Biomedical subjects

I L Kron

Publications and source records attributed to I L Kron.

At least 55 records · Page 3Linked to original sources

PubMed2000

Attenuation of lung reperfusion injury after transplantation using an inhibitor of nuclear factor-kappaB.

A central role for nuclear factor-kappaB (NF-kappaB) in the induction of lung inflammatory injury is emerging. We hypothesized that NF-kappaB is a critical early regulator of the inflammatory response in lung ischemia-reperfusion injury, and inhibition of NF-kappaB activation reduces this injury and improves pulmonary graft function. With use of a porcine transplantation model, left lungs were harvested and stored in cold Euro-Collins preservation solution for 6 h before transplantation. Activation of NF-kappaB occurred 30 min and 1 h after transplant and declined to near baseline levels after 4 h. Pyrrolidine dithiocarbamate (PDTC), a potent inhibitor of NF-kappaB, given to the lung graft during organ preservation (40 mmol/l) effectively inhibited NF-kappaB activation and significantly improved lung function. Compared with control lungs 4 h after transplant, PDTC-treated lungs displayed significantly higher oxygenation, lower PCO(2), reduced mean pulmonary arterial pressure, and reduced edema and cellular infiltration. These results demonstrate that NF-kappaB is rapidly activated and is associated with poor pulmonary graft function in transplant reperfusion injury, and targeting of NF-kappaB may be a promising therapy to reduce this injury and improve lung function.

Animals↗

PubMed1999

Does a focal neurologic deficit contraindicate operation in a patient with endocarditis?

BACKGROUND: As many as 40% of patients with left-sided bacterial endocarditis will sustain a neurologic insult. The importance of a neurologic change as an indication or a contraindication for valve replacement remains controversial. METHODS: We performed a retrospective analysis of the records of 33 patients admitted to the University of Virginia Health Sciences Center between January 1, 1978, and June 30, 1996, with a diagnosis of endocarditis and a neurologic change. RESULTS: All 33 patients had echocardiographic or pathologic evidence of left-sided endocarditis; 23 were seen with focal neurologic findings and had a mortality rate of 22% (5 of 23), and 10 patients were seen with nonfocal, diffuse encephalopathy and had a mortality rate of 60% (6 of 10) (p<0.05). Of the 33 patients, 14 underwent operation and 19 were treated medically. The mortality rate was 21.4% (3 of 14) in the surgical group and 42.1% (8 of 19) in the medical group (p = not significant). In 71% (10 of 14) of the surgical patients, the operation was done within 1 week of the neurologic event. Additional neurologic deterioration occurred in 18.2% (2 of 11) of survivors in the surgical group and 9.1% (1 of 11) in the medical group (p = not significant). CONCLUSIONS: Choosing therapy for a patient with endocarditis and a neurologic change remains a difficult challenge. Initial findings of nonfocal, global dysfunction on examination are a predictor of a poor outcome. By comparing surgical and medical groups derived from the same series of patients, it is clear that patients with bacterial endocarditis and central nervous system changes face substantial mortality regardless of intervention. However, these data demonstrate that when compared with a similar group of medical patients, surgical patients who require and receive operation early in the course of their illness do comparatively well. Improving outcomes by delaying surgical intervention may serve to "select out" hardier patients but will lead to the death of patients who might benefit from such intervention.

Adult↗

PubMed1999

Reduced neutrophil infiltration protects against lung reperfusion injury after transplantation.

BACKGROUND: There is evidence that lung ischemia reperfusion injury is a result of the activation of components of the inflammatory cascade. However, the role of neutrophils in lung reperfusion injury continues to be a source of controversy. METHODS: Using an isolated, whole blood-perfused, ventilated rabbit lung model, we sought to characterize the pattern of reperfusion injury and investigate the contribution of neutrophils to this injury. Donor rabbits underwent lung harvest after pulmonary arterial prostaglandin E1 injection and Euro-Collins preservation solution flush. Group I lungs (n = 8) were immediately reperfused without ischemic storage. Group II lungs (n = 8) were stored for 18 h at 4 degrees C before reperfusion. Group III lungs (n = 10) underwent 18 h of ischemic storage and were reperfused with whole blood that was first passed through a leukocyte-depleting filter. All lungs were reperfused for 2 h. RESULTS: Arterial oxygenation in group III progressively improved, and was significantly higher than that of group II after 2 h of reperfusion (272.58+/-58.97 vs 53.58+/-5.34 mm Hg, p = 0.01). Both pulmonary artery pressure and pulmonary vascular resistance were significantly reduced in group III when compared with group II (27.85+/-1.45 vs 44.15+/-4.77 mm Hg, p = 0.002; and 30,867+/-2,323 vs 52,775+/-6,386 dynes x sec x cm(-5), p = 0.003, respectively). Microvascular permeability in group III lungs was reduced to 73.98+/-6.15 compared with 117.16+/-12.78 ng Evans blue dye/g tissue in group II (p = 0.005). Group III myeloperoxidase activity was 56.92+/-6.31 deltaOD/g/min compared with 102.84+/-10.41 delta0d/g/min in group II (p = 0.002). CONCLUSIONS: Leukocyte depletion of the blood reperfusate protects against microvascular permeability and significantly improves pulmonary graft function. The neutrophil plays a major role in amplifying lung injury later during reperfusion, and this lung ischemia reperfusion injury may be reversed through the interruption of the inflammatory cascade and the interference with neutrophil infiltration.

Animals↗

PubMed1999

Spinal cord protection during aortic cross-clamping using retrograde venous perfusion.

BACKGROUND: Paraplegia remains a devastating complication following thoracic aortic operation. We hypothesized that retrograde perfusion of the spinal cord with a hypothermic, adenosine-enhanced solution would provide protection during periods of ischemia due to temporary aortic occlusion. METHODS: In a rabbit model, a 45-minute period of spinal cord ischemia was produced by clamping the abdominal aorta and vena cava just below the left renal vessels and at their bifurcations. Four groups (n = 8/group) were studied: control, warm saline, cold saline, and cold saline with adenosine infusion. In the experimental groups, saline or saline plus adenosine was infused into the isolated cavae throughout the ischemic period. Clamps were removed and the animals to recovered for 24 hours before blinded neurological evaluation. RESULTS: Tarlov scores (0 = paraplegia, 1 = slight movement, 2 = sits with assistance, 3 = sits alone, 4 = weak hop, 5 = normal hop) were (mean +/- standard error of the mean): control, 0.50 +/- 0.50; warm saline, 1.63 +/- 0.56; cold saline, 3.38 +/- 0.26; and cold saline plus adenosine, 4.25 +/- 0.16 (analysis of variance for all four groups, p < 0.00001). Post-hoc contrast analysis showed that cold saline plus adenosine was superior to the other three groups (p < 0.0001). CONCLUSION: Retrograde venous perfusion of the spinal cord with hypothermic saline and adenosine provides functional protection against surgical ischemia and reperfusion.

Animals↗

PubMed1999

Protection in the failing heart.

Myocardial protection for surgical procedures on the failing heart can be broken down into three areas. The first area involves selection of the appropriate patient with enough myocardial viability and contractile reserve to permit a substantial cross-clamp time. Secondly, there should be adequate targets to revascularize or adequate tissue for reparative surgery. Thirdly, and most importantly, antegrade and retrograde blood cardioplegia given in sufficient amounts to satisfy myocardial oxygen needs is of prime importance.

Cardioplegic Solutions↗

PubMed1999

Preservation of intercostal arteries during thoracoabdominal aortic aneurysm surgery: a retrospective study.

OBJECTIVE: The purpose of this article was to examine the influence of reimplantation of patent intercostal and lumbar arteries on the incidence of postoperative paraplegia/paraparesis in patients undergoing clamp-and-sew surgical repair of thoracoabdominal aortic aneurysms. METHODS: Data from January 1987 through December 1997 were retrospectively collected on 132 patients. Ninety-one patients in group I underwent aneurysm repairs before January 1995 and did not undergo intercostal artery reimplantation. Group II included the more recent 41 patients who had vessels between the eighth thoracic intercostal and the second lumbar arteries reimplanted to the graft or preserved at the aortic anastomoses. RESULTS: The operative mortality rate was 13.2% (12/91) in group I and 4.9% (2/41) in group II (P =.22). The incidence of postoperative paraplegia was significantly lower in the more recent cohort of patients (8.8% [8/91] in group I vs 0% [0/41] in group II, P =.05). The overall rate of spinal cord dysfunction was lowered from 9.9% (9/91) in group I to 2.4% (1/41) in group II (P =.17). However, a multivariable logistic regression analysis identified only aneurysm extent (Crawford type I and type II) as a predictor of less postoperative spinal cord injury (P =.08). The average aortic crossclamp time in group I was 30.3 +/- 11.5 (SD) minutes, and the time of aortic occlusion in group II was not significantly prolonged, with an average crossclamp time of 31.0 +/- 21.0 (SD) minutes (P =. 88). CONCLUSIONS: An aggressive approach to maintain intercostal artery patency during clamp-and-sew repair of thoracoabdominal aortic aneurysms may effectively lower the incidence of spinal cord injury without prolonging aortic crossclamp time.

Aged↗

PubMed1999

Selective adenosine-A2A activation reduces lung reperfusion injury following transplantation.

BACKGROUND: The adenosine-A2A receptor on the neutrophil is responsible for several anti-inflammatory actions. We hypothesized that DWH-146e, a selective adenosine-A2A agonist, would reduce lung reperfusion injury following transplantation. METHODS: We used an isolated, whole blood-perfused, ventilated rabbit lung model. Donor rabbits underwent lung harvest after pulmonary arterial PGE1 injection and Euro-Collins preservation solution flush, and lungs were preserved for 18 hours at 4 degrees C. Group I lungs (n = 9) served as control subjects. Group II lungs (n = 9) were reperfused with whole blood that was first passed through a leukocyte-depleting filter. In group III (n = 9), DWH-146e was added to the blood reperfusate (25 microg/kg) immediately before reperfusion and was administered throughout the reperfusion period (1 microg/kg/min). All lungs were reperfused for 30 minutes. RESULTS: Arterial oxygenation in group II and group III was significantly higher than that of group I after 30 minutes of reperfusion (514.27 +/- 35.80 and 461.12 +/- 43.77 vs 91.41 +/- 20.58 mm Hg, p < .001). Pulmonary vascular resistance was significantly reduced in group III (22,783 +/- 357 dynes x s x cm(-5)) compared to both group II and group I (31,057 +/- 1743 and 36,911 +/- 2173 dynes x s x cm(-5), p < .001). Airway compliance was improved in groups II and III when compared to group I (1.68 +/- 0.08 and 1.68 +/- 0.05 vs 1.36 +/- 0.13, p = .03). Microvascular permeability in group III was reduced to 106.82 +/- 17.09 compared with 165.70 +/- 21.83 ng Evans blue dye per gram of tissue in group I (p = .05). Group III myeloperoxidase activity was 39.88 +/- 4.87 compared with 88.70 +/- 18.69 deltaOD/g/min in group I (p = .03); group II myeloperoxidase activity was 56.06 +/- 7.46. CONCLUSIONS: DWH-146e reduced lung neutrophil sequestration and dramatically improved pulmonary graft function. Neutrophils are important components of the inflammatory cascade of reperfusion injury and their source may include both the circulating blood and the lung graft itself. Selective adenosine-A2A activation interrupts the neutrophil-mediated inflammatory response and reduces lung reperfusion injury following transplantation.

Adenosine↗

PubMed1998

Effect of implantable cardioverter-defibrillator implantation on surgical morbidity in the CABG Patch Trial. Surgical Investigators of the Coronary Artery Bypass Graft Patch Trial.

BACKGROUND: The Coronary Artery Bypass Graft (CABG) Patch Trial tested the hypothesis that prophylactic insertion of an implantable cardioverter-defibrillator (ICD) improves survival rates after high-risk CABG. We compared group-specific perioperative morbidity and mortality rates. METHODS AND RESULTS: Patients were randomized intraoperatively to undergo CABG (control subjects, n = 454) or CABG plus ICD implantation (n = 446). There were no significant differences between groups in the incidence of diabetes, ejection fraction < 0.25, end-diastolic pressure, prior myocardial infarction, or congestive heart failure. Cardiopulmonary bypass time averaged 106 minutes in control subjects and 127 minutes in the ICD group. At the inception of the trial, investigators were concerned that ICD therapy could increase surgical mortality rates or the incidence of shock, bleeding, congestive heart failure, arrhythmias, or deep sternal wound infection. Of these, only sternal wound infection was significantly more frequent in the ICD group (2.2% versus 0.4%, P < 0.05). Also more common in the ICD group were infection at a wound or catheter site (12% versus 6%), urinary tract infection (4% versus 1%), pneumonitis (8% versus 4%), respiratory insufficiency (13% versus 8%), transient central nervous system deficit (6% versus 2%), and psychotic reaction (4% versus 1%). The all-cause death rate was 6.7% in the ICD group and 4.6% for control patients (P = NS) at the time of the last surgical death, postoperative day 48. CONCLUSIONS: Epicardial ICD insertion during CABG is associated with an increase in perioperative infection. Although reporting bias may have influenced the data, if ICD insertion is indicated in CABG patients, metachronous endocardial implantation should be considered.

Adult↗

PubMed1998

Nitric oxide potentiates acute lung injury in an isolated rabbit lung model.

BACKGROUND: The effect of inhaled nitric oxide (NO) treatment on pulmonary function in the setting of adult respiratory distress syndrome is controversial. We examined the effect of inhaled NO on pulmonary function in an isolated rabbit lung model of oleic acid (OA)-induced acute lung injury. We hypothesized that NO would decrease pulmonary artery pressure and improve oxygenation. METHODS: Rabbit heart-lung blocks were isolated, flushed in vivo, harvested, and immediately perfused with whole blood and ventilated with 50% oxygen (O2). Pulmonary artery pressure was determined every 15 seconds for 60 minutes of perfusion. Oxygenation was determined by blood gas analysis of pulmonary venous effluent at 0, 20, 40, and 60 minutes after initiation of OA infusion. Rabbits were randomized into four study groups: saline control; OA control, which received a 20-minute infusion of 50% OA/ethanol solution; NO treatment (20 ppm NO inhaled before OA infusion); and NO control, which underwent NO (20 ppm) pretreatment, followed by saline infusion. Pulmonary artery pressure, oxygenation (arteriovenous O2 difference), compliance, and wet/dry lung weight were determined. RESULTS: Pretreatment with NO caused significant increases in pulmonary artery pressure (NO treatment versus NO control and saline control; no significant difference between NO treatment group and OA control group), and did not improve oxygenation in our model. CONCLUSIONS: Contrary to our hypothesis, pretreatment with NO potentiates acute lung injury in our isolated lung model. There was significant exacerbation of pulmonary hypertension and no improvement in oxygenation. Further investigation of the possible deleterious effects of NO in acute lung injury are needed, especially in the early acute phases of this process.

Animals↗

PubMed1998

Replacing the atherosclerotic ascending aorta is a high-risk procedure.

BACKGROUND: Improved techniques in cerebral and myocardial protection have made replacement of the chronically aneurysmal ascending thoracic aorta a safe and effective procedure. We hypothesized that patients with severe ascending or aortic arch atherosclerosis were at greater risk for operative complications during ascending aortic replacement because of the diffuse nature of their atherosclerotic process. METHODS: We retrospectively analyzed the records of 17 patients who received ascending aortic replacement during elective coronary artery bypass grafting (CABG) because of the intraoperative finding of severe atherosclerosis. All 17 patients underwent tube graft replacement of the ascending aorta under hypothermic circulatory arrest and retrograde cerebral perfusion before coronary artery bypass grafting. The outcomes for these patients were compared with those of a control group of 89 consecutive patients who underwent replacement for ascending thoracic aortic aneurysm. RESULTS: The hospital mortality rate for replacement of the ascending thoracic aorta for severe atherosclerosis was 23.5% (4/17) versus 2.25% (2 of 89) for the control group (p=0.006). The incidence of cerebrovascular accident in the atherosclerotic group was 17.6% (3/17) and 3.37% (3/89) for the control group (p=0.051). Nine of 17 atherosclerotic patients (52.9%) had operative morbidity. Only 20.2% (18 of 89) of the control patients had nonfatal postoperative complications. CONCLUSIONS: The severely atherosclerotic ascending aorta is a marker of diffuse atherosclerosis. Despite improved techniques of myocardial and cerebral protection, we have been unable to duplicate our success with ascending thoracic aneurysm repair. Preoperative screening of the ascending aorta by chest computed tomography may be appropriate in select high-risk patients to determine operability.

Aged↗

PubMed1998

Inhibition of inducible nitric oxide synthase after myocardial ischemia increases coronary flow.

BACKGROUND: The role of nitric oxide synthase in myocardial ischemia-reperfusion injury is complex. Our hypothesis was that inducible nitric oxide synthase has a role in the regulation of coronary flow after ischemia. METHODS: Four groups of isolated blood-perfused rabbit hearts underwent sequential periods of perfusion, ischemia, and reperfusion (20, 30, and 20 minutes). Two groups underwent 40 minutes of perfusion. Ischemic groups received saline vehicle, N omega-nitro-L-arginine methyl ester (L-NAME) or the highly specific inducible nitric oxide synthase inhibitor 1400W in low or high doses during reperfusion. Two nonischemic groups were treated with saline vehicle or 1400W during the last 20 minutes of perfusion. Left ventricular developed pressure and coronary flow were measured after each perfusion period. Ventricular levels of myeloperoxidase and cyclic guanosine monophosphate were measured at the end of the second perfusion period. RESULTS: Coronary flow was significantly increased in both 1400W groups versus L-NAME (p < 0.001) and in high-dose 1400W versus control (p < 0.001). Coronary flow was not significantly different between the nonischemic groups. Left ventricular developed pressure was not significantly different among the ischemic groups or between the two nonischemic groups. There were no differences in cyclic guanosine monophosphate levels in any of the ischemic hearts. Myeloperoxidase levels were significantly elevated in L-NAME versus high-dose 1400W, nonischemic 1400W, and nonischemic saline groups (p < 0.02). CONCLUSIONS: Highly selective inhibition of inducible nitric oxide synthase results in increased coronary flow after ischemia but not after continuous perfusion. This occurs with decreased neutrophil accumulation and a trend toward increased contractility without elevation of cyclic guanosine monophosphate levels.

Animals↗

PubMed1998

Simultaneous coronary artery bypass grafting and abdominal aneurysm repair decreases stay and costs.

BACKGROUND: Patients with large (> or = 5.0 cm) abdominal aortic aneurysms (AAA) frequently have marked associated coronary artery disease. We hypothesized that a single operation for coronary artery bypass grafting (CABG)/AAA would provide equivalent, if not improved, patient care while decreasing postoperative length of stay and hospital costs compared with staged procedures. METHODS: Eleven patients to date have undergone a combined procedure at our institution. Ten underwent CABG followed by AAA repair, whereas one patient received an aortic valve replacement before aneurysm repair. We performed a retrospective analysis comparing the postoperative length of stay and hospital costs for this single procedure to a combined cohort of 20 randomly selected patients who either received AAA repair (n = 10) or standard CABG (n = 10) during the same time period. RESULTS: No operative mortality has been reported. There were no episodes of neurologic deficit or cardiac complication after these procedures. The postoperative length of stay was significantly decreased for the CABG/AAA group compared with the combined postoperative length of stay for the AAA plus CABG group (7.44+/-0.88 days versus 14.10+/-2.00; p = 0.012). Total hospital costs were also significantly decreased for the CABG/AAA group compared with total hospital costs for the AAA plus CABG group ($22,941+/-$1,933 versus $34,076+/-$2,534; p = 0.003). CONCLUSIONS: A single operation for coronary revascularization and AAA repair is safe and effective. Simultaneous CABG and AAA repair substantially decreases postoperative length of stay and hospital costs while avoiding possible interim aneurysm rupture and repeat anesthesia.

Aged↗

PubMed1998

Heparin preserves nitric oxide activity in coronary endothelium during ischemia-reperfusion injury.

BACKGROUND: Brief episodes of ischemia followed by reperfusion adversely affect endothelial vasomotor function. We hypothesized that heparin may impart a protective effect on the coronary endothelium during ischemia-reperfusion injury possibly via the nitric oxide pathway. METHODS: Eighteen anesthetized dogs were randomly assigned to one of two treatment groups: saline solution or bovine heparin (6.0 mg x kg intravenously). A flow probe and cannula were placed in the left anterior descending artery. Functional recovery of the coronary endothelium was assessed after 15 minutes of ischemia and during 120 minutes of reperfusion after acetylcholine and nitroprusside challenge. In a separate group (n = 10), nitric oxide activity was measured as nitrate/nitrite levels and cyclic guanosine monophosphate levels in the left anterior descending artery. RESULTS: Control dogs displayed a significant decrease in percent change of left anterior descending artery flow at 15, 30, and 60 minutes of reperfusion (67%+/-8%, 76% +/-11%, and 84%+/-8%) when compared with preischemic values (108+/-6; p < 0.01). Heparinized dogs, however, showed preservation of coronary endothelial function after acetylcholine challenge throughout reperfusion. Heparin-treated dogs also displayed a significant increase in nitrate/nitrite levels during reperfusion (37.3+/-4.1 micromol/L) when compared with the saline group (24.3+/-0.8 micromol/L; p < 0.03). Left anterior descending artery levels of cyclic guanosine monophosphate were also significantly increased after heparin administration (3.0+/-0.3 pmol/mg) when compared with ischemia-reperfusion alone (0.7+/-0.1 pmol/mg; p < 0.03). CONCLUSIONS: Heparin preserves the vasoregulatory function of the coronary endothelium during brief episodes of ischemia-reperfusion injury, in part, via the nitric oxide pathway. Administration of heparin may have important therapeutic implications in the prevention of coronary endothelial dysfunction associated with reperfusion injury.

Animals↗

PubMed1998

Preservation with 8-bromo-cyclic GMP improves pulmonary function after prolonged ischemia.

BACKGROUND: Cyclic guanosine monophosphate (cGMP) is a potent second messenger for the nitric oxide pathway in the pulmonary vasculature. Increased cytosolic cGMP levels elicit pulmonary vasodilatation resulting in decreased pulmonary vascular resistance and maximized pulmonary function after ischemia-reperfusion injury. We hypothesized that the addition of a membrane-permeable cGMP analogue (8-bromo-cGMP) to a Euro-Collins (EC) preservation solution would ameliorate pulmonary reperfusion injury better than prostaglandin E1 injection alone after prolonged hypothermic ischemia. METHODS: All lungs from New Zealand White rabbits (weight, 3 to 3.5 kg) were harvested en bloc, flushed with EC solution, and reperfused with whole blood for 30 minutes. Group 1 lungs (immediate control) were immediately reperfused. Group 2 lungs (control) were stored inflated at 4 degrees C for 18 hours before reperfusion. Groups 3 and 4 lungs were flushed with EC solution containing 200 micromol/L 8-bromo-cGMP and stored at 4 degrees C for 18 and 30 hours, respectively. Fresh, nonrecirculated venous blood was used to determine single-pass pulmonary venous-arterial oxygen gradients at 10-minute intervals. Assays for cGMP, cyclic adenosine monophosphate, nitric oxide synthase activity, and myeloperoxidase were performed on all lung tissue samples. Wet to dry weight ratios were determined after 2 weeks of passive desiccation. RESULTS: Oxygenation (venous-arterial oxygen gradient), pulmonary artery pressure, pulmonary vascular resistance, and edema formation were significantly improved in groups 3 and 4 (addition of 8-bromo-cGMP to EC plus 18 or 30 hours of hypothermic ischemia). Hypothermic storage (groups 2, 3, and 4) decreased both nitric oxide synthase activity and myeloperoxidase levels compared with immediate reperfusion (group 1). CONCLUSIONS: These results suggest that the addition of a membrane-permeable cGMP analogue to an EC pulmonary flush solution improves pulmonary function after prolonged storage compared with EC and prostaglandin (E1) preservation alone. The finding of myeloperoxidase reduced levels after hypothermic storage and subsequent reperfusion may suggest a more important role for pulmonary hemodynamic control in mitigating pulmonary reperfusion injury.

Alprostadil↗

PubMed1998

Hypothermic circulatory arrest does not increase the risk of ascending thoracic aortic aneurysm resection.

OBJECTIVE: The purpose of this study was to investigate the safety and efficacy of a period of deep hypothermic circulatory arrest (DHCA) during elective replacement of the ascending thoracic aorta. SUMMARY BACKGROUND DATA: DHCA has been implemented in ascending thoracic aortic aneurysm resection whenever the anatomy or pathology of the aorta or arch vessels prevents safe or adequate cross-clamping. Profound hypothermia and retrograde cerebral perfusion have been shown to be neurologically protective during ascending aortic replacement under circulatory arrest. METHODS: The authors conducted a retrospective analysis of 91 consecutive patients who underwent repair of chronic ascending thoracic aortic aneurysms from 1986 to present. The authors hypothesized that patients undergoing DHCA with or without retrograde cerebral perfusion during aneurysm repair were at no greater operative risk than patients who received aneurysm resection while on standard cardiopulmonary bypass. RESULTS: There were no significant differences in hospital mortality, stroke rate, or operative morbidity between patients repaired on DHCA when compared to those repaired on cardiopulmonary bypass. CONCLUSIONS: DHCA with or without retrograde cerebral perfusion does not result in increased morbidity or mortality during the resection of ascending thoracic aortic aneurysms. In fact, this technique may prevent damage to the arch vessels in select cases and avoid the possible complications associated with cross-clamping a friable or atherosclerotic aorta.

Aged↗

PubMed1998

Protective roles of nitric oxide and testosterone in endotoxemia: evidence from NOS-2-deficient mice.

Lipopolysaccharide (LPS)-induced septic shock, which triggers nitric oxide (NO) overproduction, multiple organ dysfunction, and death, can be affected by gender and sex hormones. We hypothesized that NO is beneficial during endotoxemia and that this beneficial effect is influenced by sex hormones. C57BL/6 wild-type (WT) mice and congenic inducible NO synthase knockout (KO) mice were injected with LPS, and mortality was recorded for 4 days. After 5 mg/kg LPS, female KO mice had significantly higher mortality than WT. After 12.5 mg/kg LPS, both male and female KO mice had significantly higher mortality than WT. Ovariectomy did not alter mortality, but orchiectomy dramatically increased mortality in KO mice. After 5 mg/kg LPS, exogenous testosterone completely prevented the increased mortality in KO female and orchiectomized KO male mice. WT survival was not affected by exogenous testosterone. After 12.5 mg/kg LPS, exogenous testosterone significantly improved survival of female KO mice. Serum enzymes and organ edema, which may not correlate with mortality, were significantly and similarly increased in both WT and KO endotoxemic mice; however, edema was not observed in KO hearts. Thus, NO plays a protective role in endotoxemia while having differential effects on different organs. Importantly, testosterone is beneficial in endotoxemia when NO production is deficient, and may be therapeutic in certain septic patients.

Animals↗

PubMed1998

Minimally invasive coronary artery bypass grafting.

Explore the source record for details and available documents.

Clinical Trials as Topic↗

PubMed1998

Successful treatment of exsanguinating aortic injury from a fractured rib.

A 57-year-old man presented in shock after a 15-foot fall from a ladder. A massive left hemothorax was present. He underwent prompt thoracotomy and was found to have a penetrating injury of the descending thoracic aorta caused by a fractured rib. Successful management of this type of aortic injury has not been previously reported.

Accidental Falls↗