Deep engraving of 3D textures is a very demanding process for the creation of master tool e. g molds, forming tools or coining dies. As these masters are uses for reproduction of 3D patterns the materials for the tools are typically hard and brittle and thus difficult to machine. The new generation of industrial femtosecond lasers provides both high accuracy engraving results and high ablation rates at the same time. Operation at pulse energies of typically 40 mu J and repetition rates in the Mhz range the detrimental effect of heat accumulation has to be avoided. Therefore high scanning speeds are required to reduce the pulse overlap below 90%. As a consequence scan speeds in the range of 25-50 m/s a needed, which is beyond the capability of galvo scanners. In this paper we present results using a combination of a polygon scanner with a high average power femtosecond laser and compare this to results with conventional scanners. The effects of pulse energy and scan speed of the head on geometrical accuracy are discussed. The quality of the obtained structures is analyzed by means of 3D surface metrology microscope as well as SEM images.

The effect of resuscitation with varying levels of O2 on pulmonary hemodynamics at birth is not well known. We hypothesized that the decrease in pulmonary vascular resistance (PVR) and subsequent response to pulmonary vasoconstrictors and vasodilators will differ following resuscitation with 21%, 50%, or 100%O2 for 30 min at birth in normal term lambs. Lambs at 141 d gestation were delivered by cesarean section and ventilated with 21% (21% Res; n = 6), 50% (50% Res; n = 6), or 100% O2 (100% Res; n = 7) for 30 min followed by ventilation with 21% O2 in all three groups. A greater decrease in PVR was seen with 50% and 100% O2 ventilation than with 21% O2 (0.21 ± 0.02, 0.21 ± 0.02, and 0.34 ± 0.05 mm Hg/mL/min/kg, respectively). Subsequent pulmonary vasoconstriction to hypoxia (10% O2) and the thromboxane analog U46619 (0.5 and 1 μg/kg/min) was similar in all three groups. After inducing a stable elevation in PVR with U46619, impaired pulmonary vasodilation to inhaled NO (59 ± 4, 65 ± 4, and 74 ± 5% of baseline PVR with 21, 50, and 100%Res, respectively) and acetylcholine infusion (67 ± 8, 75 ± 6, and 87 ± 4% of baseline PVR with 21, 50, and 100%Res, respectively) and rebound pulmonary hypertension following their withdrawal were observed in the 100%Res group. We conclude that, while ventilation with 100% O2 at birth results in a greater initial decrease in PVR, subsequent pulmonary vasodilation to NO/acetylcholine is impaired.

PURPOSE: In our fetal lamb model of PPHN, created by prenatal ligation of the ductus arteriosus, we found that endothelial NO gene expression is attenuated and that this may contribute to abnormal vasoreactivity and muscularization of the pulmonary circulation in fetal hypertension. This study characterizes changes in the cardiac muscle mass and wall thickness and pulmonary physiology in this model.

Activation of sGC by Nitric Oxide (NO) appears to be essential for the pulmonary vasodilation that allows the establishment of gas exchange by the lungs at birth. The relative role of each segment of the pulmonary vasculature of the newborn in this activation of sGC is not known. Immunohistochemistry using the B4 antibody to the 82 kDA subunit of rat sGC (cross reacts with the sheep) was used to study differences along the pulmonary vasculature in fetal sheep. Specific staining was confined to vascular smooth muscle layers. At 1:6400 dilution, all veins stained positively, whereas the largest positively stained artery was 200mm. All vessels at the level of small terminal and respiratory bronchioles and alveolar ducts stained intensely positive. This pattern of differential staining between small and large pulmonary arteries supports previous physiologic studies in fetal sheep lung showing decreased sensitivity to NO in pulmonary arteries greater than 500 mm in diameter but sustained activity in pulmonary veins. Our data supports a role for sGC activation in regulating tone in the intraacinar arteries and veins of the newborn pulmonary circulation.

An incidence of sensorineural hearing loss (SNHL) in infants surviving PPHN as high as 53% has been reported (Pediatrics. 81(5):650-6, 1988). However, one study reported an incidence as low as 0% in infants with similar echocardiographic and/or catheterization criteria (Pediatrics. 90(3):392-6, 1992). This latter study differs from all previous reports in that none of the infants were hyperventilated. Other confounders in these studies include dysmaturity, infection and the use of ototoxic drugs. In addition, PPHN has a variety of etiologies and no single method of management. Since there may be site-specific differences not only in management, but in the incidence of hearing loss, we looked at our own institution's experience.

Pulmonary hypertension in humans is characterized by significant increases in cell proliferation and extracellular matrix protein production in pulmonary vascular wall cells [1]. The fibroproliferative response in neonatal pulmonary hypertension is particularly exuberant compared with changes observed in adults, yet the reasons for these age-related differences remain, for the most part, obscure (Fig. 1).

Persistent pulmonary hypertension of the newborn (PPHN) is associated with chronic intrauterine events. Acute nitric oxide (NO) inhibition attenuates the normal increase in pulmonary blood flow at birth. We investigated whether chronic NO inhibition in utero causes persistent pulmonary hypertension. 11 fetal lambs received either a continuous infusion of N omega-nitro-L-arginine (an NO synthesis inhibitor) or 0.9% saline. Before infusion, acetylcholine (dependent upon endogenous NO production) and sodium nitroprusside (which releases its own NO) produced potent pulmonary vasodilation. After 10.5 +/- 1.5 d of infusion, acetylcholine did not produce pulmonary vasodilation in N omega-nitric-L-arginine-treated fetal lambs, but did in saline-treated fetal lambs; sodium nitroprusside produced pulmonary vasodilation in both groups. Immediately after birth, at 140 d of gestation, during the 3-h study period, mean pulmonary arterial pressure did not decrease in N omega-nitro-L-arginine-treated lambs; the increase in pulmonary blood flow and decrease in pulmonary vascular resistance were markedly attenuated compared to saline-treated lambs. These hemodynamic derangements were reversed by L-arginine. There were no anatomic abnormalities in the pulmonary circulation. Chronic NO inhibition in utero reproduces many of the physiologic derangements of PPHN. Intrauterine events which result in endothelial dysfunction and inhibition of NO may produce the physiologic derrangements of PPHN.

We evaluated the effect of hypoxia on the response of unanesthetized lambs (age 2-10 days) to hemorrhage of 50% of their measured blood volume over 30 min. All 15 lambs breathed 5% CO2 beginning 15 min. before hemorrhage and continuing for 90 min. after. The 5 lambs in Group I breathed 21% O2 throughout, the 5 in Group II breathed 9% O2 for the 15 min. prior to hemorrhage and then 21% O2, and the 5 in Group III breathed 9% O2 throughout the experiment. Organ blood flow was determined by radioactive microsphere technique and HR, BP, Hct, PO2, PCO2 and pH were measured 20 min. before, immediately before, at 2/3 of, at the end of, and at 90 min. after the hemorrhage. Group I had 4 survivors, Group II had 1, and Group III had none. The mortality in Group III was significantly greater than that in Group I (p≤0.05 Fischer exact). During the hemorrhage, BP and Hct fell similarly in all groups. In Group I, brain blood flow rose progressively throughout the experiment. In Group III, it rose with onset of hypoxia and then fell progressively thereafter. In Group II, it ran an intermediate course rising with the onset of hypoxia and then falling to baseline where it remained until shortly before death. Multiple regression analysis revealed a positive regression of brain blood flow on BP in Group III. We conclude that hypoxia during hemorrhage increases mortality and disrupts cerebral autoregulation.