Local control in breast cancer. Old and new lines and analysis of our experience.

The great interest in early breast cancer is caused by hope in the future of treating especially early cancers, extending the indications to a local conservative treatment of the breast with a more and more efficient general treatment. The GIVIO work has proved that the major part of Italian surgeons and gynaecologist don't accept the FIGO protocol. We report our experience (similar to the major part of general surgical division like GIVIO experience) and our results. W. Wood, at ASCO 1991, has indicated the role and optimal techniques for breast conservation in early breast cancer. New lines and our experience have induced us to draw up a new protocol in early breast cancer: we did not carry out Halsted mastectomy because a local invasion of muscle or muscle aponeurosis are treated with local excision and radiotherapy; if the tumour's size is more than 3 cm we did a radical mastectomy because like many authors these cancers have a worse prognosis; under 3 cm we carried out the lumpectomy with the techniques indicated by W. Wood at ASCO 91; we remove the lymph nodes of level 3 only if the axillary lymph nodes are clinically suspected. So we think the same results of local and general control with a lower morbidity are obtained; we are considering introducing neoadjuvant chemotherapy, to increase the indication for a breast conservation treatment.

[The pre- and postoperative and follow-up use of the tumor markers MCA, CA-125 and CA-19-9]. / Utilizzazione pre- e postoperatoria e nel follow-up dei markers tumorali MCA, CA 125, CA 19,9.

The paper describes the authors' personal experience of the use of tumour markers, above all during postoperative follow-up as well as during the evaluation of the response to adjuvant and other forms of chemotherapy. The authors affirm that the use of these markers is fundamental for a correct evaluation and rapid treatment, above all in the identification and treatment of recidivation.

Autonomic nervous control of fundic secretion of somatostatin and antral secretion of gastrin and somatostatin in pigs.

By selective catheterization of gastric veins, we studied the secretion of gastrin and somatostatin from the antrum and of somatostatin from the gastric fundus-corpus region in anaesthetized pigs with or without acute adrenalectomy. The secretion was studied during electrical stimulation of the vagus nerves and the splanchnic nerves and simultaneous irrigation of gastric lumen with fluids of high, low, and neutral pH. The corpus-fundus somatostatin response to vagal stimulation was biphasic with a short-lasting initial increase followed by a lasting inhibition, which was little influenced by intraluminal pH or adrenalectomy. In pigs with intact adrenals, antral somatostatin secretion was increased by vagal stimulation, whereas in adrenalectomized pigs, the effect was inhibitory. The vagally induced inhibition was abolished when the intragastric pH was kept at pH 2. The antral gastrin secretion was strongly stimulated by vagal stimulation. The magnitude of the secretory response was inversely related to the pre-stimulatory somatostatin levels, but not to the nerve stimulation responses. Splanchnic stimulation increased arterial blood pressure and gastric blood flow, but had inconsistent effects on somatostatin and gastrin secretion.

Autonomic nervous control of gastric somatostatin and gastrin release.

In anesthesized pigs the cut peripheral ends of splanchnic and vagal nerves were electrically stimulated in 5 min periods, and blood for somatostatin and gastrin determination collected from the right and left gastroepiploic veins and from the left femoral artery. The experimental animals were randomly allocated to two groups, one of which underwent acute bilateral adrenalectomy prior to the experiments. Gastroepiploic vein bloodflow increased in both groups during vagal as well as splanchnic stimulation. Mean systemic bloodpressures increased at least 70% during splanchnic stimulation. Prestimulatory somatostatin concentration was significantly higher in the left than in the right gastroepiploic vein. During vagal stimulation the somatostatin output from the gastric fundus decreased in both experimental groups, most pronounced though, in the adrenalectomized group. The somatostatin output from the antrum increased in the group with intact adrenals, and decreased in the adrenalectomized group (the difference is significant), thus indicating a role for circulating catecholamines in the regulation of somatostatin secretion. During splanchnic stimulation somatostatin output increased, but a marked fluctuation was observed in both groups. The arterial somatostatin concentration was unaffected of the nervous stimulation. In both groups gastrin concentration increased at least 10-fold with vagal stimulation, and significant changes from the prestimulatory level were not observed during splanchnic stimulation.

Nervous control of gastro-pancreatic somatostatin secretion in pigs.

The influence of the autonomic nervous system on the secretion of somatostatin from the antral and the fundic parts of the stomach and from the pancreas of the pig was investigated in experiments involving electrical stimulation of the vagal nerves and the splanchnic nerves in (1) intact, anesthetized pigs and (2) isolated perfused preparations of (a) antrum with intact vagal supply, (b) pancreas with intact vagal supply, (c) pancrease with intact sympathetic supply. The results clearly demonstrated that parasympathetic activity inhibits D-cell function in all gastro-pancreatic tissues; antral gastrin secretion was inversely correlated to somatostatin secretion and it is suggest that antral D-cell secretion participates in the control of gastrin secretion; the inhibitory effect of Gastric Inhibitory Polypeptide (GIP) as well as intraluminal HCl on gastrin secretion may be exerted via the stimulatory effect of both on somatostatin secretion. The sympathetic innervation of the pancreas is also clearly inhibitory to the pancreatic somatostatin secretion, whereas sympathetic nervous activity influences little the gastric somatostatin release.