Small optic suspensions for Advanced LIGO input optics and other precision optical experiments.

We report on the design and performance of small optic suspensions developed to suppress seismic motion of out-of-cavity optics in the input optics subsystem of the Advanced Laser Interferometer Gravitational Wave Observatory. These compact single stage suspensions provide isolation in all six degrees of freedom of the optic, local sensing and actuation in three of them, and passive damping for the other three.

Coulomb expansion of laser-excited ion plasmas.

We determine the electric field in mm-sized clouds of cold Rb+ ions, produced by photoionization of laser-cooled 87Rb atoms in a magneto-optical trap, using the Stark effect of embedded Rydberg atoms. The dependence of the electric field on the time delay between the ion plasma production and the probe of the electric field reflects the Coulomb expansion of the plasma. Our experiments and models show expansion times <1micros.

High-angular-momentum states in cold Rydberg gases.

Cold, dense Rydberg gases produced in a cold-atom trap are investigated using spectroscopic methods and time-resolved electron counting. Optical excitation on the discrete Rydberg resonances reveals long-lasting electron emission from the Rydberg gas ( >20 ms). Our observations are explained by lm-mixing collisions between Rydberg atoms and slow electrons that lead to the population of long-lived high-angular-momentum Rydberg states. These atoms thermally ionize slowly and with large probabilities.

Ponderomotive optical lattice for Rydberg atoms.

We propose to use the ponderomotive energy of Rydberg electrons in standing-wave light fields to form an optical lattice for Rydberg atoms. Application of the Born-Oppenheimer approximation shows that, with readily achievable experimental parameters, atoms in any Rydberg state can be trapped. Realization of this scheme would extend the benefits of atom trapping to highly excited atoms.

Removal of infected pacemaker leads with deep hypothermic circulatory arrest and open surgical exploration of the superior vena cava and innominate veins.

Despite the use of transvenous methods for extraction of infected leads, failed attempts may result in retained lead fragments. Retained lead fragments may be a focus of continued infection leading to sepsis. We present two patients in which conversion from cardiopulmonary bypass to hypothermic circulatory arrest allowed direct visualization, using venotomies in the superior vena cava and innominate vein to achieve complete removal of retained pacemaker lead fragments. Use of venotomies in the extracardiac venous system is a technical addition to prior descriptions of lead extraction using deep hypothermia and circulatory arrest.

Segmental pulmonary vascular resistance following wood smoke inhalation.

OBJECTIVES: To locate the specific site (i.e., pulmonary arteries, veins, or capillaries) of increased pulmonary vascular resistance after wood smoke inhalation and to demonstrate whether the prostanoids, thromboxane B2 or 6-keto-prostaglandin F1 alpha, play a role in these vascular resistance changes. DESIGN: Prospective, randomized, controlled trial. SETTING: Laboratory at a university medical center. SUBJECTS: Five mongrel dogs. INTERVENTIONS: The isolated canine left lower lobe preparation was used to measure changes in the pressure drop across the pulmonary arteries, veins, and capillaries. The left lower lobe was surgically isolated and perfused by a pump primed with autologous blood. The arterial and venous occlusion technique and the vascular pressure-flow relationship were used to assess changes in pulmonary vascular resistance. After baseline measurements, the left lower lobe was exposed to wood smoke for 2.5 mins and measurements were repeated. MEASUREMENTS AND MAIN RESULTS: Smoke exposure caused an immediate (5 mins post-inhalation) increase in the total pressure gradient across the lobe (baseline = 9.8 +/- 0.5 torr [1.3 +/- 0.06 kPa]); smoke inhalation = 24.3 +/- 3.9 torr [3.24 +/- 0.5 kPa]; p < .05). Total pressure drop was partitioned longitudinally into pressure drops across arteries, veins, and the middle vessels. The increase in total pressure drop was associated with a moderate increase in the pressure drop across the middle vessels (baseline = 1.1 +/- 0.2 torr [0.14 +/- 0.02 kPa]; smoke inhalation = 5.2 +/- 1.1 torr [0.69 +/- 0.14 kPa]; p < .05); a large increase in the pressure drop across the veins (baseline = 4.8 +/- 1.3 torr [0.64 +/- 0.17 kPa]; smoke inhalation = 20.7 +/- 3.4 torr [2.7 +/- 0.45 kPa]; p < .05), and no significant change in the pressure drop across the arteries (baseline = 3.7 +/- 0.4 torr [0.49 +/- 0.05 kPa]; smoke inhalation = 4.8 +/- 0.5 torr [0.64 +/- 0.06 kPa]; p = NS). Increases in the pressure drop across the middle and venous vessels were transient and no longer significantly different from baseline 15 mins after smoke inhalation. Similarly, analysis of the pulmonary artery/blood flow data demonstrated that the mean slope and pressure intercept were greater than baseline only at 5 mins postsmoke inhalation (p < .05). Thromboxane B2 did not significantly change from baseline values after smoke exposure and prostaglandin F1 alpha demonstrated a slight but significant decrease 30 mins postsmoke. Pulmonary edema was measured gravimetrically (wet/dry weight ratio) and smoke significantly increased lung water in the left lower lobe (wet/dry weight ratio = 6.55 +/- 0.4) as compared with the normal left upper lobe (wet/dry weight ratio = 4.97 +/- 0.2). CONCLUSIONS: We conclude that smoke causes an intense but transient increase in the pressure drop across the venous segment that may accelerate the formation of pulmonary edema, which is not mediated by changes in thromboxane B2 or prostaglandin F1 alpha.

Effect of early versus delayed hypoxic environment on neonatal rabbits.

We developed a low-cost, nonsurgical small animal model simulating the condition of cyanotic heart disease. Six groups of New Zealand white rabbits were studied: Group (1-C), 1-week-old control rabbits (n = 9) reared in room air; Group (1-H), 1-week-old rabbits placed in a hypoxic environment (10% O2) at birth (n = 5); Group (1-H-3), 1-week-old rabbits (n = 11) reared in room air for 3 days and then placed under hypoxic conditions identical to those for Group (1-C); Group (4-C), 4-week-old control rabbits (n = 12); Group (4-H), 4-week-old rabbits placed in hypoxia since birth (n = 11); Group (4-H-3), 4-week-old rabbits kept in room air after birth for 3 days (n = 7) before being exposed to hypoxia. Animals were anesthetized, heparinized, and instrumented for measurement of hemodynamic parameters. Right ventricular (RV) hypertrophy and hematocrit were assessed. Lung tissue was analyzed using quantitative morphometric techniques to assess arterial size, number, and muscularity. Group (1-H) and Group (4-H) developed RV hypertrophy, pulmonary hypertension, and erythrocytosis. The RV hypertrophy developed rapidly, as early as 1 week of age and became so pronounced by 4 weeks as to result in high mortality rate (35%). None of the animals in Groups (1-H-3) or (4-H-3) died while chronic changes of hypoxemia still developed. Placing rabbits after birth in room air for 3 days before exposing them to hypoxia appeared to play a protective role, moderating the development of pulmonary hypertension and severe RV hypertrophy. The effects of hypoxia appear to be at least partially dependent on the time of exposure. Utilizing our low-cost model will allow future work, including study of the effects of chronic hypoxemia on systemic ventricle exposed to an ischemic insult.

Exosurf treatment following wood smoke inhalation.

Pulmonary surfactant deactivation is an important factor in the pathophysiology caused by wood smoke inhalation. Surfactant replacement is beneficial in treatment of surfactant-deficient neonates and possibly the adult respiratory distress syndrome (ARDS). In this study, the effect of exogenous Exosurf treatment for acute wood smoke injury was examined in four groups of rabbits. All groups were anaesthetized, placed on a ventilator, and surgically prepared for haemodynamic, peak airway pressure (P(aw)), and blood gas measurements. Rabbits were monitored for 2 h following smoke or sham smoke inhalation. At the conclusion of the experiment pulmonary oedema and surfactant function were measured. A Control group (n = 5) was followed without intervention. A Smoke group (n = 4) was ventilated with wood smoke for 3 min. A third group (Smoke+Exo, n = 4) was subjected to smoke followed by pulmonary instillation of Exosurf (5 ml/kg). Saline (5 ml/kg) was instilled into the lungs of the fourth group (n = 3) as a control for Exosurf instillation. Saline, Smoke and Smoke+Exo all significantly lowered PO2 and elevated P(aw) compared to baseline and the Control group. Exosurf treatment did not reduce the pulmonary oedema or restore surfactant function caused by smoke exposure. This study indicates that wood smoke inhalation acutely damages the lung and that administration of Exosurf by instillation is not an effective treatment.

Recovery of hypoxic neonatal hearts after cardioplegic arrest.

OBJECTIVES: Surgery for repair of congenital heart defects in the infant may be affected by hypoxia associated with the defect. The effects of chronic hypoxia on systemic ventricular function are not well characterised and few studies have considered myocardial preservation in the hypoxic neonatal heart. The aim was to determine how chronic hypoxia would affect left ventricular function in neonatal rabbit hearts subjected to global ischaemia. METHODS: Hearts from rabbits one, four, and six weeks of age and raised at 9% O2 were compared with hearts from rabbits raised in ambient air. Haemodynamic variables were measured with an isolated heart preparation before and after cardioplegic arrest. Creatine kinase was measured during reperfusion and myocardial oxygen consumption (MVO2) during ischaemia. RESULTS: At all ages, hypoxic hearts had significantly lower peak dP/dt and contractility index (dP/dt/left ventricular pressure (LVP)) than normoxic controls. After ischaemia and reperfusion, one week hypoxic hearts did not differ significantly in recovery from controls. Four week hypoxic hearts had significantly higher stroke volume and aortic flow, and six week hearts had significantly higher coronary flow than age matched controls. Contractility index did not show significant differences between hypoxic and control animals at any age. Hypoxic hearts released less creatine kinase in the coronary effluent during reperfusion than did control hearts of similar age. Six week hypoxic hearts had significantly higher MVO2 measured during the second administration of cardioplegia compared with six week control hearts but MVO2 did not differ significantly at one and four weeks of age. CONCLUSIONS: Despite reduced baseline function, chronically hypoxic immature rabbit hearts can recover from an ischaemic insult as well as age matched controls, with less evidence of myocardial necrosis. This parallels clinical findings in cyanotic infants.