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Biomedical subjects

A T Ali

Publications and source records attributed to A T Ali.

At least 19 recordsLinked to original sources
PubMed2001

Vascular delay and intermittent stimulation: keys to successful latissimus dorsi muscle stimulation.

BACKGROUND: The goal of this study was to obtain physiologically significant increases in peak left ventricular (LV) systolic pressure and stroke volume with latissimus dorsi muscle (LDM) stimulation in cardiomyoplasty (CMP). We hypothesized that preserving LDM integrity by vascular delay and intermittent stimulation would significantly increase LDM cardiac assistance. METHODS: In 4 control dogs and 12 dogs that had undergone a vascular delay (VD) procedure, LV dysfunction was induced by intracoronary microsphere injections. Cardiomyoplasty surgery was performed 14 days later, followed by progressive LDM conditioning. In the control dogs and in 6 of the VD dogs, the LDM was stimulated 24 hours per day (VD plus constant stimulation [CS]). In the other 6 VD dogs, LDMs were stimulated on a daily schedule of 10 hours on and 14 hours off (VD plus interrupted stimulation [IS]). Latissimus dorsi muscle stimulated beats were compared with nonstimulated beats 9 weeks later. RESULTS: In the control dogs, LDM stimulation had minimal effects. In VD + CS and VD + IS, LDM stimulation increased peak LV pressure, stroke volume, stroke work, and stroke power (p < 0.05). However, these changes were greater in the VD + IS group, in which LDM stimulation increased peak aortic pressure by 17.6 +/- 1.7 mm Hg, peak LV pressure by 19.7 +/- 1.1 mm Hg, peak positive LV dp/dt by 398 +/- 144 mm Hg per second, stroke volume by 5.1 +/- 0.7 mL, stroke work by 10.9 +/- 0.9 gm.m, and stroke power by 122.7 +/- 11.6 gm.m per second (p < 0.05 compared with VD + CS). Quantitative morphometric analysis showed minimal LDM degeneration in the VD + IS group (7.5% +/- 1.1%), and VD + CS group (10.5% +/- 4.5%) compared with the control group (29.5% +/- 4.5%, p < 0.05). CONCLUSIONS: VD and IS considerably increased the LV assistance with LDM stimulation. Further studies of this combined approach to CMP should be planned.

Animals↗
PubMed2000

Transthoracic ultrasonography is an alternative to subxyphoid ultrasonography for the diagnosis of hemopericardium in penetrating precordial trauma.

BACKGROUND: Surgeon-performed ultrasonography is increasingly becoming part of the initial evaluation of patients after blunt or penetrating trauma. Currently, most institutions obtain a subxyphoid or subcostal view of the heart and pericardial space, and a three-view ultrasonogram of the abdomen to detect blood in the pericardial sac or in three dependent abdominal areas. METHODS: A left parastemal standard transverse transthoracic view is described in addition to the aforementioned views. This facilitates the visualization of the pericardial sac when a subxyphoid or subcostal view cannot be obtained because of anatomical reasons (narrow subxyphoid space) or local factors (pain, fractures, subcutaneous emphysema, or chest wall contusion). RESULTS: The transthoracic view can be useful in patients where the subxyphoid view is difficult to obtain through the conventional approach. In most patients an excellent view of the pericardial sac and ventricles can be obtained and, therefore, expedites the diagnosis and treatment of patients with hemopericardium. CONCLUSION: Surgeon-performed ultrasonography has become the diagnostic test of choice for patients suspected of having hemopericardium and cardiac tamponade. Transthoracic ultrasonography is an excellent alternative for those patients where a subxyphoid or subcostal view to visualize the pericardial sac and heart cannot be obtained owing to local or anatomical factors.

Abdominal Injuries↗
PubMed1999

Vascular delay of the latissimus dorsi provides an early hemodynamic benefit in dynamic cardiomyoplasty.

OBJECTIVES: Dynamic cardiomyoplasty (CMP) as a surgical treatment for chronic heart failure improves functional class status for most patients. However, significant hemodynamic improvement with latissimus dorsi muscle (LDM) stimulation has not been consistent. The current protocols do not allow early LDM stimulation after CMP surgery. We hypothesized that vascular delay of LDM would increase myocardial assistance after CMP and allow early (48-h) LDM stimulation after CMP. METHODS: Mongrel dogs (n = 24) were divided in four groups: 1) controls (n = 6), single-stage CMP; 2) Group ES (n = 6), single-stage CMP with early LDM stimulation beginning 48 h, postoperatively; 3) Group VD (n = 6), vascular delay of the LDM followed by CMP without early LDM stimulation, and 4) Group VDES (n = 6), vascular delay of LDM (14-18 days), followed by CMP with early stimulation (48 h postoperatively). Two weeks after CMP, global cardiac dysfunction was induced by injecting microspheres into the left coronary artery. LDM-assisted (S) beats were compared with nonstimulated beats (NS) by measuring aortic pressure (AoP), LV pressure, aortic flow, and by calculating first derivative of LV contraction (+/-dP/dt), stroke volume (SV), and stroke work (SW). RESULTS: In ES, LDM stimulation had no effect on the hemodynamic parameters. In the other groups, LDM stimulation significantly (p < 0.05) increased AoP, LVP, dP/dt, SV, and SW. However, these increases were much larger in VD and VDES. In VD, LDM stimulation increased peak AoP by 21.5+/-3.8 mm Hg, LVP by 22.1+/-4.1 mm Hg, dP/dt by 512+/-163 mm Hg/sec, SV by 10.4+/-2.3 mL, and SW by 22.1+/-5.4 g/m(-1). Similarly, in VDES, LDM stimulation increased peak AoP by 24.1+/-4.7 mm Hg, LVP by 26.2+/-4.3 mm Hg, dP/dt by 619+/-47 mm Hg/sec, SV by 6.5+/-0.7 mL, and SW by 16.7+/-4.1 g/m(-1). CONCLUSIONS: In dogs with global LV dysfunction, CMP after vascular delay resulted in a significant improvement in hemodynamic function measured 2 weeks after surgery. This improvement was not provided by single-stage CMP with or without early stimulation. Vascular delay of the LDM before surgery may play an important role for early benefit after CMP, shorten the overall muscle training period, as well as increase hemodynamic response to LDM stimulation.

Animals↗
PubMed1998

Preconditioning of the latissimus dorsi muscle in cardiomyoplasty: vascular delay or chronic electrical stimulation.

OBJECTIVES: In standard single stage cardiomyoplasty (CMP), the latissimus dorsi muscle (LDM) is not preconditioned prior to surgery. We hypothesized that latissimus dorsi preconditioning by vascular delay or by chronic electrical stimulation would result in an improved LV hemodynamic function early (14 days) after CMP. METHODS: Mongrel dogs had preconditioning of the latissimus dorsi by a vascular delay procedure followed by CMP 14-18 days later (group I VD). Dogs in group II underwent 4 weeks of chronic stimulation (CS) of the latissimus dorsi (2 V/30 Hz, six bursts/min) followed by CMP. The latissimus dorsi muscle was fully stimulated from 48 h after cardiomyoplasty in both groups (2 V/30 Hz, three bursts/min). Two weeks after myoplasty, injecting 2.0-3.0 x 10(5) 90 microm latex microspheres in the left main coronary artery induced global cardiac dysfunction. Hemodynamic function was then evaluated for latissimus dorsi muscle assisted (S) beats and non-stimulated beats (NS) in each group by measuring peak systolic aortic pressure (AOP), left ventricular pressure (LVP) and end diastolic pressure (LVEDP), and by calculating maximum and minimum dP/dt. RESULTS: Dogs with vascular delay of the latissimus dorsi showed a marked increase for all hemodynamic indices (AOP: 23.9+/-2.5%, LVP: 23.5+/-2.2%, max dP/dt: 49.4+/-3.3%) for LDM assisted (S) beats compared to non-stimulated beats (P < 0.001). Animals with chronic electrical training did not demonstrate a significant increase in any hemodynamic parameter with LDM stimulation. CONCLUSION: Preconditioning the LDM may play an important role in providing early cardiac assistance in CMP. Preconditioning the LDM with vascular delay resulted in improving performance of the LDM with consistent increases in LV hemodynamics. This was not observed after preconditioning with chronic electrical stimulation. Vascular delay of the latissimus dorsi can significantly improve muscle performance in CMP and could provide hemodynamic assistance early after surgery.

Animals↗
PubMed1998

Evidence for improved cerebral function after minimally invasive bypass surgery.

BACKGROUND: Neurological impairment is a major cause of morbidity after cardiac surgery and may be associated with occurrence of cerebral microemboli generated during cardiopulmonary bypass (CPB). This study evaluates cerebral dysfunction following coronary artery surgery on-pump and off-pump. METHODS: Neurological outcome was evaluated in 322 patients with a coronary artery bypass graft (CABG). Conventional CPB was used (on-pump) in 305 patients and in 17 patients no CPB was used (off-pump). Intraoperatively, a pulsed-wave transcranial Doppler with a 2-MHZ probe measured high-intensity transient signals (HITS) by ultrasonic insonnation of the middle cerebral artery indicating the presence of emboli within the vessel lumen. Transcranial near-infrared spectroscopy measured cerebral venous oxygen saturation for adequate perfusion. Postoperatively, all patients were subjected to the antisaccadic eye movement (ASEM) test, a sensitive indicator of neurocognitive deficits secondary to frontal lobe dysfunction. RESULTS: While there was no significant difference in O2 saturation, the number of microemboli HITS generated was significantly higher in the on-pump group than the off-pump group. In the off-pump group, 16 (94%) of 17 patients had perfect scores on the ASEM test, while only 108 (35.4%) of 305 patients achieved a perfect score in the on-pump group (p < 0.01). Furthermore, while all patients in the off-pump group achieved at least 90%, 28% (86/305) in the on-pump group scored "zero" on the ASEM test. CONCLUSION: Cerebral dysfunction as evidenced by ASEM errors is common following coronary bypass on-pump, but rare with off-pump bypass surgery. Cerebral microemboli generated during CPB may account for this difference.

Cardiopulmonary Bypass↗
PubMed1997

Preventing gastroepiploic artery spasm: papaverine vs calcium channel blockade.

UNLABELLED: The gastroepiploic artery (GEA) is a highly vasoactive artery gaining wider acceptance as a conduit for coronary artery bypass surgery. A variety of agents are used to dilate the GEA prior to grafting; however, little is known about the duration of their effect in the immediate postoperative period. This study evaluated three calcium channel blockers and papaverine in preventing graft spasm. METHODS: Porcine GEA segments (10-12 cm in length) were connected to a computer-controlled perfusion system with a constant in-flow pressure and distal resistance to simulate bypass flow (80-100 ml/min). Norepinephrine (NE; 10(-9) to 10(-5) M) was given in incremental doses at baseline before the vasodilator, immediately after (0 hr), and again at 2 hr after the vasodilator. Changes in flow and ED50 were recorded. Group INT (N = 25) received papaverine (PAP), diltiazem, nifedipine (NFP), or verapamil (VPL) intraluminally, while group EXT (N = 25) received the same dilators externally. RESULTS: All arteries showed dose-dependent vasoconstriction to NE prior to treatment. Immediately after receiving the vasodilator, arteries in both groups (INT and EXT) showed initial protection against NE-induced spasm with the exception of arteries receiving NFD externally. However, at 2 hr, for group INT, only VPL and NFD prevented NE-induced graft spasm (VPL: 40.4 +/- 6.8 ml/min vs 17.9 +/- 3.3 ml/min and NFD: 27.0 +/- 6.5 ml/min vs 13.1 +/- 0.9 ml/min, P < 0.02). In group EXT, after 2 hr, only VPL- and PAP-treated grafts showed resistance to NE-induced vasospasm (VPL: 35.6 +/- 7.3 ml/min vs 15.0 +/- 6.9 ml/min and PAP: 47.4 +/- 15.1 ml/min vs 8.0 +/- 2.0 ml/min, P < 0.001). CONCLUSIONS: Papaverine, a lipophilic vasodilator, when given externally on the perivascular fat of the GEA, prevented graft spasm for up to 2 hr. In contrast, intraluminally applied papaverine did not show graft protection against NE-induced spasm. Nifedipine prevented NE-induced spasm only when given intraluminally. Verapamil proved to be the most potent and versatile vasodilator with effective graft protection of up to 2 hr whether applied externally or internally and was the preferred agent for protecting against GEA spasm.

Animals↗
PubMed1997

Natural honey prevents ischaemia-reperfusion-induced gastric mucosal lesions and increased vascular permeability in rats.

OBJECTIVE: It has been proposed that natural honey may contain a 'sucralfate-like' substance. Recent studies have shown that sucralfate affords protection against ischaemia-reperfusion-induced injuries in the rat stomach. Therefore, the effect of honey was studied on ischaemia-reperfusion-induced gastric lesions, intraluminal bleeding, vascular permeability and non-protein sulphhydryls (NP-SH) in the rat stomach. METHODS: Rats were subjected to 30 min of gastric ischaemia in the presence of 100 mM HCl and reperfusion period of 60 min. Intraluminal bleeding was assessed macroscopically and the gastric lesions were graded microscopically under an inverted microscope. Vascular permeability was quantified by measuring spectrophotometrically the extravasated Evans blue dye in the stomach. NP-SH levels were measured spectrophotometrically. A luminol-dependent chemiluminescence method was used to assess antioxidant effects of honey in vitro. RESULTS: There were significantly more gastric lesions, more severe intraluminal bleeding, more leakage of Evans blue and depletion of NP-SH during the reperfusion period as compared to controls. Pre-treatment with honey (0.078-0.625 g/kg, orally) or dimethyl sulphoxide (0.02-0.08 g/kg, intraperitoneally) 30 min before the ischaemia-reperfusion dose-dependently reduced the gastric lesions and intraluminal bleeding and decreased the vascular permeability. Furthermore, honey reversed the ischaemia-reperfusion-induced depletion of NP-SH levels and inhibited the luminol-dependent chemiluminescence induced in a cell-free xanthine-xanthine oxidase system. CONCLUSION: These results suggest that gastric protection by honey may be a result of its antioxidant effect. It is suggested that this property of honey may be due to the presence of a 'sucralfate-like' substance.

Animals↗
PubMed1997

Sucralfate attenuates gastric mucosal lesions and increased vascular permeability induced by ischaemia and reperfusion in rats.

Recent evidence suggests that oxygen-derived free radicals are involved in mediating gastric microvascular and parenchymal cell injuries induced by ischaemia and reperfusion. Therefore, the effect of the locally acting anti-ulcer drug, sucralfate, was studied on ischaemia and reperfusion (e.g. induced gastric lesions, intraluminal bleeding, changes in vascular permeability and non-protein sulfhydryl levels in the rat stomach). Allopurinol was used as a known standard antioxidant drug. Rats were subjected to 30 min of gastric ischaemia in the presence of 100 mmol/L hydrochloric acid and reperfusion periods of 15, 30 or 60 min duration. The gastric lesions were assessed microscopically under an inverted microscope. The vascular permeability was quantified by measuring the extravasated Evans blue in the stomach. There were significantly greater numbers of gastric lesions, intraluminal bleeding and leakage of Evans blue during all reperfusion periods as compared with those of ischaemia, with maximum effects occurring at 60 min following reperfusion. Pretreatment with sucralfate (31.25-250 mg/kg, p.o.) or allopurinol (12.5-50 mg/kg, i.p.) 30 min before the procedure, dose-dependently reduced the gastric lesions, intraluminal bleeding, and decreased the vascular permeability induced by ischaemia and reperfusion. Furthermore, sucralfate dose-dependently reverses the ischaemia and reperfusion-induced depletion of mucosal non-protein sulfhydryl levels and inhibited the superoxide radical production in both cell-free xanthine-xanthine oxidase and in the stimulated polymorphonuclear cellular systems. These results suggest that the protection produced by sucralfate against gastric injury may be due to its antioxidant effects.

Allopurinol↗
PubMed1997

Variable effects of cardiomyoplasty on left ventricular function.

Cardiomyoplasty (CMP) has been considered as a possible treatment for patients with heart failure. Symptomatic improvements occur almost uniformly among survivors with CMP, but changes in left peak ventricular systolic pressure (PVSP) and stroke volume vary in patients. This study examined whether there is variability present shortly after cardiomyoplasty surgery. Cardiomyoplasty was performed in 11 mongrel dogs with normal ventricular function. Nine to twelve days after CMP, left ventricular (LV) function was evaluated by simultaneously measuring LV volume (conductance catheter) and pressure (Millar catheter). The latissimus dorsi muscle (LDM) was stimulated synchronously with ventricular systole in a ratio of 1:4 to 1:7 to avoid muscle fatigue. Data were analyzed on a beat by beat basis. The PVSP, and maximum dP/dt (+dP/dt) increased, but the absolute value of minimum dP/dt (-dP/dt) decreased in stimulated beats in 7 dogs while 4 dogs did not respond. The net changes in stimulated beats versus nonstimulated beats of PVSP were 6.1 +/- 1.8 mm Hg (4.3%), of stroke work was 4.5 +/- 1.9 gm x m (29.5%), of +dP/dt was 185 +/- 47 mm Hg/s (8%), and of -dP/dt was 168 +/- 43 mm Hg/s (7.8%) (p < 0.05) for all these net changes in the responding group while these variations were not significant in the nonresponding group. From the results of our study, active LDM assist improves left ventricular systolic function, occurring in only 7 of 11 experiments. This improvement is inconsistent and varied individually. The integrity of the LDM, tightness of wrapping, and adhesions might contribute to the variability which is present early after surgery and before the LDM is converted into a fatigue resistance muscle.

Animals↗
PubMed1996

Evaluation of the long-term effectiveness of extraluminal and intraluminal vasodilators in an in vitro porcine model of arterial graft spasm.

OBJECTIVE: Postoperative graft spasm is a concern when arterial conduits are used because there may be insufficient arterial graft flow. Intraoperatively, vasodilators are used to increase flow and prevent spasm, but little is known about their duration of effectiveness. METHODS: To examine this we attached porcine gastroepiploic and internal thoracic arteries (GEA, n = 48; ITA, n = 24, 10-12 cm long) to a computer-controlled perfusion system (constant inflow pressure 80 mm Hg) with a fixed outflow resistance. Norepinephrine (10(-9)-10(-5) M) was incrementally added to the perfusate at baseline (B), then immediately (h+0) and 2 h (h+2) after the vessels were treated with 30 min of extraluminal or intraluminal nitroglycerin, nitroprusside, verapamil or papaverine. RESULTS: At (B), norepinephrine caused a dose-dependent decrease in flow in both the ITAs and GEAs. In the ITAs, at (h+0), both extraluminal and intraluminal papaverine and, to a lesser extent nitroprusside, increased initial flow and decreased graft sensitivity to norepinephrine. At (h+2), only extraluminal papaverine sustained this maximal effect (ED50 for extraluminal papaverine at (B) 2.6 E(-7) vs. (h+2) 1.3 E(-6), P = 0.01). For the GEAs, at (h+0), both extraluminal and intraluminal verapamil, papaverine, nitroprusside and nitroglycerin attenuated flow reduction due to norepinephrine. At (h+2), only extraluminal papaverine, extraluminal verapamil and intraluminal verapamil were effective in preventing norepinephrine-induced spasm (ED50 for extraluminal papaverine at (B) 1.0 E(-7) vs. (h+2) 6.4 E(-6) (P = 0.004); extraluminal verapamil at (B) 1.2 E(-7) vs. (h+2) 4.0 E(-6); intraluminal verapamil at (B) 5.8 E(-7) vs. (h+2) 5.7 E(-6), P = 0.005). CONCLUSION: Verapamil-and papaverine-treated arteries have a greater duration of efficacy in resisting spasm than arteries treated with nitroglycerin and nitroprusside. In the ITA, extraluminal administration of papaverine is most efficacious, possibly due to the prolonged exposure afforded by this route of administration. The effects of verapamil and papaverine are more prolonged in the GEA when administered extraluminally, potentially due to absorption in the perivascular fat-pad and subsequent slow release. The results of this study suggest that extraluminally administered verapamil and papaverine appear to be the preferred vasodilators for preventing arterial graft spasm in the postoperative period. This may be especially important when multiple arterial grafts are used.

Animals↗
PubMed1995

Management of tissue breakdown and exposure associated with orbital hydroxyapatite implants.

A new surgical approach for the management of tissue breakdown and exposure of an orbital hydroxyapatite (HA) implant is presented. The implant was placed after evisceration of an atrophic globe. Tissue breakdown and exposure developed 3 weeks after implantation. After a 3-month waiting period for spontaneous healing, a pedicled conjunctival flap from the lower eyelid was fashioned to cover the defect. This technique can be used to cover conjunctival defects over HA implants and is specifically recommended for large defects.

Adolescent↗
PubMed1995

The role of nitric oxide and sulphydryls in gastric mucosal protection induced by sodium cromoglycate in rats.

The role of endogenous nitric oxide and sulphydryls in gastric protection afforded by sodium cromoglycate against ethanol-induced gastric lesions was studied in rats. Drugs were administered either intraperitoneally (i.p.) or subcutaneously (s.c.) 30, 45 or 60 min before oral administration of ethanol. Administration of cromoglycate before ethanol dose-dependently inhibited ethanol-induced gastric lesions. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide biosynthesis, dose-dependently aggravated gastric lesions and reduced cromoglycate-induced gastric protection. The attenuating effect of L-NAME on gastric protection elicited by cromoglycate was reversible by pretreatment with L-arginine but not by D-arginine. On the other hand, ethanol-induced gastric lesions were found to be associated with a reduction of nonprotein sulphydryl content of glandular stomachs. Pretreatment with cromoglycate prevented non protein sulphydryl depletion and afforded protection. Pretreatment with N-ethylmaleimide, a sulphydryl blocker, caused dose-dependent enhancement of ethanol-induced gastric lesions and further depletion of non protein-sulphydryl. Treatment with N-ethylmaleimide before cromoglycate reduced the gastric protection that was associated with depletion of nonprotein sulphydryls. Furthermore, combined N-ethylmaleimide and L-NAME pretreatment caused a greater aggravation of ethanol-induced gastric lesions and significantly produced a higher reduction of the protective effects of cromoglycate. However, pretreatment with L-arginine only partially restored the protective effects of cromoglycate. These results suggest that the protective effects of cromoglycate may be dependent on the maintenance of a critical level of both endogenous nitric oxide and nonprotein sulphydryls in the gastric mucosa.

Animals↗
PubMed1991

Prevention of ethanol-induced gastric lesions in rats by natural honey, and its possible mechanism of action.

The effects and the mechanism of natural honey on absolute ethanol-induced gastric lesions were studied in rats. Drugs and/or honey were administered subcutaneously or orally to 48-h fasted animals at different time intervals before oral administration of ethanol (0.5 ml/100 g). Mucosal damage and pH were measured 1 h later. Honey afforded protection against gastric damage and reversed the changes in pH induced by ethanol. The effects of honey were dose- and time-dependent. Thus, pretreatment with honey (1.25 g/kg) 30 min before ethanol provided more than 80% protection. On the other hand, administration of honey simultaneously with or 5 min after ethanol failed to offer protection. The cyclooxygenase inhibitor indomethacin (IND) did not alter the protective effects when given before or after honey. The protective effects of honey could be reversed by treatment with the sulfhydryl (SH) blocker N-ethylmaleimide (NEM). Combined IND and NEM treatment caused greater reduction of the protective effects, but the values were not significantly different from those obtained with NEM alone. Thus, the gastroprotective effects of honey appeared to be mediated through SH-sensitive processes. Furthermore, the protective effects were supported by both macroscopic and microscopic findings. It is suggested that honey may be used clinically in preventing/reducing ethanol-induced gastric lesions in humans.

Animals↗
PubMed1984

Effects of non-steroidal anti-inflammatory drugs on lymphocyte activation.

Guinea-pig lymph node lymphocytes were stimulated with mitogen (phytohaemagglutinin) in vitro and lymphocyte activation was measured by tritiated thymidine incorporation (DNA synthesis). Inclusion of non-steroidal anti-inflammatory drugs (NSAIDs) in the culture medium at therapeutic concentrations, frequently exerted an inhibitory effect. Such inhibition could not be attributed to the ability of these drugs to inhibit cyclo-oxygenase or lipoxygenase enzymes. Inhibition by salicylates was not associated with cytotoxic or cytopathic effects, since inhibition was only evident when the drugs were included in the early phase of culture. Other NSAIDs exhibited varying degrees of toxicity, which in some instances may account for observed inhibition. The effects on lymphocyte activation of selective inhibitors of pathways of arachidonic acid metabolism, do not support the proposition that the generation of prostaglandins, thromboxanes, leukotrienes or related compounds is an obligatory step during lymphocyte activation.

Animals↗
PubMed1982

Enhancement of lymphocyte activation by BW755C in vitro.

BW755C considerably enhances the increased DNA synthesis of lymphocytes responding to mitogen stimulation. This effect is evident at much lower concentrations of BW755C than are required to inhibit cyclooxygenase or lipoxygenase enzymes. This suggests that in vivo effects of BW755C may not solely depend upon modification of arachidonic acid metabolism.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗