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Biomedical subjects

Robert M Mentzer

Publications and source records attributed to Robert M Mentzer.

At least 19 recordsLinked to original sources
PubMed2006

The A2a/A2b receptor antagonist ZM-241385 blocks the cardioprotective effect of adenosine agonist pretreatment in in vivo rat myocardium.

There is increasing evidence for interactions among adenosine receptor subtypes in the brain and heart. The purpose of this study was to determine whether the adenosine A(2a) receptor modulates the infarct size-reducing effect of preischemic administration of adenosine receptor agonists in intact rat myocardium. Adult male rats were submitted to in vivo regional myocardial ischemia (25 min) and 2 h reperfusion. Vehicle-treated rats were compared with rats pretreated with the A(1) agonist 2-chloro-N(6)-cyclopentyladenosine (CCPA, 10 mug/kg), the nonselective agonist 5'-N-ethylcarboxamidoadenosine (NECA, 10 mug/kg), or the A(2a) agonist 2-[4-(2-carboxyethyl)phenethylamino]-5'-N-methylcarboxamidoadenosine (CGS-21680, 20 mug/kg). Additional CCPA- and NECA-treated rats were pretreated with the A(1) antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 100 mug/kg), the A(2a)/A(2b) antagonist 4-(-2-[7-amino-2-{2-furyl}{1,2,4}triazolo{2,3-a} {1,3,5}triazin-5-yl-amino]ethyl)phenol (ZM-241385, 1.5 mg/kg) or the A(3) antagonist 3-propyl-6-ethyl-5[(ethylthio)carbonyl]-2-phenyl-4-propyl-3-pyridine carboxylate (MRS-1523, 2 mg/kg). CCPA and NECA reduced myocardial infarct size by 50% and 35%, respectively, versus vehicle, but CGS-21680 had no effect. DPCPX blunted the bradycardia associated with CCPA and NECA, whereas ZM-241385 attenuated their hypotensive effects. Both DPCPX and ZM-241385 blocked the protective effects of CCPA and NECA. The A(3) antagonist did not alter the hemodynamic effects of CCPA or NECA, nor did it alter adenosine agonist cardioprotection. None of the antagonists alone altered myocardial infarct size. These findings suggest that although preischemic administration of an A(2a) receptor agonist does not induce cardioprotection, antagonism of the A(2a) and/or the A(2b) receptor blocks the cardioprotection associated with adenosine agonist pretreatment.

Adenosine A2 Receptor Antagonists↗
PubMed2006

Successful management of recalcitrant groin lymphorrhoea with the combination of intraoperative lymphatic mapping and muscle flap.

Recalcitrant groin lymphorrhoea in high-risk patients remains a problem. In this report, a cardiac transplant patient with recalcitrant groin lymphorrhoea was successfully treated with a combination of intraoperative lymphatic mapping and sartorius muscle flap. We believe that the combined use of these two treatment options offers a more effective approach for surgical treatment of recalcitrant groin lymphorrhoea and should be considered when managing this difficult clinical problem, especially in high-risk patients.

Groin↗
PubMed2006

National Surgical Quality Improvement Program (NSQIP) risk factors can be used to validate American Society of Anesthesiologists Physical Status Classification (ASA PS) levels.

OBJECTIVE: The purpose of this study was to determine the relationship between the American Society of Anesthesiologists' Physical Status (ASA PS) classifications and the other National Surgical Quality Improvement Program (NSQIP) preoperative risk factors. BACKGROUND: The ASA PS has been shown to predict morbidity and mortality in surgical patients but is inconsistently applied and clinically imprecise. It is desirable to have a method for validating ASA PS classification levels. METHODS: The NSQIP preoperative risk factors, including ASA PS, were recorded from a random sample of 5878 surgical patients on 6 services between October 1, 2001 and September 30, 2003 at the University of Kentucky Medical Center. Mortality, morbidity, costs, and length of stay were obtained and compared across ASA PS levels. The ability of 1) ASA PS alone, 2) the other NSQIP risk factors, and, 3) all factors combined to predict outcomes was analyzed. A model using the other NSQIP risk factors was developed to predict ASA PS. RESULTS: ASA PS alone was a strong predictor of outcomes (P < 0.01). However, the other NSQIP risk factors were better predictors as a group. There was significant interdependence between the ASA PS and the other NSQIP risk factors. Predictions of ASA PS using the other factors showed strong agreement with the anesthesiologists' assignments. CONCLUSIONS: The NSQIP risk factors other than ASA PS can and should be used to validate ASA PS classifications.

Anesthesiology↗
PubMed2006

What do faculty observe of medical students' clinical performance?

BACKGROUND: An earlier study of our faculty's evaluation of junior medical students indicated that performance ratings were unreliable and reflected 1 underlying dimension. Other researchers have obtained similar results. PURPOSE: The purpose of this study was to identify which aspects of students' clinical performance faculty actually observe. METHODS: We analyzed the responses of 9 faculty members to an open-ended questionnaire concerning which aspects of clinical performance attending faculty observe. We also reviewed and summarized the written comments of 331 faculty evaluations of third-year medical students. RESULTS: Analysis of the questionnaires and evaluations indicated that faculty members gauge medical knowledge, professionalism, and clinical reasoning skills from direct interaction with students. History-taking and physical examination skills are inferred from the quality of verbal presentations. Faculty have little basis for evaluating other important aspects of clinical performance. CONCLUSIONS: Faculty primarily observe medical students' cognitive skills and professionalism. Faculty have little basis for evaluating most other features of clinical performance.

Clinical Competence↗
PubMed2005

Delayed adenosine A1 receptor preconditioning in rat myocardium is MAPK dependent but iNOS independent.

Adenosine A1 receptor delayed preconditioning (PC) against myocardial infarction has been well described; however, there have been limited investigations of the signaling mechanisms that mediate this phenomenon. In addition, there are multiple conflicting reports on the role of inducible nitric oxide synthase (iNOS) in mediating A1 late-phase PC. The purpose of this study was to determine the roles of the p38 and extracellular signal-regulated kinase (ERK) mitogen-activated protein kinases (MAPKs) in in vivo delayed A1 receptor PC and whether this protection at the myocyte level is due to upregulation of iNOS. Myocardial infarct size was measured in open-chest anesthetized rats 24 h after treatment with vehicle or the adenosine A1 agonist 2-chloro-N6-cyclopentyladenosine (CCPA; 100 microg/kg ip). Additional rats receiving CCPA were pretreated with the p38 inhibitor SB-203580 (1 mg/kg ip) or the MAPK/ERK kinase (MEK) inhibitor PD-098059 (0.5 mg/kg ip). At 24 h after CCPA administration, a group of animals was given the iNOS inhibitor 1400 W 10 min before ischemia. Treatment with CCPA reduced infarct size from 48 +/- 2 to 28 +/- 2% of the area at risk, an effect that was blocked by both SB-203580 and PD-098059 but not 1400 W. Ventricular myocytes isolated 24 h after CCPA injection exhibited significantly reduced oxidative stress during H2O2 exposure compared with myocytes from vehicle-injected animals, and this effect was not blocked by the iNOS inhibitor 1400 W. Western blot analysis of whole heart and cardiac myocyte protein samples revealed no expression of iNOS 6 or 24 h after CCPA treatment. These results indicate that adenosine A1 receptor delayed PC in rats is mediated by MAPK-dependent mechanisms, but this phenomenon is not associated with the early or late expression of iNOS.

Adenosine↗
PubMed2005

In vivo adenosine receptor preconditioning reduces myocardial infarct size via subcellular ERK signaling.

The protective effects of adenosine receptor acute preconditioning (PC) are well known; however, the signaling mechanism mediating this effect has not been determined in in vivo models. The purpose of this study was to determine the role of the extracellular signal-regulated kinase (ERK) pathway in mediating adenosine PC in in vivo rat myocardium. Open-chest rats were submitted to 25 min of coronary artery occlusion and 2 h of reperfusion. ERK activation was assessed by measuring total and dually phosphorylated p44/42 ERK isoforms in nuclear and/or myofilament, mitochondrial, cytosolic, and membrane fractions. Adenosine receptor PC with the A1/A2a agonist 1S-[1a,2b,3b,4a(S*)]-4-[7-[[2-(3-chloro-2-thienyl)-1-methylpropyl]amino]-3H-imidazo[4,5-b]pyridyl-3-yl]cyclopentane carboxamide (AMP-579) reduced infarct size from 49 +/- 3% to 29 +/- 3%, an effect that was blocked by the mitogen-activated protein kinase-ERK inhibitor U-0126. ERK isoforms were present in all fractions, with the greatest expression in the cytosolic fraction and the least in the mitochondrial fraction. AMP-579 treatment increased preischemic p44/42 ERK phosphorylation in all fractions 2.7- to 6.9-fold. Reperfusion increased ERK isoform activation in all fractions, but there were no differences between control and AMP-579 hearts. Preischemic increases in phospo-p44/p42 ERK with AMP-579 were blunted by U-0126, although only in mitochondrial and membrane compartments. The PC effects of AMP-579 on infarct size and ERK were blunted by both the A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine and, surprisingly, the A2a antagonist ZM-241385. These results indicate that the unique adenosine receptor agonist AMP-579 exerts its beneficial effects in vivo via both A1 and A2a receptor modulation of subcellular ERK isoform signaling.

Animals↗
PubMed2005

Aged rat myocardium exhibits normal adenosine receptor-mediated bradycardia and coronary vasodilation but increased adenosine agonist-mediated cardioprotection.

The purpose of this study was to determine whether aged myocardium exhibits decreased responsiveness to adenosine A1 and A(2a) receptor activation. Studies were conducted in adult (4-6 months) and aged (24-26 months) Fischer 344 x Brown Norway hybrid (F344 x BN) rats. Effects of the adenosine A1/A(2a) agonist AMP579 were measured in isolated hearts and in rats submitted to in vivo regional myocardial ischemia. Aged isolated hearts exhibited lower spontaneous heart rates and higher coronary resistance, as well as normal A1- and A(2a)-mediated responses. There was no difference in control infarct size between adult and aged rats; however, AMP579 treatment resulted in a 50% greater infarct size reduction in aged rats (18 +/- 4% of risk area) compared to adult rats (37 +/- 3%). These findings suggest that adenosine A1 and A(2a) receptor-mediated effects are not diminished in normal aged myocardium, and that aged hearts exhibit increased adenosine agonist-induced infarct reduction.

Aging↗
PubMed2005

Preoperative risk factors and surgical complexity are more predictive of costs than postoperative complications: a case study using the National Surgical Quality Improvement Program (NSQIP) database.

OBJECTIVE: This single-center study tested the hypothesis that preoperative risk factors and surgical complexity predict more variation in hospital costs than complications. BACKGROUND: Complications after surgical operations have been shown to significantly increase hospital cost. The impact on complication-related costs of preoperative risk factors is less well known. METHODS: The National Surgical Quality Improvement Program (NSQIP) preoperative risk factors, surgical complexity, and outcomes, along with hospital costs, were analyzed for a random sample of 5875 patients on 6 surgical services. Operation complexity was assessed by work RVUs (Centers for Medicare and Medicaid Services Resource Based Relative Value Scale). The difference in mean hospital costs associated with all variables was analyzed. Multiple linear regression was used to determine the cost variation associated with all variables separately and combined. RESULTS: Fifty-one of 60 preoperative risk factors, work RVUs, and 22 of 29 postoperative complications were associated with higher variable direct costs (P < 0.05). Linear regressions showed that risk factors predicted 33% (P < 0.001) of cost variation, work RVUs predicted 23% (P < 0.001), and complications predicted 20% (P < 0.001). Risk factors and work RVUs together predicted 49% of cost variation (P < 0.001) or 16% more than risk factors alone. Adding complications to this combined model modestly increased prediction of costs by 4% for a total of 53% (P < 0.001). CONCLUSION: Preoperative risk factors and surgical complexity are more effective predictors of hospital costs than complications. Preoperative intervention to reduce risk could lead to significant cost savings. Payers and regulatory agencies should risk-adjust hospital cost assessments using clinical information that integrates costs, preoperative risk, complexity of operation, and outcomes.

Databases as Topic↗
PubMed2005

Changing the paradigm for transfusing the anemic patient in an acute care environment.

Blood is a precious and vital resource in medicine. Its importance in maintaining human life is second only to the oxygen it transports. Nearly 300,000 blood product transfusions occurred in Kentucky last year. While donor attrition from the pool is inevitable, recruiting efforts have resulted in an overall stable donor population in the state over the last five years. Roughly 5% of community members who are eligible to donate do so each year. Despite our effort to constantly recruit new donors, there is evidence to suggest that clinicians are less than rigorous in their efforts to conserve and to be accountable for this precious human product. For example, the indications for blood transfusions are often not documented in up to a third of the cases, and arbitrary transfusion "triggers" are often the criteria used to justify transfusion rather than the patient's clinical condition. Recent development of evidence-based criteria for prevention and treatment of anemia combined with technological advances suggest that a major paradigm shift in the clinical use of red cells is warranted.

Acute Disease↗
PubMed2004

Acute adenosine preconditioning is mediated by p38 MAPK activation in discrete subcellular compartments.

Although acute adenosine preconditioning (PC) is well established, the signaling pathways mediating this cardioprotection remain unclear. Because adenosine receptor agonists activate p38 MAPK and this kinase has been implicated in ischemic and pharmacological PC, the purpose of this study was to determine the role of p38 MAPK in acute adenosine receptor PC. The role of p38 MAPK activation in discrete subcellular compartments during ischemia-reperfusion was also determined. The following groups were used in an in vivo rat ischemia-reperfusion model: 1) control (10% DMSO i.v.), 2) the A(1)/A(2a) adenosine receptor AMP-579 (50 microg/kg i.v.), 3) AMP-579 + the A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 100 microg/kg i.v.), 4) AMP-579 + the p38 MAPK inhibitor SB-203580 (1 mg/kg i.v.), and 5) SB-203580 alone. p38 MAPK activation was measured by Western blot analysis in cytosolic, mitochondrial, membrane, and nuclear/myofilament fractions obtained from hearts at preischemic, ischemic, and reperfusion time points. A significant reduction in infarct size was observed with AMP-579 PC, an effect blocked by DPCPX or SB-203580 pretreatment. AMP-579 treatment was associated with a significant increase in p38 MAPK activation in the nuclear/myofilament fraction before ischemia, whereas no activation of this kinase occurred during ischemia or reperfusion. In contrast, p38 MAPK was activated in the mitochondrial fraction by ischemia and in the cytosolic, mitochondrial, and membrane fractions by reperfusion in the control group. SB-203580 blocked the AMP-579-induced increase in phosphorylation of the downstream p38 substrate activating transcription factor-2. These results suggest a role for p38 MAPK activation in discrete subcellular compartments in acute adenosine A(1) receptor PC.

Adenosine↗
PubMed2004

Adenosine A1/A2a receptor agonist AMP-579 induces acute and delayed preconditioning against in vivo myocardial stunning.

The purpose of this study was to determine whether the adenosine A1/A2a receptor agonist AMP-579 induces acute and delayed preconditioning against in vivo myocardial stunning. Regional stunning was produced by 15 min of coronary artery occlusion and 3 h of reperfusion (RP) in anesthetized open-chest pigs. In acute protection studies, animals were pretreated with saline, low-dose AMP-579 (15 microg/kg iv bolus 10 min before ischemia), or high-dose AMP-579 (50 microg/kg iv at 14 microg/kg bolus + 1.2 microg.kg(-1).min(-1) for 30 min before coronary occlusion). The delayed preconditioning effects of AMP-579 were evaluated 24 h after administration of saline vehicle or high-dose AMP-579 (50 microg/kg iv). Load-insensitive contractility was assessed by measuring regional preload recruitable stroke work (PRSW) and PRSW area. Acute preconditioning with AMP-579 dose dependently improved regional PRSW: 129 +/- 5 and 100 +/- 2% in high- and low-dose AMP-579 groups, respectively, and 78 +/- 5% in the control group at 3 h of RP. Administration of the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (0.7 mg/kg) blocked the acute protective effect of high-dose AMP-579, indicating that these effects are mediated through A1 receptor activation. Delayed preconditioning with AMP-579 significantly increased recovery of PRSW area: 64 +/- 5 vs. 33 +/- 5% in control at 3 h of RP. In isolated perfused rat heart studies, kinetics of the onset and washout of AMP-579 A1 and A2a receptor-mediated effects were distinct compared with those of other adenosine receptor agonists. The unique nature of the adenosine agonist AMP-579 may play a role in its ability to induce delayed preconditioning against in vivo myocardial stunning.

Acute Disease↗
PubMed2004

Surveillance venous duplex is not clinically useful after total joint arthroplasty when effective deep venous thrombosis prophylaxis is used.

The early detection of deep venous thrombosis (DVT) and treatment with systemic anticoagulation to prevent pulmonary embolism (PE) are essential in the management of patients undergoing total joint arthroplasty (TJA). However, improvements in prophylactic measures have significantly decreased the occurrence of DVT in these patients. The purpose of this study was to determine whether routine postoperative duplex surveillance for DVT remains clinically useful. The medical records of all patients undergoing total knee or total hip arthroplasty between October 1997 and January 2002 at a University Hospital and its Veterans Affairs (VA) affiliate were reviewed. The type of operation and occurrence of complications (e.g., DVT, PE, and hemorrhage) were noted. All patients were treated postoperatively with both enoxaparin 30 mg b.i.d. and bilateral lower extremity sequential compression devices (SCDs). A venous duplex scan was performed prior to discharge. Three hundred ninety-eight patients underwent 441 TJAs for 149 hips and 292 knees. The average age was 65 years (range, 23-95). Venous duplex scans were performed within 1 week (median, 4 days) of operation. Initial inpatient scans revealed acute, ipsilateral DVT in five patients (1.3%). Three patients experienced documented PE-one as an inpatient and two after hospital discharge; both outpatients had negative inhospital duplex scans. One of the 398 patients did not have a duplex scan as an inpatient and returned 6 weeks later with a popliteal DVT. Complications included one upper gastrointestinal hemorrhage, and one patient died postoperatively of unknown causes. These data demonstrate that routine postoperative venous duplex scans rarely found DVT (5 of 398 patients) after TJA when effective prophylaxis was used. Furthermore, surveillance scanning did not enable reliable prediction of PE. Therefore, we conclude that postoperative inpatient surveillance duplex scans for DVT provide very minimal benefit and that a routine screening program is not clinically useful for patients managed with effective DVT prophylaxis.

Adult↗
PubMed2004

The p38 MAPK inhibitor SB203580 blocks adenosine A(1) receptor-induced attenuation of in vivo myocardial stunning.

There is considerable evidence implicating a key role for p38 mitogen-activated protein kinase (MAPK) in ischemic and pharmacological preconditioning against myocardial infarction. However, there have been few, if any, studies examining the role of p38 MAPK in the protection of stunned myocardium. The purpose of this study was to determine whether p38 MAPK plays a role in the adenosine A(1) receptor anti-stunning effect in in vivo porcine myocardium. Regional myocardial stunning in anesthetized, open-chest pigs was induced by 15 min of left anterior descending coronary artery (LAD) occlusion and 3 h of reperfusion (RP). Animals were treated with either vehicle (n = 5), AMP579 (70 microg/kg i.v.; 25 microg/kg bolus + 1.5 microg/kg/min for 30 min prior to ischemia, n = 5), the p38 MAPK inhibitor SB203580 (0.25 mg/kg i.v. bolus, n = 4) or a combination of SB203580 plus AMP579 (n = 5). Regional ventricular function was monitored by measurements of segment shortening and load insensitive parameters including preload recruitable stroke work (PRSW) and PRSW area (PRSWA). The ischemic area at risk was similar in all groups and there was no necrosis in any heart. Treatment with AMP579 significantly improved reperfusion regional PRSW and PRSWA compared to vehicle controls. The p38 inhibitor SB203580 alone did not alter the extent of myocardial stunning, but it abolished the beneficial effect of AMP579 pretreatment. These results provide the first evidence that p38 MAPK activation may play an important role in the mechanism by which adenosine agonists attenuate myocardial stunning.

Adenosine A1 Receptor Antagonists↗
PubMed2004

Evaluating alternative risk-adjustment strategies for surgery.

BACKGROUND: Comparison of institutional health care outcomes requires risk adjustment. Risk-adjustment methodology may influence the results of such comparisons. METHODS: We compared 3 risk-adjustment methodologies used to assess the quality of surgical care. Nurse reviewers abstracted data from a continuous sample of 2,167 surgical patients at 3 academic institutions. One risk adjustor was based on medical record data (National Surgical Quality Improvement Program [NSQIP]) whereas the other 2, the DxCG and Charlson Comorbidity Index (CCI), primarily used International Classification of Disease-9 (ICD-9) codes. Risk-assessment scores from the 3 systems were compared with each other and with mortality. RESULTS: Substantial disagreement was found in the risk assessment calculated by the 3 methodologies. Although there was a weak association between the CCI and DxCG, neither correlated well with the NSQIP. The NSQIP was best able to predict mortality, followed by the DxCG and CCI. CONCLUSION: In surgical patients, different risk-adjustment methodologies afford divergent estimates of mortality risk.

Evidence-Based Medicine↗
PubMed2004

The preischemic combination of the sodium-hydrogen exchanger inhibitor cariporide and the adenosine agonist AMP579 acts additively to reduce porcine myocardial infarct size.

BACKGROUND: We tested whether the combination of two known cardioprotective agents, the type-1 sodium-hydrogen exchanger inhibitor cariporide plus the adenosine A(1)/A(2a) receptor agonist AMP579 ([1S-[1a,2b,3b, 4a(S*)]]-4-[7-[[2-(3-chloro-2-thienyl)-1-methylpropyl]amino]-[(3)H]-imidazo[4,5-b]pyridyl-3-yl]cyclopentane carboxamide), acted additively to reduce myocardial infarct size. STUDY DESIGN: Pigs underwent 1 hour of coronary artery occlusion and 3 hours reperfusion. Vehicle-treated controls were compared with animals treated before ischemia with low-dose and high-dose cariporide and AMP579, and low-dose cariporide plus AMP579. The effects of both agents, alone and in combination, were also tested in isolated porcine polymorphonuclear neutrophils (PMNs). The PMN respiratory burst was induced with phorbol 12-myristate 13-acetate and quantified by the increase in 2',7'-dichlorofluorescein fluorescence, measured by flow cytometry. RESULTS: Infarct size in the control pigs was 65 +/- 1% of the area at risk. Cariporide dose-dependently reduced infarct size to 39 +/- 2% and 24 +/- 3% in the low- and high-dose groups, respectively. Infarct size was 54 +/- 3% in the low-dose AMP579 group and 47 +/- 3% with high dose. The combination of low doses of cariporide and AMP579 reduced infarction to 25 +/- 6% of the area at risk. In the PMN studies, cariporide and AMP579 alone had no effect on 2',7'-dichlorofluorescein fluorescence, but the combination of the two agents reduced the PMN 2',7'-dichlorofluorescein increase to 79 +/- 5% of the vehicle control response. CONCLUSIONS: The preischemic combination of low doses of cariporide and AMP579 decreased myocardial infarct size more than either agent used alone in low concentration, indicating an additive effect of the two agents. Given the effects that cariporide plus AMP579 combination exerted on PMN activity, it appears that this combination has the potential to reduce PMN-mediated effects during myocardial reperfusion.

Animals↗
PubMed2004

Sodium-hydrogen exchange inhibition attenuates in vivo porcine myocardial stunning.

BACKGROUND: Inhibition of the sodium-hydrogen exchanger isoform 1 with HOE-642 (cariporide) has been shown to protect against ischemia-reperfusion injury and to decrease myocardial cell death in numerous animal preparations; however the effects of cariporide in stunned myocardium are not as well understood. We sought to determine whether cariporide attenuated myocardial stunning in vivo. METHODS: Open chest anesthetized pigs (22-33 kg) were subjected to 15 min of left anterior descending coronary artery (LAD) occlusion followed by 3 h of reperfusion. Regional ventricular function was assessed by segment shortening. Contractility was measured by stroke work and by load-insensitive preload recruitable stroke work and preload recruitable stroke work area. Vehicle or HOE-642 (1 mg/kg, IV) was administered 10 min before LAD occlusion. RESULTS: Cariporide treatment significantly improved postischemic segment shortening, stroke work, preload recruitable stroke work, and preload recruitable stroke work area and had no systemic hemodynamic effects. After 3 h of reperfusion, control animals recovered 33% +/- 4% and 33% +/- 3% of preischemic LAD segment shortening and preload recruitable stroke work area values, respectively, whereas animals treated with HOE-642 recovered 59% +/- 6% and 57% +/- 6%, respectively (p < 0.05). Seven (39%) of 17 control animals exhibited ventricular fibrillation during reperfusion; none of the cariporide-treated pigs fibrillated. CONCLUSIONS: Sodium-hydrogen exchange inhibition can attenuate postischemic myocardial stunning in addition to its well-described anti-infarct properties. Inhibition of the sodium-hydrogen exchanger may be beneficial in patients susceptible to postischemic myocardial dysfunction associated with cardiac surgery.

Animals↗
PubMed2004

Replantation: past, present, and future.

The reattachment of completely severed parts has only been a clinical reality for 40 years. During that time there has been a shift in focus from refining technical aspects and improving success rates to assessing functional outcomes and better defining the indications for replantation. Although replantations are most frequently performed in academic environments, all practitioners should understand the basic indications for replantation as well as the principles of preservation of tissue. The advances in microsurgery and replantation over the past four decades have revolutionized the way reconstructive surgeons restore form and function to the body, and have laid the groundwork for new advances in composite tissue allotransplantation and tissue engineering.

Decision Making↗