The aim of this study was to assess postoperative opioid prescribing patterns, usage, and pain control after common vascular surgery procedures in order to develop patient centered best-practice guidelines. We performed a prospective review of opioid prescribing after seven common vascular surgeries at a rural, academic medical center from December 2016 to July 2017. A standardized telephone questionnaire was prospectively administered to patients (n = 110) about opioid use and pain management perceptions. For comparison we retrospectively assessed opioid prescribing patterns (n = 939) from July 2014 to June 2016 normalized into morphine milligram equivalents (MME). Prescribers were surveyed regarding opioid prescription attitudes, perceptions, and practices. Opioids were prescribed for 78% of procedures, and 70% of patients reported using opioid analgesia. In the prospective group, the median MMEs prescribed were: VEIN (31, n = 16), CEA (40, n = 14), DIAL (60, n = 17), EVAR (108, n = 8), INFRA (160, n = 16), FEM TEA (200, n = 11), and OA (273, n = 4). The median proportion of opioids used by patients across all procedures was only 30% of the amount prescribed across all procedures (range 14-64%). Patients rated the opioid prescribed as appropriate (59%), insufficient (16%), and overprescribed (25%), and pain as very well controlled (47%), well controlled (47%), poorly controlled (4%), and very poorly controlled (2%). In conclusion, we observed significant variability in opioid prescribing after vascular procedures. The overall opioid use was substantially lower than the amount prescribed. These data enabled us to develop guidelines for opioid prescribing practice for our patients.

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This study was conducted to determine whether gestational changes in maternal uterine artery reactivity are primarily driven by local vs. systemic factors. Rats underwent surgical ligation of one oviduct, thereby restricting implantation and pregnancy to one uterine horn while maintaining a gestational endocrine milieu. Uterine arcuate arteries were isolated and cannulated to evaluate reactivity. Vessels from the implanted horn were significantly more sensitive to phenylephrine and less sensitive to sodium nitroprusside than those from the non-implanted horn; endothelial basal calcium levels were only increased in the implanted horn. Conversely, there were no differences in sensitivity to acetylcholine, or its effects on endothelial cell calcium, although efficacy was greater in vessels from the implanted vs. non-implanted horn. These findings demonstrate that local factors are predominant in inducing changes in vascular smooth muscle function, while endothelial adaptations result from an interplay between local and systemic factors, with distinct effects attributable to each.

This study investigated how vasoconstriction (tone), wall tension, smooth muscle activation, and vascular wall deformation influence resistance artery vasodilator reactivity. Resistance arteries, from two different regional circulations (splanchnic, uterine) and from pregnant and non-pregnant rats, were cannulated and pressurized, or mounted on a wire myograph under isometric conditions prior to being exposed to both endothelium-dependent (acetylcholine, ACh) and -independent (sodium nitroprusside, SNP) vasodilator agonists. A consistent pattern of reduced vasodilator sensitivity was noted as a function of extent of preconstriction for both agonists noted in pressurized arteries. A similar pattern regarding activation was noted in wiremounted arteries in response to SNP but not ACh. Wall tension proved to be a major determinant of vascular smooth muscle vasodilator reactivity and its normalization reversed this pattern, as more constricted vessels were more sensitive to ACh relaxation without any change in SNP sensitivity, suggesting that endothelial deformation secondary to vasoconstriction augments its vasodilator output. To our knowledge, this is the first study to dissect out the complex interplay between biophysical forces impinging on VSM (pressure, wall tension), the ambient level of tone (vasoconstriction, smooth muscle cell activation), and consequences of cellular (particularly endothelial) deformation secondary to constriction in determining resistance artery vasodilatory reactivity.