Effects of phenylephrine or volume loading on right ventricular function in patients undergoing myocardial revascularization.

The acute effects of phenylephrine (PHE) administration or intravascular volume loading on right ventricular (RV) function were examined in 34 patients undergoing elective coronary artery surgery. After anesthetic induction with sufentanil and midazolam, 20 patients received PHE to treat hypotension and increase systemic arterial pressure 20% above baseline values. PHE effectively restored arterial pressure without changing stroke index (SI), although RV ejection fraction (RVEF) declined (41.3% to 37.6%) with concomitant increases in RV end-diastolic volume index (RVEDVI) (86.3 to 97.5 mL/m2) and RV end-systolic volume index (51.8 to 63.4 mL/m2). In the first 6 to 8 hours after surgery, 18 patients received intravascular volume expansion with 5% albumin when the clinical perfusion state was inadequate and accompanied by pulmonary artery occlusion pressure (PAOP) less than 15 mmHg and a hemoglobin level greater than 8 g/dL. Volume loading with 500 mL of albumin increased SI(27.0 to 31.8mL/m2), PAOP (12.2 to 15.4 mmHg) and RVEDVI (69.0 to 86.5 mL/m2), although RVEF declined (39.3% to 37.6%). Baseline values of RVEF and SI (but not PAOP or right atrial pressure [RAP]) were lower in 9 of 18 patients who exhibited declines in RVEF after volume loading, and RAP was a poor indicator of RVEDVI (r = 0.17). RVEDVI (but not RAP or PAOP) had significant correlation with SI during volume loading. There was no relationship between the presence of hemodynamically significant right coronary artery stenoses requiring revascularization or other perioperative factors with the response to PHE before revascularization or to volume loading after revascularization.(ABSTRACT TRUNCATED AT 250 WORDS)

Neutrophils are not necessary for ischemia-reperfusion lung injury.

The role of neutrophils (PMNs) in ischemia-reperfusion injury after lung transplantation is unclear. If PMNs are involved in ischemia-reperfusion injury in the intact rat, then PMNs should sequester in the injured lung and PMN-depleted rats should develop less injury. Group A rats were treated with a rabbit anti-rat PMN antibody causing profound neutropenia (less than 100 PMNs/microL) and group B with control serum (greater than 2,000 PMNs/microL). Rats were anesthetized and left lung ischemia was sustained for 90 or 180 minutes by clamping the bronchus and the pulmonary artery and vein. Lung injury was quantified by the accumulation of radiolabeled (125I) albumin in ischemic left and nonischemic right lungs (cpm per gram of lung/cpm per gram of blood). Ischemia caused significant lung injury (p less than 0.05) in both PMN-depleted (albumin leak index: 90 min, 0.208; 180 min, 0.218) and nondepleted (90 min, 0.222; 180 min, 0.241) animals compared with nonischemic controls (depleted: 90 min, 0.050; 180 min, 0.100; nondepleted: 90 min, 0.063; 180 min, 0.101); microscopy also demonstrated lung injury. The injury was not associated with PMN sequestration as shown by light microscopy. Thus, we conclude that PMNs are not necessary for ischemia-reperfusion injury and PMN-depletion does not attenuate ischemia-reperfusion injury.

Injection sclerotherapy-induced esophageal strictures. Risk factors and prognosis.

Injection sclerotherapy (IS) has become an effective modality for the treatment of bleeding esophageal varices. Despite improvements in equipment, sclerosant solutions and operator technique, injection sclerotherapy-induced esophageal strictures (ISES) remain a significant cause of patient morbidity. To analyze the risk factors and prognosis of ISES, the records of 117 patients who underwent IS over a 6-year period at a single teaching institute were reviewed. The predictive value of multiple risk factors including the patient's age, Child's risk classification, previous bleeding episodes, etiology of varices, cumulative amount of sclerosant used, and the number of IS treatments were determined using ANOVA. A P value of less than 0.05 was considered significant. In all cases, a free-hand injection technique, flexible endoscopes and sodium morrhuate were used. During a mean follow-up period of 228 days (1-1,469 days), 41 patients (35%) died and 24 patients (20.5%) developed symptomatic strictures. The cumulative amount of sclerosant used (81.4 +/- 9.5 ml) and the number of IS treatments (6.5 +/- 0.7) required in the stricture group was significantly greater than in the nonstricture group (49.1 +/- 2.7 and 4.0 +/- 0.3, respectively). The risk of stricture formation did not correlate with the volume of sclerosant injected per treatment, cause of varices, number of previous bleeds, or Child's hepatic risk class. A mean of 3.6 +/- 4.5 dilations was required for treatment of established strictures and 18 patients (75%) required r 4 dilations. One esophageal perforation occurred following dilation. Mortality correlated with hepatic risk class as 30/41 (73%) of deaths occurred in Child's C patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Neutrophils are not necessary for induction of ischemia-reperfusion lung injury.

Ischemia-reperfusion lung injury limits lung transplantation. Neutrophil activation and/or xanthine oxidase-mediated purine degradation may cause toxic oxygen metabolite production and lung injury. We investigated whether circulating blood elements are involved in the pathogenesis of ischemia-reperfusion lung injury. Isolated rat lungs were perfused with physiological salt solution (PSS) stabilized with Ficoll until circulating blood elements were not detected in the lung effluent. Lungs were then rendered ischemic by stopping ventilation and perfusion for 45 min at room temperature. Lung injury occurred and was quantitated by the accumulation of 125I-bovine serum albumin into lung parenchyma and alveolar lavage fluid during reperfusion. Lung injury occurred, in the absence of circulating blood elements, when ischemic lungs were reperfused with PSS-Ficoll solution alone. Reperfusion with whole blood or PSS-Ficoll supplemented with human or rat neutrophils did not increase lung injury. Furthermore, during lung ischemia, the presence of neutrophils did not enhance injury. Experiments using PSS-albumin perfusate and quantitating lung injury by permeability-surface area product yielded similar results. Microvascular pressures were not different and could not account for the results. Toxic O2 metabolites were involved in the injury because addition of erythrocytes or catalase to the perfusate attenuated the injury. Thus reperfusion after lung ischemia causes injury that is dependent on a nonneutrophil source of toxic O2 metabolites.

Amrinone versus conventional therapy in pulmonary hypertensive patients awaiting cardiac transplantation.

Pulmonary hypertension is associated with an increased perioperative mortality for orthotopic heart transplantation. A transpulmonary gradient greater than 15 mm Hg or a pulmonary vascular resistance greater than 5 Woods units increases mortality secondary to right heart failure. This study compares amrinone with conventional therapy in 38 transplant candidates with pulmonary hypertension. All patients had elevated transpulmonary gradient, pulmonary vascular resistance, or both. Group 1 (n = 21) received prolonged continuous intravenous amrinone therapy, whereas group 2 (n = 16) received high-dose oral diuretics, digitalis, and captopril. Both groups 1 and 2 had decreased pulmonary hypertension, transpulmonary gradient, and pulmonary vascular resistance. However, amrinone was more effective, with a 86% response rate versus 63% response for conventional therapy. Survival awaiting transplantation was significantly higher in group 1 (20 of 22, 91%) than in group 2 (10 of 16, 63%). Although both groups 1 and 2 had significantly decreased pulmonary vascular resistance, only group 2 had significantly decreased systemic vascular resistance. Comparison of pulmonary vascular resistance after therapy showed that the response in group 1 (amrinone) was significantly lower than the response in group 2 (conventional therapy), suggesting that amrinone may function as a direct vasodilator of the pulmonary vasculature. There were no operative deaths or episodes of perioperative right heart failure in either group. Amrinone appears to be more effective and safe than conventional therapy in the treatment of prospective heart transplant candidates with pulmonary hypertension.