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Biomedical subjects

R Cartier

Publications and source records attributed to R Cartier.

At least 91 records · Page 5Linked to original sources

Combined endarterectomy of the internal carotid artery and persistent hypoglossal artery: an unusual case of carotid revascularization.

Persistence of the hypoglossal artery is an unusual congenital abnormality of the carotid arterial system, and the simultaneous occurrence of atheromatous disease in the internal carotid artery and persistent hypoglossal artery is even more uncommon. Carotid surgery in this situation is challenging, and the surgeon must be aware of potential inherent pitfalls. A 74-year-old woman with asymptomatic stenosis of both internal carotid and hypoglossal arteries associated with occlusion of the contralateral internal carotid artery underwent successful revascularization. The anatomy of this unusual lesion and the surgical strategies, which included cranial nerve dissection and mandibular subluxation, are reviewed.

Aged↗

[Effect of cyclosporin A dosage on the vascular tone of the thoracic aorta of rats].

Cyclosporine A (CyA) is known to affect the local release of endothelial-derived relaxing factor (EDRF). However, evidence that CyA could specifically alter endothelial signal transduction is not well understood. Experiments were designed to assess dose-dependent effect of CyA on vascular reactivity-specificity of the rat thoracic aorta. Three groups of rats (n = 10) were treated for 4 weeks with oral CyA 15 mg/kg/day (Gr 1), CyA 30 mg/kg/day (Gr 2), and olive oil (Gr 3), the CyA vehicle. At the end of the period, animals were euthanized and the thoracic aorta harvested for isometric assessment of endothelial and smooth muscle function in organ chambers. Maximal endothelial-dependent relaxation (Rmax) to acetylcholine dose-response was similarly affected in rats treated with CyA [Rmax (%): Gr 1: 33 +/- 8, Gr 2: 28 +/- 2, Gr 3:51 +/- 7, *p < 0.05]. At the opposite, response to adenosine diphosphate [Rmax (%): Gr 1: 11 +/- 2, Gr 2:24 +/- 3*, Gr 3:7 +/- 2, *p < 0.01] and histamine [dose-response CE50 (log M): Gr 1: +/- 12 +/- 0.05, Gr 2: +/- 5.45 +/- 0.05*, Gr 3: -4.85 +/- 0.08, *p < 0.05] were significantly enhanced in animals exposed to 30 mg/kg/day. Endothelium-independent relaxation to sodium nitroprusside (SNP) was comparable in all groups and dose-response to depolarizing (KCl) and non-depolarizing (norepinephrine) contractile agents were not affected either. These experiments suggest that CyA does not affect second messenger (cyclic-GMP) activation by an EDRF analogue (SNP) whereas signal transduction coupled to muscarinic, purinergic, and histaminergic receptors are either inhibited or enhanced by CyA in dose-dependent manner in the rat aortic model.

Animals↗

[Effect of vitamin E on the endothelial function of the regenerated aorta in rats following direct arterial injury].

Fibromuscular intimal injury is frequent after coronary or peripheral angioplasty. Peroxidation of circulating and membrane lipids have been implicated in intimal hyperplasia and endothelial dysfunction following direct arterial trauma. The aim of this study was to evaluate the effects of natural membrane antioxidant, vitamin E (VE), on the vascular reactivity of the regenerated endothelium. A first group of rats (n = 10) was pretreated with VE 100 IU/kg/day for a week before undergoing aortic (thoracic) endothelial denudation with a Fogarty catheter. Rats were then fed with the same VE supplemented diet for a 2-month period. A second group (n = 10), was similarly denudated and fed with soya oil (SO), VE vehicle, for the same period. A third group (n = 10) was denuded and used as control (CL). Endothelial-dependent and independent relaxations were assessed in organ chambers with acetylcholine (ACH), adenosine diphosphate (ADP), histamine (HIS), 5-hydroxytryptamine (5-HT) and sodium nitroprusside (SNP). Endothelial regeneration was evaluated with Evans blue staining. Vascular relaxation to SNP was not affected either by the regeneration process or the VE supplementation. However, endothelial-dependent relaxation to ACH and HIS were significantly impeded in the regenerated endothelium compared to control but was not influenced by the VE or the SO supplementation. Vascular contraction to 5-HT was significantly decreased in VE group compared to the other groups. Morphometric studies with Evans blue staining showed over 95% regeneration of the endothelial surface of the denuded aortas. Our results suggest that in spite of a complete anatomical regeneration, endothelial cells did not resume predenudation function. Endothelial-independent relaxation was preserved in all groups indicating that smooth muscle function was not altered by the regenerating process. The presence of dietary supplement of VE (up to 20 fold the daily requirement) did not prevent the endothelial dysfunction to ACH and HIS but attenuated the vaso-contraction to 5-HT and then could contribute to decreased vascular tone in endothelium-regenerated vessels.

Animals↗

[Effect of cyclosporin A on the reactivity of the pulmonary vascular network in dogs].

UNLABELLED: Aside to its immunosuppressive effects, cyclosporine A (CyA) is known as a vasoconstrictor agent. The vasoconstriction appears to be related to an endothelial release of thromboxane A2 (TxA2) and endothelium as well as a decrease endothelial production of nitric oxide. However, no data is available on the effects of CyA on pulmonary artery (PA) network. We designed experiments to study the CyA effects on canine pulmonary artery vasoregulation. Resistance vessels were studied in vivo using a lung (n = 6) steady rate delivery autoperfusion model. The CyA was infused in the left pulmonary artery at incremental doses of 5, 10, and 20 mg; CyA dosage, sampled in the left atrium, were respectively 515 +/- 67, 580 +/- 97, and 1024 +/- 84 nmol/L. No significant increase in tension were registered regardless of the dose infused. Conductance vessels were studied in vitro using third division PA segments (n = 6) suspended for isometric force measurement in organ chambers. PA segments were precontracted (phenylephrine 10(-6) M) and subsequently exposed to incremental dose of CyA and cremophor (CR), the CyA vehicle. CyA specifically induced a dose-dependent contraction. The maximal contraction observed were 159 g +/- 13% with CyA exposure and 106 +/- 3% with the CR (p < 0.05). This contraction was abolished by indomethacin (cyclooxygenase inhibitor), pinane thromboxane A2 (TxA2 antagonist), dexamethasone (phospholipase A2 inhibitor), neomycin (phospholipase C inhibitor), and endothelial mechanical denudation. CONCLUSIONS: In the canine model, in vivo infusion of CyA does not affect pulmonary resistance arteries. However, in vitro, on pulmonary conductance arteries, CyA induces an endothelium-dependent vasoconstriction. This constriction appears to be related to a TxA2 release mediated by a phospholipase A2 phospholipase C pathway.

Animals↗

[Effect of the ventricular preload on the basal and stimulated coronary circulation of the isolated rat heart].

Langendorff perfused isolated rat heart is a common model for coronary blood flow study. Left ventricular preload can both increase coronary blood flow by direct inotropic effect or decrease it by rising transmural tension. Experiments were designed to determine optimal preload conditions for observation of basal (CBF) and 5-hydroxytryptamine (5-HT) stimulated coronary blood flow (SCBF) in the isolated rat heart model. Rat hearts (n = 6) were harvested and stabilized in the Langendorff apparatus and a left ventricular balloon was inserted and inflated at different volumes (0.05 to 0.4 ml) to stimulate preload. Left ventricular systolic (LVSP), diastolic (LVDP), myocardial oxygen consumption (MVO2) and extraction (MEO2) were also measured. Under basal conditions, optimal LVSP was obtained at 0.2 ml (111 +/- 15 mmHg). MVO2 was optimal at 0.2 ml of preload and decreased thereafter while MEO2 remained stable. Optimal CBF was reached at 0.2 ml of preload. Under 5-HT stimulation, CBF increased significantly (CBF: 8.2 +/- 0.6 ml/min vs SCBF: 16.4 +/- 1.0 ml/min, p < 0.01) while left ventricular hemodynamics did not differ from basal observations. At preload volume > 0.2 ml a significant drop in SCBF was observed (0 ml: 16.4 +/- 1 ml/min vs 0.4 ml: 11 +/- 1 ml/min, p < 0.01). MVO2 and MEO2 followed the same pattern observed under basal conditions. In basal and stimulated conditions, a hyperemic flow was also seen after deflation of the balloon with preload > = 0.2 ml in both CBF and SCBF suggesting myocardial oxygen debt. We conclude that in the Langendorff model preload affects coronary flow under both basal and 5-HT stimulation. A volume > 0.2 ml for rats of 350-400 g can impede CBF and generate myocardial oxygen debt as suggested by a decreased MVO2 and a post-deflation hyperemic flow. Left ventricular preload should be maintained under 0.2 ml for optimal coronary blood flow study in the Langendorff perfused rat heart model.

Animals↗

Clentiazem and diltiazem preserve endothelium-dependent relaxation following global rat heart ischemia.

OBJECTIVE: To evaluate the effects of the calcium channel blocker diltiazem and its chloride derivative clentiazem on coronary vasoregulation of isolated rat hearts exposed to ischemia-reperfusion. Diltiazem has been reported to prevent postreperfusion myocardial damage but its beneficial effects on coronary blood-flow regulation remain uncertain. METHODS: Two groups of hearts were pretreated with a 10 min infusion of either diltiazem (10(-9) to 10(-6) mol/L) or clentiazem (10(-9) to 10(-7) mol/L) (n = 6 for each concentration) and exposed to 30 mins of no-flow ischemia. Another group (n = 6) received no pretreatment and was used as control. Endothelium-dependent and -independent relaxation were tested by assessing coronary flow increase to 5-hydroxytriptamine (10(-6) mol/L) and sodium nitroprusside (10(-5) mol/L) infusions, respectively, and were assessed before and after ischemia-reperfusion. Left ventricular pressure, dP/dt and coronary basal flow were also recorded. Postreperfusion results are expressed as a percentage of pre-ischemic value. Dunnet variance analysis was used to compare means of pretreated groups with the control group. RESULTS: Endothelium-dependent relaxation was significantly improved with both drugs. Optimal preservation was obtained with diltiazem 10(-6) mol/L (66 +/- 4%) and clentiazem 10(-7) mol/L (83 +/- 4%), whereas endothelial response was almost abolished in control hearts (6 +/- 11%, P < 0.01). Clentiazem was found to be more potent than diltiazem at low concentration (10(-9) mol/L, clentiazem 89 +/- 13% versus diltiazem 3 +/- 16%, P < 0.05). Optimal endothelium-independent relaxation preservation was achieved at 10(-8) mol/L in both groups (diltiazem 86 +/- 4%, clentiazem 82 +/- 8%, control 47 +/- 10%, P < 0.05). Left ventricular pressure and dP/dt were not affected by any pretreatment. However, postreperfusion coronary basal flow was significantly increased in control hearts. CONCLUSION: This study indicated that pre-ischemic infusion of diltiazem and clentiazem enhances endothelium-dependent and -independent coronary artery relaxation following reperfusion in the isolated rat heart model, without affective ventricular hemodynamics, and contributes to preservation of coronary artery autoregulation.

Animals↗

Orotracheal intubation of rats by transillumination.

We described a new technique of orotracheal intubation in the rat. This technique is performed under direct vision by transillumination to obtain a better view of the rat's small and distant vocal cords. We also emphasize overextension of the neck to allow for a more direct path to the animal's trachea. This technique is easily learned, is atraumatic, and does not depend on expensive equipment.

Animals↗

2,3-Butanedione monoxime preserves coronary artery endothelium-dependent relaxation during myocardial ischemia in the isolated rat heart.

OBJECTIVE: To evaluate the potential benefit of 2,3-butanedione monoxime (BDM) in preserving endothelium-dependent coronary artery relaxation during myocardial ischemia. MATERIALS AND METHODS: Langendorff-perfused rat heart model. Endothelium-dependent and independent relaxations were tested with infusion of 5-hydroxytryptamine (10(-6) mol/L) and sodium nitroprusside (10(-5) mol/L), respectively. Four groups of hearts (n = 6) were used. Group 1 was perfused with BDM (25 mmol/L) without ischemia for 30 mins. Group 2 was perfused for 10 mins with BDM and exposed to 30 mins of no flow ischemia (37 degrees C). Group 3 was perfused with cold (4 degrees C) nonoxygenated BDM (30 mins) and group 4 (control) was exposed to 30 mins of no flow ischemia alone. Left ventricular pressure (LVP), left ventricular pressure first derivative (dP/dt) and coronary basal flow were evaluated before treatment and after 30 mins of reperfusion. RESULTS: BDM perfusion alone (group 1) did not affect coronary reactivity. Preservation of endothelium-dependent and -independent relaxation was significantly enhanced after ischemia in groups 2 and 3 (BDM-treated) compared with group 4 (control). No significant benefit was found regarding LVP and dP/dt in all groups. Postreperfusion coronary flow was decreased in all hearts except the controls (group 4), suggesting a residual BDM intrinsic effect on coronary flow. CONCLUSION: These experiments suggest that BDM can enhance preservation of coronary artery endothelium-dependent and -independent relaxation during myocardial ischemia in the isolated rat heart.

Animals↗

Effects of modified St Thomas' Hospital solution on coronary artery endothelium dependent relaxation in the isolated rat heart.

Addition of magnesium to a preservation solution such as St Thomas's Hospital solution has been shown to improve myocardial preservation. High concentration of magnesium can affect coronary artery endothelial-dependent relaxation. Isolated rat hearts were studied in the Langendorff apparatus to investigate whether magnesium-enriched hyperkalemic cardioplegic solution (HCS) could alter coronary endothelial function. Hearts in group 1 (n = 8) were perfused for 30 mins with a standard hyperkalemic cardioplegic solution (potassium chloride 24 mmol/L). Hearts in group 2 (n = 8) were perfused with modified St Thomas' Hospital solution (MST) containing 16 mmol/L of magnesium chloride and 24 mmol of potassium chloride. The endothelium dependent and endothelium independent relaxation of the coronary arteries were respectively assessed by infusing 5-hydroxytryptamine (5-HT) (1 x 10(-6) mol/L) and sodium nitroprusside (SNP) (1 x 10(-5) mol/L) before and after perfusion of cardioplegic solutions. Hearts in group 2 showed a reduction of the 5-HT-induced coronary flow increase following the MST exposure (before, 8.66 +/- 0.86 mL/min; after, 5.66 +/- 0.97 mL/min, P < 0.01) whereas hearts in group 1 were not significantly affected (before, 8.00 +/- 0.68 mL/min; after, 6.99 +/- 1.02 mL/min, not significant), suggesting endothelial dysfunction in the former. Coronary flow response to SNP was not affected in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Effects of cyclosporine A on the reactivity of the aorta with regenerated endothelium in rats].

Cyclosporine A (CyA) affects vascular reactivity but its effect on local vascular tone following endothelial regeneration is unknown. Experiments were designed to study the effects of CyA on endothelial and smooth muscle reactivity of endothelium-regenerated arteries. Three groups of rats (n = 8) were subjected to aortic mechanical denudation. Subsequently a first group was treated 8 weeks with CyA (20 mg/kg) and a second one with an equivalent volume of CyA vehicle: olive oil (OL). A last group was submitted to a standard diet and represented the control group (CTL). After 8 weeks, aortic rings were suspended in organ chambers for assessment of endothelial and smooth muscle function. Maximal endothelial dependent relaxation to acetylcholine (CyA: 52 +/- 3%, OL: 50 +/- 4%, CTL: 48 +/- 5%; p = NS), adenosine diphosphate (CyA: 30 +/- 7%, OL: 18 +/- 2%, CTL: 24 +/- 5%; p = NS) and histamine (CyA: 38 +/- 6%, OL: 43 +/- 4%, CTL: 47 +/- 5%; p = NS) were comparable among all groups. In aortic segments studies without endothelium, increased contraction to serotonine was significantly lessened in the OL group (CyA: 259 +/- 43%, OL: 153 +/- 11%, CTL: 243 +/- 24%; p < 0.05). Maximal tension to cumulative doses of norepinephrine was increased in rings without endothelium treated with CyA (CyA: 5.8 +/- 0.6 g, OL: 4.2 +/- 0.5 g, CTL: 4.0 +/- 0.2 g; p < 0.05). All these differences were abolished in rings studied with endothelium. Endothelial independent relaxation to sodium nitroprusside were similar among all groups. In conclusion, CyA does not specifically affect endothelium-dependent relaxation of the regenerated aortic endothelium. However, our model suggests that CyA increases vascular tone mediated by increased smooth muscle sensitivity to norepinephrine and serotonine but these effects are prevented by the regenerated endothelium. This experiment demonstrates the ability of the regenerated endothelium to prevent CyA-induced vascular toxicity.

Animals↗

[In vitro endothelial dysfunction after cold storage: comparison with various preservative solutions].

Optimal solution for endothelial function preservation during cold storage for organ transplant has not yet been defined. To assess this issue, rat aortic rings (n = 28) were stored for 4 hours at 4 degrees C in different preservation solutions: Krebs Ringer (KR), normal saline (NS), rat blood (RB), and the University of Wisconsin solution (UW). Subsequently, rings were suspended in organ chambers for endothelial and smooth muscle assessment. Endothelial-dependent relaxation responses were tested by exposure to cumulative doses of acetylcholine (ACH), adenosine diphosphate (ADP), and histamine (HIS). Smooth muscle function was evaluated by exposure to norepinephrine (NE) and sodium nitroprusside (SNP). A fifth group not submitted to a storage period was used as control (CTL, n = 7). Results are expressed as maximal relaxation (%) from initial precontraction level. Compared to the CTL group, all storage groups showed a significant decrease in endothelial-dependent relaxations to ACH, ADP and HIS (p < 0.05). Among the stored groups, endothelial-dependent relaxation to ACH was significantly decreased in the NS group when compared to the UW group (p < 0.05). Endothelial-independent relaxation to SNP was comparable for all groups. However significant hypercontractility to NE was observed for all stored groups compared to the control group (p < 0.01). A significant decrease in ADP response was observed with NS and RB storage when compared to KR (p < 0.01). In conclusion, cold storage affects both endothelial and smooth muscle function by decreasing endothelial-dependent responses to ACH, ADP and HIS and increasing smooth muscle reactivity to NE. However, endothelial dysfunction was lessened with UW or KR storage compared to NS or RB.

Adenosine↗

[Effect of pentoxifylline on the vascular toxicity secondary to cyclosporine in rats].

Chronic administration of cyclosporine (CyA) has been shown to affect local vascular tone. Pentoxifylline (PTX), a xanthine-derived vasoactive agent, has been reported to prevent CyA toxicity but its effect on CyA-related increased vascular tone remains uncertain. In vitro experiments were designed to study the effects of PTX on endothelium-dependent and independent vasorelaxation of the rat thoracic aorta. Three groups of rats (n = 10) were respectively treated for 4 weeks with CyA (30 mg/kg/day), CyA and PTX (40 mg/kg/day), and CyA and PTX (80 mg/kg/day). At the end of the period, rings (4-5 mm) of aorta were harvested and suspended in organ chambers containing Krebs Ringer solution (37 degrees C, 95% O2, 5% CO2) for assessment of endothelial and smooth muscle reactivity. Endothelium-dependent relaxation to acetylcholine was significantly enhanced in animals treated with CyA and PTX (40 mg/kg/day) compared to those exposed to CyA alone (p < 0.05). Response to histamine and adenosine diphosphate was not affected. However, the use of PTX (80 mg/kg/day) significantly deteriorated the endothelial response to the same drugs (p < 0.05) suggesting a detrimental effect of PTX at this concentration. Endothelial-independent relaxation to sodium nitroprusside was comparable in all groups. The results suggest the clinical benefit reported with the use of PTX on patients chronically exposed to CyA may partly be due to an improvement of the vascular endothelial function. However, the toxicity encountered at high dose should cautioned its use in clinical setup.

Animals↗

[Effect of solutions of preservation on the vascular reactivity of human saphenous veins].

It is mandatory to preserve the vascular tone regulation of the saphenous vein in order to optimize its performance as a vascular conduit. To determine the optimal preservation solution, human saphenous vein segments (3-4 cm) were harvested, stored for 60 minutes in different preservation solutions and studied in organ chambers for endothelial and smooth muscle assessment. A 1st group (n = 10) was stored in the heparinized blood of the patient (SH), a 2nd group (n = 10) in physiologic saline solution (NaCl) and a 3rd group (n = 10) in Krebs Ringer (KR) solution. All solutions were maintained at room temperature (21 degrees C). Each preserved segment was paired to a control segment, harvested in the same patient, and studied before storage. Following 60 minutes of preservation decreased endothelial-dependent relaxation to acetylcholine and histamine was observed among the group stored in KR (p = 0.06 and p < 0.02 respectively) compared to the other groups. Endothelium-independent relaxation to sodium nitroprusside was not affected regardless of the solution used. However, veins stored in SH disclosed an increased contractility to norepinephrine (p < 0.04). When intergroup variability was considered (by variance analysis), no significant difference was seen between each group. This study suggests that KR and SH were not as efficient as NaCl in preserving saphenous endothelial function. Furthermore, storage in SH increased smooth muscle response to catecholamine. In this experimental setup, 0.9% NaCl solution is an acceptable preservation solution of the saphenous vein.

Blood↗

[Effects of acute rejection on the endothelium-dependent relaxation of coronary arteries of the transplanted heart in dogs].

Chronic rejection has been linked to premature coronary atherosclerosis in heart transplantation and may be related to altered vascular reactivity. However, the effect of acute rejection on coronary reactivity remains uncertain. To evaluate this aspect, coronary artery reactivity was studied during acute rejection in a canine model of heart transplantation. Two groups of mongrel dogs (n = 7) (20 to 30 kg) underwent heterotopic heart transplantation (cervical position), and received either no treatment (noTx) or cyclosporine (CyA), 10 mg/kg/day. On day 7, recipient native (NH) and grafted hearts (GH) were harvested and 4-mm rings from the circumflex coronary artery were studied in organ chambers for endothelium and smooth muscle reactivity. At the harvesting, GHnoTx displayed a grade IV/IV histologic rejection while GHCyA (CyA dosage 250-350 nM) reached grade IIIa-IV. Intimal hyperplasia was found in coronary arteries of treated and non-treated GH [4/7 (noTx) vs 3/7 (CyA)]. Endothelium-dependent relaxation to thrombin was impaired in GH compared to NH and was not influenced by CyA treatment [EC50 (-log M): GHnoTx: 1.12 +/- 0.18 vs NHnoTx: 1.67 +/- 0.16 (p = 0.06); GHCyA: 0.99 +/- 0.22 vs NHCyA: 1.64 +/- 0.09 (p = 0.02)]. Conversely, endothelium-dependent relaxation to 5-hydroxytryptamine (5-HT) was enhanced in both CyA-treated and noTx groups [EC50 (-log M); GHnoTx: 5.96 +/- 0.12 vs NHnoTx: 5.54 +/- 0.14 (p = 0.046); GHCyA: 6.65 +/- 0.19 vs NHCyA: 5.66 +/- 0.16 (p = 0.004)]. A facilitating effect of CyA on 5-HT was also seen in GH [GHnoTx vs GHCyA (p = 0.01)], suggesting a CyA intrinsic effect. Responses to acetylcholine and adenosine diphosphate were similar in all groups as well as endothelium-independent relaxation to sodium nitroprusside and contractile response to KCl and PGF2 alpha. We conclude that, in our model, acute rejection does not specifically impair cGMP-mediated relaxation but affects in a receptor-specific manner the endothelium-dependent relaxation. CyA did not prevent these effects but furthermore appeared to enhance the coronary endothelial sensitivity to 5-HT.

Acute Disease↗

[Assessment of the need for organ transplantation in Quebec].

OBJECTIVES: To evaluate the demand for organs for transplantation and to recommend a reorganization of transplantation services in Quebec. DESIGN: Retrospective study. SETTING: Province of Quebec, 1988 to 1992. PATIENTS: All patients on waiting lists for organ transplantation and patients who received transplants registered in national data banks. MAIN OUTCOME MEASURES: The actual annual demand for organ transplantation and the rate of transplantations performed. RESULTS: The rates of heart transplantation were lower than the actual annual demand, which resulted in many patients dying while awaiting transplantation. The actual annual demand for heart transplantation decreased during the last 5 years from 10.9 per million people in 1987 to 6.7 in 1992. The rates of heart transplantation in Quebec were higher than the Canadian average. The actual demand for lung transplantation was only 2.9 per million people on average in 1992. Demand for liver transplantation increased annually, reaching 8.6 per million in 1992. The rate of transplantation increased likewise but remained insufficient. The demand for kidney transplantation reached 27.2 per million people in 1992, and the transplantation rate was 17.8. CONCLUSIONS: Taking into account the actual demand for and supply of organ transplantation, to insure high-quality service and to control costs associated with organ transplantation, we recommend that the present system in Quebec be reorganized so that transplantations are performed in 12 centres: 7 for kidney transplantation, 2 for hearts, 2 for livers and 1 for lungs.

Databases, Factual↗

Hydromorphone patient-controlled analgesia (PCA) after coronary artery bypass surgery.

We conducted a study to compare the effectiveness of patient-controlled analgesia (PCA) technique to conventional analgesic therapy (CAT) after coronary artery bypass graft (CABG). The PCA group received hydromorphone 0.1 mg.hr-1 basal infusion and bolus doses of 0.2 mg Q 5 min (maximum 1.2 mg.hr-1) while the CAT group received morphine 2.5 mg iv Q 30 min prn until extubation followed by prn meperidine 1 mg.kg-1 im Q 4 hr or acetaminophen 325 mg with codeine 30 mg po (1 or 2 tablets) when oral intake was possible. The degree of pain was assessed using a Visual Analogue Scale (VAS) starting after extubation and every 6-8 hr for the next 60 hr. Holter monitoring was initiated one hour after patient arrival in the Intensive Care Unit (ICU) and continued for 72 hr. Other measured variables were pulmonary function, sedation, side effects and total opioid requirements. Results show that the day-to-day VAS pain score decreased in the PCA group (P < 0.001) while it remained unchanged in CAT patients. The PCA patients had lower VAS pain scores at extubation (P < 0.05). During the third postoperative day, the PCA group had a lower VAS pain score, a lower incidence of severe pain defined as a score > 5 on the VAS scale, and a reduced incidence of myocardial ischaemia (P < 0.01). However, there was no difference in the duration, severity, area under the curve (AUC), or heart rate during ischaemic events. Postoperative pulmonary function was abnormal in both groups (NS) with minimal recovery by the fourth day.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗