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Bilateral lesions of the hypothalamic paraventricular nuclei (PVN) induce hyperphagia and obesity, and ghrelin stimulates appetite in rodents and humans. Conversely, corticotrophin-releasing hormone (CRH) and melanotan-II (MT-II, a synthetic structural homologue of alpha-melanocyte-stimulating hormone, alphaMSH) inhibit feeding behavior. The purpose of the present study was to determine whether these peptides are involved in the hyperphagia and obesity induced by PVN lesions. After bilateral electrolytic lesions of the PVN, rats were given ghrelin intraperitoneally (i. p.), or intracerebroventricular (i. c. v.) infusion of CRH or MT-II. We measured the cumulative food intake (FI) for 4 h after ghrelin injection in rats fed AD LIB, and the changes in FI at 15 min, 30 min, 1 h, and 2 h after infusion of CRH and MT-II in rats fasted for 24 h. Ghrelin significantly increased cumulative FI, with maximal response 3 h and 4 h after injection, and at these times, the FI of PVN-lesioned rats was greater than that of sham-operated rats. CRH significantly decreased FI in all experimental animals, but at 1 h, there was a more powerful inhibitory effect on FI in the PVN-lesioned group than in the sham-operated group. MT-II decreased FI in sham-operated, but not in PVN-lesioned rats. Thus, ghrelin and CRH showed more potent orexigenic and anorectic effects in PVN-lesioned rats, respectively, but MT-II lost its inhibitory action on feeding behavior. These results suggest that the hyperphagia and obesity induced by PVN lesions may be related to an increased orexigenic action of ghrelin due to the destruction of endogenous CRH and alphaMSH receptors.

Sixty-four patients who were operated on within 4 days after acute subarachnoid hemorrhage are included in this study. All patients underwent preoperative computed tomographic (CT) scanning, and the amount and distribution of subarachnoid blood clot were noted. Operation was carried out by the frontobasal lateral approach, and the subarachnoid clot was removed by microsurgical suction-irrigation after clipping of the aneurysm. Immediate postoperative CT scanning was performed to evaluate the completeness of the subarachnoid blood clot removal. The presence or absence of postoperative vasospasm was determined with angiography performed between the 7th and 10th postoperative days. All patients were, of course, also evaluated for evidence of neurological deterioration. Approximately two-thirds of the patients in this series showed high density subarachnoid blood clot on the preoperative CT scan. The postoperative CT scans showed that it was possible to remove the majority of the blood clot except that located in the frontal interhemispheric fissure, the posterior part of the insular cistern on the approached side, and all of the insular cistern on the contralateral side. There was no spasm or only mild spasm in any site where the blood clot had been successfully removed. Delayed neurological deficits occurred only in those cases in which subarachnoid blood clot remained in the cisterns. These results suggest that it is possible to prevent intracranial arterial spasm and associated neurological deterioration by early operation and removal of clotted blood from the subarachnoid space.

These results suggest that the hyperphagia and obesity induced by PVN lesions may be related to an increased orexigenic action of ghrelin, but not NPY.

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