Minimally invasive endoscopically assisted remodelation (MEAR) of sagittal craniosynostosis: an alternative technique to open and endoscopic procedures with cranial orthosis time span reduction.

INTRODUCTION: Sagittal craniosynostosis represents the most frequent simplex skull suture pathology. There are currently several operative approaches to this defect. Minimally invasive techniques are preferred for young infants. Since July 2017, we have employed endoscopically assisted craniectomies followed by cranial orthosis. Gradually, we have developed our modified technique, the minimally invasive endoscopically assisted remodelation (MEAR). SURGICAL TECHNIQUE: MEAR is a combination of principles gained from classical cranial vault remodeling techniques and minimal invasive approaches. The long and wider lateral osteoectomies performed in the parietal and occipital bones along with loosening of the periosteum and dura adhesions at the lambdoid sutures lead to early correction of parieto-occipital dimensions. RESULTS: Thirty-one consecutive patients with scaphocephaly underwent MEAR. The median preoperative cephalic index of 67 units (P25:63.3, P75:70) was improved to a median postoperative cephalic index of 77 units (P25:75, P75: 81). Sufficient correction was achieved in all patients. Cranial orthosis was needed for a median of 1.5 months (P25:1, P75:2). We had no major surgical complications in this pilot series. CONCLUSIONS: With MEAR, we have achieved good cosmetic results. Duration of cranial orthosis was significantly shortened compared to conventional endoscopic-assisted procedures.

Regulation of phospholipid degradation and biosynthesis in the heart by isoprenaline: effect of mepacrine.

We investigated the effect of isoprenaline (IPRO), a beta-mimetic catecholamine, on incorporation (32P)Pi into phospholipids of the mouse left ventricle in vivo. All experimental groups of male mice received an injection of (32P)Pi (250 MBq x kg-1 b.w.) intraperitoneally two hours prior to sacrifice. A single dose of IPRO (5 mg x kg-1 b.w.) was injected one hour before killing. IPRO increased the specific radioactivity of phosphatidylcholine (PC) by a factor of 1.8, diphosphatidylglycerol (DPG) 2.1, sphingomyelin (SM) 3.5, phosphatidylinositol (PI) 1.7, phosphatidylserine (PS) 1.7, phosphatidylglycerol (PG) 1.7, phosphatidic acid (PA) 2.0 compared to control values. On the other hand, IPRO is also known to stimulate phospholipid degradation by activation of phospholipase A2. That is why we used mepacrine (50 mg x kg-1 b.w.), a phospholipase inhibitor, to find a possible link between biosynthesis and degradation of phospholipids. Pretreatment with mepacrine two hours prior to sacrifice suppressed IPRO stimulated incorporation of (32P)Pi into phospholipids nearly to control levels. Mepacrine itself did not significantly influence the specific radioactivity of phospholipids. We conclude that phospholipase A2 inhibitor, mepacrine, is able to prevent IPRO-stimulated incorporation into phospholipids, suggesting a feedback relation between their biosynthesis and degradation in the myocardium.

Changes in the phospholipid content in the left heart ventricle of male mice during repeated administration of isoprenaline.

1. Male mice were injected 5 mg/kg isoprenaline (IPRO) daily and the heart weight, dry weight and phospholipid content in the left ventricle determined 24 hr after the last injection on days 1, 3, 5 and 10. 2. The phospholipid content sinks during the experiment, but the onset of the change is different in different phospholipids: for diphosphatidylglycerol it is clearly significant after 3 days, for phosphatidylcholine and phosphatidylethanolamine after 5 days and for sphingomyelin after 10 days; the relative amplitude of the change in this latter phospholipid was greatest of all. 3. If IPRO is given for 3 days and physiological saline for next 7 days, the content of some phospholipids (PE, SM and PG) continued to decrease. This suggests an important delayed effect of IPRO action.

The effect of isoprenaline on the phospholipid content of the compact and spongious musculature of the carp ventricular myocardium.

1. After a single injection of 40 mg kg-1 of isoprenaline to the carp, lysophospholipids appear in the tissue of the heart ventricle, ethanolamine plasmalogens increase and choline plasmalogens decrease; phosphatidylinositol is lowered in the spongious layer only. 2. Daily administration of 5 mg kg-1 of the drug leads, after 5 doses, to a dramatic decrease of the diphosphatidylglycerol content; during the subsequent 5 and 10 doses a return to normal values occurs. Shifts in plasmalogens are similar to those found after a single high dose. Some other phospholipids change significantly. 3. All changes reveal that the spongious musculature is more sensitive to the drug than the compact one.

Phospholipid content in the compact and spongious musculature of the carp heart (Cyprinus carpio).

The phospholipid content of the spongious and compact musculature of the heart of the carp (Cyprinus carpio) was compared. The content of phospholipids is higher in the spongious musculature, the greatest difference being in the content of diphosphatidylglycerol: 2.53 mumol P . g-1 wet weight in the spongious layer and 1.29 mumol P . g-1 wet weight in the compact one. In both tissues plasmalogens represent 20-27% of the tissue content of choline and ethanolamine phosphoglycerides.