, jugular thrombosis, peritoneal adhesions, and laminitis) or to a control group, in which active hemostasis was unlikely. Within 2 to 24 hours after admission, nonsurvivors developed lower protein C content than did survivors. Protein C content and plasminogen activity became low during hospitalization in horses with strangulating obstructions and in horses having surgery. The results from the grouping by specific diagnosis must be considered pilot data because the numbers of horses in each subgroup were small. Although not statistically significant, trends were noticed in protein C and plasminogen: (1) horses with intestinal ischemia and endotoxemia developed low protein C content and plasminogen activity, (2) protein C content became low in horses that developed peritoneal adhesions or laminitis, and (3) plasminogen activity became low in horses that developed jugular thrombosis. Low protein C content or low plasminogen activity, or both, may be useful as predictors for outcome and for these specific complications of equine colic.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of a linseed oil enriched diet on endotoxin-induced sequelae: differential in vitro and in vivo effects.

Endotoxin stimulates macrophages to synthesize membrane-associated inflammatory mediators including eicosanoids and procoagulant activity (PCA). Alpha linolenic acid, a component of linseed oil, is metabolized to eicosapentaenoic acid, which may replace arachidonic acid in membrane phospholipids. Thus, ingestion of linseed oil may alter the generation of eicosanoids, PCA and other membrane-dependent responses. This study compared the in vitro endotoxin-induced synthesis of eicosanoids and expression of PCA by peritoneal macrophages obtained from rats fed a control diet and rats fed a diet enriched with linseed oil. The effect of endotoxin on in vivo plasma eicosanoid concentrations, leukogram, and microvascular permeability were determined. Endotoxin (5 ug/ml) stimulated synthesis of iTxB2, i6-keto PGF1 alpha and expression of PCA by macrophages in vitro. These in vitro responses of macrophages from linseed oil fed rats were significantly less than those of macrophages from control rats. In contrast, there were no significant differences in in vivo responses to endotoxin. The fatty acid composition of total lipids and phospholipids in liver and plasma from linseed oil fed rats and control rats were not different. These composite data suggest several possibilities: (1) linseed oil may have effects independent of alpha-linolenic acid on macrophage function, (2) linseed oil may alter the fatty acid composition of macrophage phospholipids prior to changing that of other tissues, and (3) the reduced in vitro responses of peritoneal macrophages may not reflect the systemic responses to endotoxin.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Effect of dietary alpha-linolenic acid on equine monocyte procoagulant activity and eicosanoid synthesis.

To investigate the effects of an omega-3 fatty acid-enriched ration on the in vitro response of equine monocytes to endotoxin, an 8-week feeding trial was conducted in which linseed oil served as the source of the omega-3 fatty acid, alpha-linolenic acid. One group of horses was fed a control pelleted ration and the other group was fed an 8% linseed oil-enriched pelleted ration. After 8 weeks of feeding, monocytes were isolated and incubated in the presence of Escherichia coli O55:B5 endotoxin for 6 hr. After 8 weeks on the rations, the mean procoagulant activity and thromboxane B2 production by endotoxin-stimulated monocytes from horses consuming the linseed oil ration decreased by 51% and 71%, respectively, compared with cells from horses consuming the control ration. There was no difference in monocyte synthesis of 12-hydroxyeicosatetraenoic acid or leukotriene B4 between groups. Fatty acid analysis of membrane phospholipids revealed a decrease in the omega-6:omega-3 ratio in monocytes from horses consuming the linseed oil ration. These data suggest that dietary supplementation with alpha-linolenic acid may modify the response to endotoxin by reducing the synthesis of potentially harmful cellular mediators.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1990

Evaluation of equine digital Starling forces and hemodynamics during early laminitis.

A carbohydrate overload model was used in 8 horses to evaluate Starling forces and hemodynamics of the digit during the prodromal stage of acute laminitis. A pump-perfused extracorporeal digital preparation was used to evaluate blood flow, arterial pressure, venous pressure, capillary pressure, isogravimetric capillary filtration coefficient, osmotic reflection coefficient, and vascular compliance. From these data, pre- and postcapillary resistances and pre- to postcapillary resistance ratios were determined. Vascular and tissue oncotic pressures were estimated from plasma and lymph protein concentrations, respectively. The osmotic reflection coefficient, an estimation of capillary permeability, was determined by means of the lymph protein wash-down technique. Using the collected data, tissue pressure in the digit was calculated by use of the Starling equation. In the isolated digit, mean isogravimetric capillary pressure was 55.13 mm of Hg, mean plasma and lymph oncotic pressures were 22.29 mm of Hg and 7.2 mm of Hg, respectively, the mean osmotic reflection coefficient was 0.66, the mean capillary filtration coefficient was 0.003 ml/min/mm of Hg/100 g, and mean interstitial fluid pressure was 44.82 mm of Hg. The high capillary pressure appeared to be caused by high vascular resistance from the venous side, predisposing to enhanced capillary filtration and interstitial fluid accumulation.

Animals↗