Biomedical subjects
Publications and source records attributed to J Stutzmann.
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In organ culture, the chondroblasts of the rat mandibular condyle cartilage inhibit the mitotic activity of the prechondroblasts. Hypertrophy of the chondroblasts decreases their inhibitory action. The hypothetical "inhibitory signal" might be a chalone-like substance.
1. Two cell types are found in the mitotic compartment of a secondary cartilage of the mandible (condylar, angular and coronoid cartilages) and of the maxillary (cartilage of the sagital suture): - the "skeletoblast", which bears a spontaneous tendancy to differentiate into an osteoblast, but which differentiates in vivo into a chondroblast; - the prechondroblast, originating from the skeletoblast and differentiating only into a chondroblast. 2. After homotransplantation of the condylar cartilage the skeletoblast no longer differentiates into a prechondroblast. The preexisting prechondroblast continues to mature into chondroblasts until exhaustion of the supply. The chondroblastic zone is soon replaced by "endochondral" bone. Mitosis of prechondroblasts soon stop in the presence of chondroblasts, probably by a chalone-like mitotic inhibitor. But, if the disappearing of the cartilage is more rapid than the transformation of prechondroblasts into chondroblasts, the prechondroblasts then resume mitosis for some time. The skeletoblast differentiates into an osteoblast when prechondroblasts have transformed into chondroblasts; only then, does it lay down periosteal-like bone.
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This study investigates the effect of enoxaparin (Lovenox, Klexane), a low-molecular-weight heparin, on edema following a photothrombotic lesion using rose bengal dye in the rat. An area of cerebral ischemia was provoked in the right hemisphere of rats. Edema developed over 24 h after the lesion, as seen comparing water content of a core sample from the right hemisphere to that of a similar sample from the left hemisphere of each rat. Enoxaparin at 0. 5 mg/kg i.v. plus 2 mg/kg s.c. reduced edema 24 h after lesion induction by 32% (p < 0.01) when the treatment was started 2 h after photothrombotic insult, with maintenance doses of 2 mg/kg s.c. enoxaparin at 6 and 18 h. When the same initial treatment with enoxaparin was started 18 h after insult, there was still a significant reduction of 20% (p < 0.01) in cerebral edema. Administration of enoxaparin 18 h after insult reduced cerebral edema in a dose-dependent manner. There was no evidence of intracranial hemorrhages in any of the animal groups and when the hemoglobin content of the brain samples was assayed by the method of Drabkin, no increase in hemoglobin content was seen compared to sham-operated animals.
Recently, we proposed the hypothesis according to which the central hypotensive effect of clonidine and related substances could be related to an action upon specific receptors, requiring the imidazoline or imidazoline-like structures, rather than alpha 2-adrenoceptors. Since then, direct evidences have been accumulated to confirm the existence of a population of imidazoline specific binding sites in the brainstem of animals and man, more precisely in the Nucleus Reticularis Lateralis (NRL) region of the ventrolateral medulla (VLM), site of the antihypertensive action of clonidine. The purification of the putative endogenous ligand of the imidazoline receptors--named endazoline--is currently being attempted from human brain extracts. This new concept might at last lead to the expected dissociation of the pharmacological mechanisms involved, on the one hand, in the therapeutic antihypertensive effect, and on the other, in their major side-effect, which is sedation. In fact, it has been recently confirmed that hypotension is mediated by the activation of imidazoline preferring receptors (IPR) within the NRL region, while sedation is attributed to the inhibition of alpha 2-adrenergic mechanisms in the locus coeruleus, which is involved in the control of the sleep-waking cycle. The IPR may constitute an interesting target for new drugs in the treatment of arterial hypertension. Finally, dysfunctions of this modulatory system which could be involved in the pathophysiology of some forms of the hypertensive disease are under investigation.
A significant increase in overall mandibular length can be achieved with a functional appliance. However this only appears possible in children with a high tissue-level growth potential and responsiveness as defined by the mandibular subperiosteal ossification rate and alveolar bone turnover rate.
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