Observations of the present study reveal that as reported in the literature [3
] the diameter of the uterine artery increases during pregnancy. This has been described as an adaptive response to increased blood flow within the uterine artery [13
], which results from enhanced vasodilator response, decreased vasoconstrictor response, alterations in active and passive mechanical properties of the uterine artery wall [15
]. A higher percentage increase in the lumen of the distal segment in comparison to the middle segment may imply that this zone creates a low pressure zone and hence allows for pooling of blood [16
]. The middle segment has the least increase in the diameter probably because of it giving off a cervical branch which makes the artery generally narrower at this point. Indeed, when arteries branch, there is an overall decrease in their luminal diameter [17
]. The overall widened lumen allows accommodation of a threefold increased blood flow [18
] to meet the demand of the developing conceptus [19
]. Failure of the uterine artery to adapt in this way during pregnancy usually leads to a poor pregnancy outcome [3
]. This study, however, did not take into account the age at pregnancy and parity states of the women, factors that could have had an effect on the histomorphology of the uterine artery.
Increased uterine wall thickness is most marked in the proximal segment. This increase is related to both hyperplasia and hypertrophy of smooth muscles [1
]. Functionally, medial hypertrophy may act as a regulator of blood supply to a target organ [22
]. Accordingly, the proximal segment of the uterine artery may be the “regulator zone” which adjusts blood flow to the uterus. Secondly, the media both in the proximal and the middle segment may provide a valve like mechanism to the upstream flow of blood and thus prevent backflow.
In the distal segment, the tunica media of the uterine artery of the gravid uterus was significantly thinner than that of the corresponding segment in the non-gravid uteri. This medial thinning of the distal segment, hitherto, unreported may be an adaptation to allow efficient blood flow with minimal impedance to the decidual arteries that supply the placenta [16
]. Indeed, previous reports on decidual arteries have demonstrated replacement of smooth muscles within the media with amorphous material [23
]. This structural modification of the media of the arteries supplying the placenta is thought to facilitate the expansion of these vessels to provide increased blood flow as pregnancy advances and their occlusion and collapse after parturition [24
]. The functional consequence of this modification may be to ensure an adequate and efficient flow of maternal blood to the placenta, thus enhancing the survival of the fetus.
Intimal thickness showed a proximo-distal decline. The proximal segment of the uterine artery had the largest evidence of thickening. This implies that this segment experiences the most wall shear stress, wall pressure, or particle deposition as it bears the highest pressure effect and turbulence after receiving its blood from a major vessel. This pattern has been observed in regions where arteries branch from the main trunk and are useful indicators of future atherosclerotic disease [25
]. The middle segment followed in thickness probably due to the branching off of the cervicovaginal artery. This being a smaller branch, the observation of reduced intimal thickening is expected. The distal segment had the least intimal thickening suggesting that low blood pressure and subsequent low wall shear stress at this region did not favor deposition of particles to result in intimal thickening. This concept has been explored before [26
The thickness of the intima in pregnancy was reduced compared to the non gravid period. Similar observations were made by Kamiya (1989) [27
], who demonstrated difficulties in identifying gravid sclerosis characterized by a thickening of the intima and a lamination of the internal elastic lamina in pregnancy and early postpartum period. Similar changes have also been described in uterine arteries of gravid guinea pigs and sow [28
]. These cyclical changes appear to be under the influence of hemodynamics, growth factors and hormones [27
]. Changes in the hormonal profile and an increase in the volume of blood flowing to the uterus could explain the decreased thickness of the intima. High levels of oestrogen during pregnancy with action in the uterine artery could be responsible for the adaptation seen [30
]. Indeed, some arteries are able to respond to changes in the internal milieu over a very short period of time [31
]. Intimal thickening in reproductive period outside pregnancy could be explained because of the lower levels of oestrogen as compared to pregnancy. Crawford et al., 1997 [32
] showed significant portions of intimal hyperplasia in women in reproductive age group and worse in post menopause when the protective effect of oestrogen was at the lowest.
The wall thickness to luminal ratio in all the segments remained constant during pregnancy. The ratio was; however, lower during pregnancy compared to non-gravid state because of the sharper increase in luminal diameter. When true values were considered, there was a progressive decline in the wall thickness parameters as opposed to the lumen in pregnancy. In non gravid uteri wall thickness parameters progressively showed constant decline as opposed to the rapid decline of the luminal diameter dimensions giving it a higher ratio. Previous literature has not described the changes in the wall thickness to luminal diameter ratio in different segments of the uterine artery but the general concept is in tandem with what has been described before about the morphology of arteries [2
]. The resultant effect of the increased ratio during pregnancy is to increase overall blood flow to the uteroplacental bed and reduce uterine vascular resistance to flow.