The purpose of this study was to compare the effects of different dosages of ethanol on ovarian morphology and function. Holtzman rats, 20 days old, were divided into groups as follows: The rats in Group I were autopsied at 20 days of age, and those in Group II were placed on ad libitum chow and water diet; the rats in Groups III and V were fed on a liquid diet containing 2.5% or 5% ethanol respectively; Groups IV and VI were pair-fed controls to Groups III and V, respectively. Rats in Groups II, III, IV, and VI were maintained on the diets for 50-55 days and killed at late proestrus-estrus, while the animals in Group V did not exhibit estrous cycles and were killed on day 55 of treatment. The average increase in body weights of rats in Groups II, III, and IV was significantly greater than the increase in body weights of rats given 5% ethanol or their pair-fed controls. In the rats treated with 5% ethanol, vaginal opening was significantly delayed from the controls, estrous cycles were absent, ovarian weights were similar to those of the 20-day-old rats, ovaries contained corpora lutea of only one estrus, uteri weighted less than controls, and histologically, the uteri and vaginae were similar to those of 20-day-old rats. However, in the rats treated with 2.5% ethanol, all of the parameters were similar to those of the controls. The average serum alcohol level for the rats on the 5% ethanol diet was 249 mg%; the serum alcohol levels were at the lower limit of detection for the rats on the 2.5% ethanol diet. The data show that ovarian function was suppressed in the rats that received the 5% ethanol but not in rats on the 2.5% ethanol diet.

The purpose of our study was to determine the origin and relation of vasa vasorum to atherosclerotic plaque at the bifurcation of the common carotid artery. We randomly selected 12 unembalmed adult human cadavers, 40-96 years of age. We prepared luminal casts of the arteries from eight cadavers and cleared the arteries from the remaining four cadavers. A network of vasa vasorum surrounding atherosclerotic plaque was observed in five luminal casts and in two cleared specimens; the vasa vasorum originated from the superior thyroid and ascending pharyngeal arteries. Three of the five luminal casts also demonstrated vasa vasorum arising directly from the internal carotid artery distal to the plaque. An extensive network of vasa vasorum was not observed in specimens from the five cadavers relatively free of gross atherosclerotic plaque. Our findings demonstrate the importance of the external carotid artery in giving rise to the vasa vasorum that supply the areas of atherosclerotic plaque. (Stroke 1989;20:1484-1487 N utrients are provided to large arteries by vasa vasorum, which supply the adventitia and outer media; the intima and inner media are supplied by diffusion from the lumen. Following the injection of lead chromate, Higginbotham et al 1 described a superficial plexus of vasa in the adventitia and deep plexus in the medioadventitial layer of the monkey aorta; the media and intima were free of vessels. Anastomoses between the plexuses were observed. Song et al 2 studied the vasa vasorum of the thoracic aortas of sheep, dogs, and pigs and observed that vasa vasorum extended into the internal elastic lamina. However, it was impossible to determine if the subintimal vessels came from the lumen of those vessels.With the development of atherosclerotic plaque there is a thickening of the intima, which precipitates a change in the vascular pattern of the area. From histologic studies of the human aorta and coronary arteries, Geiringer 3 proposed that vessels from the adventitia and the lumen extend into the plaque. However, vascularization from the lumen was observed only when a portion of the arterial Received December 5, 1988; accepted May 16, 1989. intima exceeded a critical depth (0.5 mm for the aorta and 0.35 mm for the first portion of the anterior descending branch of the left coronary artery). Barger et al 4 studied the vasa of carotid arteries by cinematography of silicone polymerinjected, cleared human hearts and observed a dense network of vasa in the area of atherosclerotic injury. However, vasa vasorum were rarely seen in the walls of normal coronary arteries.The bifurcation of the common carotid artery is predisposed to the development of atherosclerotic lesions. The plaques can exhibit intramural hemorrhage, 5 which may give rise to thromboemboli, resulting in transient ischemic attacks and/or stroke. A knowledge of the vascularization of carotid atherosclerotic plaque may assist in the understanding of its sequela. Therefore, our study was designed to determine the origin of the vasa vasorum and th...

No abstract