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Biomedical subjects

B Discigil

Publications and source records attributed to B Discigil.

11 recordsLinked to original sources
PubMed2005

The combined effect of iloprost and N-acetylcysteine in preventing spinal cord ischemia in rabbits.

OBJECTIVES: This study investigated the cytoprotective effects of N-acetylcysteine (NAC) and iloprost on spinal cord ischemia in an experimental model. MATERIALS AND METHODS: Thirty-five (male) New Zealand white rabbits were included in five study groups (n=7, each group). One group served as Sham. Rabbits in other groups had their abdominal aorta cross-clamped just above the iliac bifurcation for 40 min. During aortic cross clamping, iloprost, NAC, both iloprost and NAC or saline (control) were infused. RESULTS: In NAC, iloprost, and iloprost+NAC groups, neurological status of rabbits (Tarlov score) 24 and 48 h after the operation was better than the control group (p<0.01), but worse than the Sham group (p<0.01). There was minimal neuronal damage in the iloprost treated groups compared to the NAC group (p<0.05). Mean viability index values in NAC, iloprost and iloprost+NAC groups were higher than the control group (p<0.01). Viability index in the NAC group was lower than the iloprost and iloprost+NAC groups. CONCLUSIONS: The use of iloprost and NAC may provide better protection from spinal cord ischemia.

Acetylcysteine↗
PubMed2004

Ionic radiocontrast inhibits endothelium-dependent vasodilation of the canine renal artery in vitro: possible mechanism of renal failure following contrast medium infusion.

To determine if radiocontrast impairs vascular relaxation of the renal artery, segments (4-5 mm in length) of canine renal artery were suspended in vitro in organ chambers to measure isometric force (95% O2/5% CO2, at 37 C). Arterial segments with and without endothelium were placed at the optimal point of their length-tension relation and incubated with 10 microM indomethacin to prevent synthesis of endogenous prostanoids. The presence of nonionic radiocontrast (iohexol, Omnipaque 350, 1 ml in 25 ml control solution, 4% (v/v)) did not alter endothelium-dependent relaxation to acetylcholine in rings precontracted with both norepinephrine and prostaglandin F2alpha (N = 6). When the rings were precontracted with prostaglandin F2alpha, the presence of ionic contrast did not inhibit the relaxation of the arteries. However, in canine renal arteries contracted with norepinephrine, the presence of ionic radiocontrast (diatrizoate meglumine and diatrizoate sodium, MD-76, 1 ml in 25 ml control solution, 4% (v/v)) inhibited relaxation in response to acetylcholine, sodium nitroprusside (N = 6 in each group), and isoproterenol (N = 5; P < 0.05). Rings were relaxed less than 50% of norepinephrine contraction. Following removal of the contrast, vascular relaxation in response to the agonists returned to normal. These results indicate that ionic radiocontrast nonspecifically inhibits vasodilation (both cAMP-mediated and cGMP-mediated) of canine renal arteries contracted with norepinephrine. This reversible impairment of vasodilation could inhibit normal renal perfusion and act as a mechanism of renal failure following radiocontrast infusion. In the adopted experimental protocol the isoproterenol-induced relaxation of renal arteries precontracted with norepinephrine was more affected, suggesting a pivotal role of the cAMP system.

Acute Kidney Injury↗
PubMed2002

Pharmacological studies on internal mammary artery bypass grafts. Action of endogenous and exogenous vasodilators and vasoconstrictors.

BACKGROUND: The purpose of this experiment was four-fold: 1) to determine the effect of currently used cardiovascular drugs on internal mammary artery (IMA) vascular tone, 2) to examine IMA reactivity to autacoids and products released from aggregating platelets, 3) to compare the vascular reactivity of the right versus left IMA, and 4) to determine whether the canine IMA was an acceptable physiological model as regards its similarity to the human IMA, which is used routinely for coronary artery bypass grafting. METHODS: To study factors that modulate the tone of IMA, bypass grafts, right and left canine IMAs were studied in vitro in organ chambers (95% O(2)/5% CO(2), pH=7.4). RESULTS: Increasing concentrations (10(-9) to 10(-4M)) of the neurotransmitter acetylcholine (ACH) and the platelet-derived products adenosine diphosphate (ADP) or serotonin (5-HT) induced vasodilatation of contracted right and left IMAs. The vasodilation caused by ACH and ADP was endothelium-dependent while serotonin acted directly on the vascular smooth muscle. Histamine and bradykinin also induced IMA vasodilation, histamine via a direct action on the smooth muscle, and bradykinin through the release of nitric oxide (NO). In canine IMAs, the calcium ionophore A23187 produced endothelium-dependent vasodilation of contracted blood vessels; this vasodilation was blocked by N(G)-nitro-L-arginine (10(-4)M), a competitive inhibitor of nitric oxide synthesis from L-arginine, and by hemoglobin (10(-5)M). Dopamine, dobutamine, and papaverine induced vasodilation of the IMA regardless of the presence or absence of an intact intima, while norepinephrine induced profound IMA vasoconstriction, which was comparable to contraction to potassium ions or the constrictor peptide endothelin. CONCLUSIONS: These experiments establish a pharmacological profile of IMA and demonstrate that endogenous and exogenous compounds can significantly alter its vascular tone.

Acetylcholine↗
PubMed2001

Late pulmonary valve replacement after repair of tetralogy of Fallot.

BACKGROUND: Pulmonary regurgitation appears to be well tolerated early after repair of tetralogy of Fallot; however, it may result in progressive right ventricular dilatation and dysfunction necessitating eventual valve replacement. Our objective was to review our experience with late pulmonary valve replacement after complete repair of tetralogy of Fallot. METHODS AND RESULTS: A total of 42 patients (16 female and 26 male) were operated on between July 1, 1974, and January 1, 1998. Mean age was 22 years (range 2-65 years). The mean interval between tetralogy repair and pulmonary valve replacement was 10.8 years (range 1.6 months-33 years). Mean follow-up was 7.8 +/- 6.0 years (maximum 23 years). Indications for pulmonary valve replacement included decreased exercise tolerance in 58%, right heart failure in 21%, arrhythmia in 14%, syncope in 10%, and progressive isolated right ventricular dilatation in 7%. Heterograft prostheses were used in 33 patients and homografts in 9. Five patients underwent isolated pulmonary valve replacement; concomitant procedures performed in 37 patients included tricuspid valve repair/replacement (n = 18), residual ventricular septal defect repair (n = 12), atrial septal defect closure (n = 4), pulmonary artery patch angioplasty (n = 17), and right ventricular outflow tract enlargement (n = 13). One patient died early (2%) of multiorgan failure. There were 6 late deaths, 3 of which were cardiac related. Survival was 95.1% +/- 3.4% and 76.4% +/- 8.9% at 5 and 10 years, respectively. Functional class of patients was improved significantly; preoperatively, 76% of patients were in New York Heart Association class III-IV, and after pulmonary valve replacement, 97% of surviving patients were in class I-II (P =.0001). Moderate to severe reduction in right ventricular function was noted on preoperative echocardiography in 59% and on late echocardiography in 18% (P =.03). Of the 5 patients who had supraventricular arrhythmias before pulmonary valve replacement, 1 had postoperative recurrence and the arrhythmia is controlled with antiarrhythmic therapy; the other 4 are in normal sinus rhythm at late follow-up. Eight patients subsequently underwent pulmonary valve re-replacement without early mortality at a mean interval of 9.0 +/- 4.2 years (range 3.8-16.8 years). Freedom from pulmonary valve re-replacement was 93.1% +/- 4.7% and 69.8% +/- 10.7% at 5 and 10 years, respectively. The only significant risk factor for re-replacement was young age at the time of the initial pulmonary valve replacement (P =.023). CONCLUSION: Late pulmonary valve replacement after tetralogy repair significantly improves right ventricular function, functional class, and atrial arrhythmias, and it can be performed with low mortality. Subsequent re-replacement may be necessary to maintain functional improvement.

Adolescent↗
PubMed2000

Exogenous hyaluronidase induces release of nitric oxide from the coronary endothelium.

OBJECTIVE: Hyaluronidase, an endogenous enzyme that hydrolyzes mucopolysaccharides, has been shown to enhance myocardial protection when added to preservation solutions. In addition, hyaluronidase infusion reduces injury to ischemic myocardium. Endothelium-derived nitric oxide is an endogenous vasodilator that prevents leukocyte adhesion to the intima and inhibits platelet adhesion and aggregation in the coronary artery. Experiments were undertaken to determine whether the protective action of hyaluronidase could be mediated by the endogenous release of nitric oxide. METHODS: Segments of coronary artery, with and without endothelium, were placed in organ chambers (25 mL) to measure isometric force. Blood vessel segments were contracted with prostaglandin F(2)(alpha) (2 x 10(-6) mol/L) and exposed to hyaluronidase (3-15 units). RESULTS: Hyaluronidase induced vasodilation of arteries with intact endothelium but not of arteries without endothelium (n = 6, P<.05). Endothelium-dependent vasodilation to hyaluronidase was blocked by N(G)-monomethyl-L -arginine (10(-5) mol/L), an inhibitor of nitric oxide synthesis from L -arginine (n = 6, P<.05). Inhibition of vasodilation by N(G)-monomethyl-L -arginine was reversed by L -arginine (10(-4) mol/L) but not D -arginine (10(-4) mol/L; n = 6, each group). Vasodilation to hyaluronidase also was inhibited by hemoglobin (2 x 10(-6) mol/L), a scavenger of the nitric oxide radical (n = 6, P<.05). CONCLUSIONS: Hyaluronidase induces the release of nitric oxide from the coronary endothelium. Because nitric oxide, an endogenous vasodilator, inhibits leukocyte adhesion to the intima in addition to inhibiting platelet adhesion and aggregation, stimulated production of endothelium-derived nitric oxide by exogenous hyaluronidase could be the mechanism of the protective action of hyaluronidase infusion.

Analysis of Variance↗
PubMed1998

Hypoxia increases vasodilator release from internal mammary artery and saphenous vein grafts.

BACKGROUND: Greater release of endothelium-derived nitric oxide is implicated in the superior patency of the internal mammary artery (IMA) used in coronary artery bypass grafting. This study compared the release of endothelium-derived nitric oxide into the lumen of the IMA and the saphenous vein under normoxic versus hypoxic conditions. METHODS: Segments of canine IMA and saphenous vein were perfused in vitro. Vasorelaxant activity was measured as vasodilatation of coronary artery smooth muscle induced by the effluent. RESULTS: Effluents from the IMA and saphenous vein caused comparable vasodilation of coronary artery smooth muscle. The vasodilatation reversed when perfusion was switched to a prosthetic conduit. Vasodilator activity from the IMA and saphenous vein was attenuated by removing the intima of the grafts or by adding N(G)-monomethyl-L-arginine (10(-4) mol/L) or N(G)-nitro-L-arginine (10(-4) mol/L), two inhibitors of nitric oxide synthesis. Indomethacin attenuated vasorelaxant activity from saphenous vein grafts but not IMA grafts (n = 10). Vasodilator release from the IMA and saphenous vein was augmented by hypoxia. This augmentation was inhibited by indomethacin (n = 10, p < 0.05). Hypoxic augmentation reversed with return to normoxia. CONCLUSIONS: The release of endothelium-derived nitric oxide and prostacyclin from bypass grafts into the lumen, particularly during hypoxemia, could promote the vasodilation of distal coronary arterial beds, enhancing myocardial perfusion.

Animals↗
PubMed1996

Endoaneurysmorrhaphy for left ventricular aneurysm. Follow-up in 69 patients.

We reviewed the cases of 69 consecutive patients who underwent physiologic reconstruction of the left ventricular cavity with an endoventricular patch (endoaneurysmorrhaphy) after aneurysmectomy. Eight patients had isolated endoaneurysmorrhaphy, 60 patients had concomitant coronary artery bypass grafting, and 1 patient had concomitant closure of an atrial septal defect. The primary indications for operation were angina pectoris (New York Heart Association functional class I or II) in 42 patients and dyspnea (functional class III or IV) in 27 patients. The preoperative left ventricular ejection fraction evaluated with ventriculography was 28.95% +/- 7.27% (mean +/- standard error of the mean). The global perioperative mortality rate was 2.8%. Total follow-up was 139.3 patient-years. The late mortality rate was 4.3% per patient-year. A marked increase was found in the mean postoperative left ventricular ejection fraction of the patients: 41.91% +/- 11.83%. Survivors were interviewed in person: their functional status was class I or II in 58 patients and class III in 3 patients. We conclude that left ventricular endoaneurysmorrhaphy results in satisfactory functional improvement and can be performed with relatively low early and late mortality rates.

Adult↗
PubMed1995

Novel technique to bioassay endocardium-derived nitric oxide from the beating heart.

Nitric oxide is a potent vasodilator and antiplatelet substance released by the vascular endothelium. In the current study, isolated rabbit hearts were perfused retrograde in the aortic root with a balanced salt solution using a Langendorff technique. To perfuse the right cardiac chambers, an inflow cannula was placed in the superior vena cava and an outflow cannula in the right ventricular apex via the pulmonary artery. To detect endocardial vasodilator production, right heart perfusate was used to bathe a "bioassay" segment of canine coronary artery denuded of endothelium. Perfusate from unstimulated hearts did not alter smooth muscle tone in the bioassay tissue. Calcium inophore, a potent stimulus for endothelial nitric oxide production, produced relaxation of the bioassay smooth muscle when added to the cardiac perfusate but not when applied directly to the bioassay segment. Cardiac effluent vasodilator activity was abolished by removal of the endocardium or addition of nitric oxide synthesis inhibitors, but not by prostanoid inhibitors. These experiments describe a practical method to bioassay endocardial nitric oxide production in the beating heart.

Animals↗
PubMed1995

Continuous retrograde cerebral perfusion supplies substrates for brain metabolism during hypothermic circulatory arrest.

Ten patients underwent replacement of ascending aorta and/or aortic arch with aneurysm or dissection, using hypothermic circulatory arrest (HCA) with retrograde cerebral perfusion (RCP). RCP was administered through the superior vena cava cannula continuously during HCA (15 degrees C to 20 degrees C). Mean HCA time was 32 minutes (range, 18-45 minutes). To assess the metabolic changes during RCP, blood samples were taken from carotid arteries and the superior vena cava cannula simultaneously, five minutes after the onset and five minutes prior to termination of continuous retrograde cerebral perfusion (CRCP) for analysis of blood gas and glucose level. One patient died intraoperatively due to left ventricular failure. Nine patients survived their operations and all except one with stroke due to partial intimal flap obstruction of innominate artery awoke neurologically intact within four to six hours. One patient died on the postoperative fifth day due to septic shock following resection of ischaemic bowel due to dissection involving the mesenteric artery. Oxygen saturation, pH and glucose level were all found to be lower in blood back-bleeding from the carotid arteries than in blood perfused through the superior vena cava cannula at all sampling times during HCA and CRCP (p < 0.05). Although oxygen and glucose extraction is not only from brain tissue, these data demonstrate the efficacy of CRCP in supplying substrates for brain protection. CRCP is a reliable method as an adjunct to HCA for brain protection.

Adult↗
PubMed1994

Effect of pulsatile flow during cardiopulmonary bypass on thyroid hormone metabolism.

Changes in thyroid hormone levels during and after cardiopulmonary bypass (CPB) are well documented. However, little is known about the effects of pulsatile flow during CPB on thyroid hormone metabolism. To examine the effect of flow pattern, a prospective study was carried out using 30 patients undergoing coronary artery bypass grafting. Fifteen patients had pulsatile flow during CPB and 15, nonpulsatile flow. Serum samples were obtained preoperatively, during bypass, and at 2 and 24 hours postoperatively. Thyroid-stimulating hormone, thyroxine (T4), triiodothyronine (T3), free T4, and free T3 levels were measured by radioimmunoassay. All measured hormone levels except free T4 and thyroid-stimulating hormone decreased after the initiation of CPB. There were no differences in preoperative values between the two groups. However, levels of T3 and free T3 during and after CPB showed a significant difference between the two groups, with a smaller decrease in patients in whom pulsatile flow was used during bypass (p < 0.05). Thyroxine, and thyroid-stimulating hormone free T4 values showed no difference between the two groups at any sampling time. These data provide support for the use of pulsatile flow during CPB to establish a more physiologic state and maintain better thyroid hormone metabolism.

Cardiopulmonary Bypass↗