Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

[EX Q]: Abstract: Cisapride is a prokinetic agent believed to facilitate acetylcholine release from the myenteric plexus of the gut. The effect of cisapride on gastric emptying of solids was studied in 9 diabetic patients, all of whom had delayed gastric emptying of indigestible solids (gastroparesis). Six patients had chronic nausea and vomiting, and 3 had no symptoms. Cisapride (5 mg) was given intravenously 15 min before ingestion of a 400-kcal test meal and 10 indigestible solid radiopaque markers. On separate days and in random order each patient also received intravenous metoclopramide (10 mg) or placebo 15 min before ingestion of the meal and markers. Mean gastric emptying of radiopaque markers, assessed by serial radiographs of the gastric region, was accelerated by metoclopramide and cisapride, but the difference reached significance only with cisapride (p less than 0.05). There was considerable intersubject variability in gastric emptying responses to cisapride and metoclopramide. No side effects occurred with either drug. This study indicates that acute, intravenous administration of cisapride accelerates gastric emptying of indigestible solids in patients with diabetic gastroparesis.
[EX A]: Effect of cisapride on gastric emptying of indigestible solids in patients with gastroparesis diabeticorum. A comparison with metoclopramide and placebo.

[EX Q]: Abstract: The records of 24 patients with malignant gliomas treated with carotid infusion of cisplatin and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) are reviewed for risk factors that might suggest the development of a permanent neurological deficit after infusion. Permanent neurological deficits were seen with doses of cisplatin as low as 69 mg/m2, although doses as high as 100 mg/m2 were tolerated by other patients. All 3 patients who developed permanent neurological deficits received fixed doses of cisplatin of 150 mg and supplied only 2 major intracranial branches from the infused carotid artery. In none of these patients was a filter used in the infusion line. Other risk factors identified in 2 of the 3 patients were diffuse neoplasm involving the region of the internal capsule and the use of an infusion pump rather than a pulsatile bolus infusion technique. The development of a permanent neurological deficit appeared unrelated to the dose of BCNU within the range utilized, and preinfusion administration of corticosteroids did not prevent neurological deficit. These possible risk factors should be considered in the future development of protocols for arterial infusion therapy of malignant gliomas.
[EX A]: Neurological deficit after carotid infusion of cisplatin and 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) for malignant glioma: an analysis of risk factors.

[EX Q]: Abstract: It is well known that LH and human CG (hCG) induce an increase in total ovarian blood flow. The effect of LH/hCG on luteal blood flow, however, is unknown. This work studies the effect of hCG on both luteal and ovarian blood flows at different stages of pseudopregnancy in adult female rats. Pseudopregnancy was induced by mating with sterile male rats. The length of pseudopregnancy was 13 +/- 1 days and, during this time, blood flow was measured by the injection of radioactive microspheres during anesthesia. At autopsy, the corpora lutea were identified and extirpated under a stereomicroscope. These, and the remaining ovary, were then counted for radioactivity and the blood flow was calculated. Progesterone levels were determined in plasma and ovarian tissues. Furthermore, the responsiveness of adenylate cyclase was tested in ovarian tissues at day 6 of pseudopregnancy. An intraarterial injection of hCG (50 IU) or vehicle (saline) was given 20 min before the blood flow determinations in anesthetized rats. The luteal blood flow was not changed by hCG on days 2, 6, and 11 of pseudopregnancy, whereas in the remaining ovary the blood flow increased more than 2-fold, thereby resulting in redistribution of the blood flow. Ten micrograms of NIH-LH-B9, tested at day 6 of pseudopregnancy, mimicked the effect of hCG. At day 6 of pseudopregnancy, hCG (50 IU) was given ip to conscious rats 200 min and 24 h before blood flow determinations. At 200 min after hCG there was a more pronounced redistribution of ovarian blood flow with a 45% reduction in luteal blood flow and a 4-fold increase in flow through the remaining ovary. LH as well as hCG doubled the progesterone content of the remaining ovary. In the corpora lutea an increased progesterone content was seen after 200 min of hCG exposure. At 24 h after hCG injection, all parameters had returned to control levels except that adenylate cyclase was nonresponsive. The increase in the total ovarian blood flow coincides with the increased steroidogenesis and these effects are likely due to release of metabolites and/or vasoactive substances. Despite this increase, the blood flow of the corpus luteum was not increased rendering vascular mechanisms unlikely as a part of the acute LH/hCG effects on corpus luteum of pseudopregnancy.
[EX A]:
Redistribution of ovarian blood flow after injection of human chorionic gonadotropin and luteinizing hormone in the adult pseudopregnant rat.