Primary mediastinal germinomas in females: a case report and review of the literature.

Primary mediastinal germinomas in females are rare. Long-term survival ranges from 50 to 81%, depending on the initial extent of disease. Initial spread occurs intrathoracically and to regional nodes with late hematogenous dissemination. The roles of surgery, radiation therapy, and chemotherapy are discussed.

Reversal of experimental pulmonary hypertension with sodium nitroprusside.

Pulmonary vascular resistance may be elevated by the use of vasoconstrictive agents or by alveolar hypoxia. The present study was designed to determine the precise vasoconstrictive effects of the two inotropic agents, dopamine and epinephrine, as well as the effects of alveolar hypoxia on the pulmonary vascular system. In addition, the vasoactive effects of a known vasodilator, nitroprusside, were studied. A canine pulmonary lobar preparation was isolated in situ with its pulmonary artery and bronchus selectively cannulated in order to maintain a constant lobar pulmonary blood flow and in order to vary the inspired oxygen concentration from 95% to 0%. Pulmonary vascular pressures were determined by direct measurements and pulmonary vascular resistance units (PVRU) were calculated. Dopamine, epinephrine, and nitroprusside were infused into the isolated pulmonary artery singly and in combination, and the inspired oxygen concentration was varied during each drug infusion. The results of the study demonstrate that dopamine, epinephrine, and alveolar hypoxia all significantly elevate pulmonary vascular resistance. When these two drugs are used together in the presence of hypoxia, the effect on pulmonary resistance is additive. Furthermore, nitroprusside prevents the elevation of pulmonary vascular resistance caused by alveolar hypoxia, and when used with dopamine or epinephrine in the presence of hypoxia, nitroprusside reduces pulmonary vascular resistance toward normal.

Oral cholecystography in assessment of acute abdominal pain.

During one year, 77 patients had oral cholecystography within five days of the onset of acute upper abdominal symptoms. These patients were not severely ill, as evidenced by the fact that only 18 were hospitalized. The patients were unselected and the results were reviewed in retrospect. Accordingly, the data cannot be critically analyzed. Nonetheless, diagnostically useful information was obtained in 57 of these cases. In 44 patients, a normal gallbladder was visualized, and in 13 patients gallstones were seen. Three conclusions are derived from this study. First, oral cholecystography can be performed within five days of the onset of acute upper abdominal symptoms with a reasonable expectation of obtaining diagnostically useful information. Second, the usually recommended delay of four to six weeks is unnecessary. Finally, this diagnostic study should be performed in the acute situation when it is not precluded by nausea, vomiting, or a severely ill patient.

Beneficial effects of pulsatile perfusion in the hypertrophied ventricle during ventricular fibrillation.

To assess the potential benefit of pulsatile perfusion inthe hypertrophied heart during fibrillation, 10 dogs with left ventricular hypertrophy, produced by previous supravalvular aortic banding, were used to compare linear and pulsatile perfusion in the fibrillating heart during total cardiopulmonary bypass. The mass spectrometer was used to measure subendocardial PCO2 and PO2 (PmCO2 and PmO2), and radioactive microspheres were utilized to measure myocardial blood flow in the same layers. Pulsatile perfusion was established using the recently develop "bubble tubing," which produces a pulse pressure of at least 20 mm Hg and can be used in a standard roller-pump apparatus. Both linear and pulsatile flows were compared at mean aortic root pressures of 80 and 50 mm Hg, and these four combinations of aortic root pressure and type of flow were employed for periods of 30 minutes each. Myocardial ischemia developed during linear coronary perfusion at 50 mm Hg, as evidenced by an elevation of PmCO2. Ischemia was not evident during pulsatile perfusion at the same mean pressure. Reversal ischemia was a result of increased myocardial blood flow and pulsatile perfusion, and this increase was shown to occur maximally in the deeper subendocardial layer. Ischemia was not eviden during linear or pulsatile perfusion at an mean perfusion pressure 80 mm Hg. Thus, if lower perfusion pressures are to be tolerated in patients with left ventricular hypertrophy, pulsatile perfusion with the bubble tubing technique may prevent the development of subendocardial ischemia or infarction.

Comparison of myocardial protection with nifedipine and potassium.

Nifedipine, a slow-channel calcium blocker, is thought to provide useful myocardial protection during prolonged total ischemia and reperfusion. An isolated, isovolumic, feline heart model was used to asses the effectiveness of nifedipine in both cardioplegic (100 microgram/10 ml) and noncardioplegic (10 microgram/10 ml) doses for providing myocardial preservation during 90 minutes of hypothermic ischemic arrest and 45 minutes of normothermic reperfusion. Use of nifedipine was compared to hypothermia (27 degrees C) alone and to hypothermia with potassium cardioplegia. Ventricular function was assessed by recovery of isovolumic left ventricular developed pressure and dP/dt. Myocardial carbon dioxide tension (PCO2) and myocardial oxygen tension (PO2) were measured by mass spectrometry. Potassium cardioplegia and the higher dose of nifedipine resulted in immediate asystole. The rates of rise of PCO were greatest in the group receiving 10 microgram nifedipine and in the control group. The rates of rise in the two cardioplegic groups were significantly lower. Recovery of ventricular function was significantly lower with low-dose nifedipine than with potassium cardioplegia. Higher dose nifedipine resulted in a return of function, which was no different than with potassium cardioplegia. Morphologic protection was better with higher dose nifedipine and potassium cardioplegia than with either low-dose cardioplegia or hypothermia alone. These results demonstrate that nifedipine in a cardioplegic dose results in preservation of myocardial structure and function that is similar to that obtained with potassium cardioplegia. In lower noncardioplegic dose, nifedipine does not appear to offer additional protection compared to hypothermia alone. Whether persistent depression of ventricular contractility will limit nifedipine's clinical usefulness as a myocardial protection agent will require further study.

Potassium-induced cardioplegia during normothermic cardiac arrest. Morphologic study of the effect of varying concentrations of potassium on myocardial anoxic injury.

Most corrective procedures as well as myocardial revascularization require a period of cardiac arrest, and numerous methods have been proposed to protect the myocardium during this ischemic episode. Potassium-induced cardioplegia is one method that appears to be of benefit in this setting. Since it is recognized that myocardial necrosis may result at very high doses of potassium, we examined the effect of varying concentrations of potassium on myocardial anoxic injury. Using an isolated rat heart preparation, we evaluated anoxic injury occurring with cardioplegic solutions containing various concentrations of K+, ranging from 15 to 200 mEq. per liter, during a 50 minute normothermic arrest followed by 60 minutes of reperfusion. The transverse histologic sections of the left ventricular myocardium were analyzed for contraction band injury by morphometric and qualitative methods. Among the 62 animals studied the least severe anoxic injury was seen with K+ cardioplegia at concentrations of 25 and 30 mEq. per liter. At lower and higher concentrations there was little difference between the hearts exposed to anoxia with or without K+ cardioplegia. Potassium administered in very high doses, i.e., 100 or 200 mEq. of K+ per liter, led to contracture and extensive myocardial cell injury. This study suggests that potassium-induced cardioplegia is effective in reducing cell injury due to anoxia, and in this model an optimal concentration range was 25 to 30 mEq. per liter.

Effects of calcium administration during post-ischemic reperfusion on myocardial contractility, stiffness, edema, and ultrastructure.

Previous investigators have suggested that calcium may play a role in the pathogenesis of myocardial cell damage following ischemia and reperfusion. Twenty-six in-situ blood perfused isovolumic canine preparations were divided into four groups. Group I dogs were maintained normocalcemic during 45 min of reperfusion following 45 min of hypothermic (27 degrees C) ischemic arrest; Group II dogs received CaCl2 (7 mg/kg) after 15 min of reperfusion; Group III dogs received citrate solution (0.8 ml/kg citrate-phosphate-dextrose [CPD]) after 15 min of reperfusion; Group IV dogs received 7 mg/kg of CaCl2 at 5 min after receiving the same citrate dose as Group III after 15 min of reperfusion. In Group II hearts, calcium improved the left ventricular contractility (P < 0.05 vs Group I) without causing additional cellular or subcellular injury. Calcium also appeared to increase myocardial stiffness (alpha(n)) compared to Group I hearts (P < 0.01). In Group III hearts, citrate reduced contractility (P < 0.01 vs Group I) and increased myocardial edema (P < 0.005 vs Group I) without any apparent improvement in cellular or subcellular preservation. In Group IV hearts, calcium reversed the depression of contractility caused by citrate, resulted in no additional morphologic injury, increased myocardial stiffness compared to Group I or Group III (P < 0.005), and minimized myocardial edema (P < 0.005 vs Group I or III). These results suggest that calcium administered after 15 min of reperfusion improves the depression of contractility that follows hypothermic ischemic arrest without causing additional myocardial damage.

Primary mucinous adenocarcinoma of the appendix with bilateral Krukenberg ovarian tumors.

After experiencing intermittent episodes of abdominal pain for two years, a 28-year-old woman developed partial small bowel obstruction. Barium enema and colonoscopy revealed the source of obstruction to be an apparent cecal carcinoma. At exploratory laparotomy a primary adenocarcinoma of the appendix with bilateral Krukenberg ovarian metastases was found. This is a rare occurrence and, to our knowledge, the first well-documented case in the English literature. These case also demonstrates difficulties in the preoperative diagnosis of adenocarcinoma of the appendix.

Effects of procaine-induced cardioplegia on myocardial ischemia, myocardial edema, and postarrest ventricular function. A comparison with potassium-induced cardioplegia and hypothermia.

The extent of myocardial protection afforded by a procaine cardioplegic solution during cardiac ischemia has been evaluated and compared with the protection seen using a potassium cardioplegic solution. An isolated cat heart model was employed, and ventricular function parameters, intramyocardial gas tensions, and postischemic myocardial edema were measured and compared following 60 minutes of induced ischemia at 37 degrees C. and 27 degrees C. There was no significant improvement in recovery of postarrest ventricular function when procaine cardioplegia was used during normothermic ischemia. When used at 27 degrees C., however, both cardioplegic solutions were associated with significantly better recovery of postarrest ventricular function, although there was less myocardial edema formation in the potassium-treated hearts. Results of this study indicate that procaine-induced cardioplegia provides myocardial protection during anoxic cardiac arrest which is additive to that afforded by hypothermia alone. In addition, procaine cardioplegia results in postarrest functional recovery which is similar to that seen with potassium cardioplegia.

Improved myocardial performance in postoperative cardiac surgical patients with sodium nitroprusside.

Myocardial performance in the immediate postoperative period was studied 49 cardiac surgical patients treated with nitroprusside alone. With a thermodilution catheter positioned in the pulmonary artery, cardiac output was calculated and cardiac index, systemic vascular resistance index, and stroke work index were derived before after treatment with nitroprusside. The drug was a administered to all patients because of elevated systemic vascular resistance index. Based on their mean arterial pressure and cardiac index before treatment, the patients fell into two groups. Group I patients (N = 25) had elevated mean arterial pressure and normal cardiac index. Group II patients (N = 24) had normal mean arterial pressure and subnormal cardiac index. Nitroprusside administration resulted in a significant reduction of systemic vascular resistance index in all patients. In Group I the mean arterial pressure was lowered significantly while cardiac index increased only slightly. In Group II there was no change in arterial pressure, but cardiac index improved significantly. The results not only confirm that nitroprusside is effective in managing postoperative hypertension, but also demonstrate that in patients with postoperative left ventricular failure, the drug can improve cardiac output by reducing systemic vascular resistance without significantly lowering arterial blood pressure.

Elemental balances during intravenous hyperalimentation of underweight adult subjects.

Intravenous hyperalimentation was done in 11 underweight adults whose body weight (body wt) was less than 85 percent of ideal. For the first 6 days, "complete formula" was infused furnishing per kilogram ideal body wt per day: 15 g glucose, 0.40 g N, 0.018 g P, 2.4 meq K, 3.0 meq Na, 2.3 meq C1, 0.5 meq Mg, 0.45 meq Ca, and 50 ml H20. Patients gained weight at an average rate of 9.0 g/kg ideal body wt/day and showed average balances/kilogram ideal body wt/day as follows: plus 0.14 g N; plus 0.012 g P; plus 0.43 meq K; plus 0.49 meq Na; plus 0.37 meq Cl; and plus 0.085 meq Ca. Application of standard equations to the elemental balances indicated weight gain consisted of 35-50 percent protoplasm, 35-50 percent extracellular fluid, 5-25 percent adipose tissus, and less than 1 percent bone. Withdrawas of N, P, Na, or K impaired or abolished retention of other elements. Removal of N halted retention P, K, Na and C1; withdrawal of K stopped retention of N and P; and removal of Na or P interrupted retention of all other elements. Weight gain continued at a rate of 1.4-3.1 g/kg ideal body wt/day despite zero or negative elemental balances of N, K, P, and sometimes Na and C1. Calculations showed that weight gain during infusion of fluids lacking N, P, K, or Na consisted largely of adipose tissue, with little or no contribution by protoplasm or extracellular fluid. Data show that repletion of protoplasm and extracellular fluid of wasted adults by intravenous hyperalimentation is retarded or abolished if N, P, Na, or K is lacking. Repletion of bone mineral does not occur in absence of Na or P but proceeds in absence of N, P, K, or Na. Thus, quality of weight gained by underfed adult patients during hyperalimentation depends on elemental composition of the infusate.