Background:The changes in the functional magnetic resonance imaging signal during anticipation, pain stimulation, and the poststimulation periods were investigated to determine whether changes in sex hormones affect brain activity.Methods: Eighteen participants were examined twice, once in the follicular phase and once in the luteal phase. Half the participants were tested first during the follicular phase, and the other half were tested first in the luteal phase.Results: The pain and unpleasantness ratings were significantly higher in the luteal phase than in the follicular. During the anticipation of pain, the prefrontal cortices were activated during the follicular phase, whereas the parahippocampal gyrus and amygdala were activated during the luteal phase. During the pain stimulation, putamen and cerebellum and precentral gyrus involving motor preparation and defense mechanism related to antinociceptive behavior were activated during the follicular phase, whereas the thalamus was activated during the luteal phase. During the poststimulation periods, the prefrontal cortices were activated during the follicular phase, whereas parahippocampal gyrus was activated during the luteal phase. The temporal pole was activated during the anticipation, pain stimulation, and poststimulation periods of the luteal phase.Conclusions: During surgical and medical procedures, requirements of anesthetic and analgesic and anxiolytic drugs may be reduced during the follicular phase and increased during the luteal phase. These results highlight the need to consider the effects of the sex hormones in women when designing clinical or neuroimaging studies or when treating patients for pain and pain-related unpleasantness.

We hypothesized that estradiol treatment would improve vascular dysfunction commonly associated with obesity, hyperlipidemia, and insulin resistance. A sham operation or 17beta-estradiol pellet implantation was performed in male lean and obese Zucker rats. Maximal vasoconstriction (VC) to phenylephrine (PE) and potassium chloride was exaggerated in control obese rats compared with lean rats, but estradiol significantly attenuated VC in the obese rats. Estradiol reduced the PE EC50 in all groups. This effect was cyclooxygenase independent, because preincubation with indomethacin reduced VC response to PE similarly in a subset of control and estrogen-treated lean rats. Endothelium-independent vasodilation (VD) to sodium nitroprusside was similar among groups, but endothelium-dependent VD to ACh was significantly impaired in obese compared with lean rats. Estradiol improved VD in lean and obese rats by decreasing EC50 but impaired function by decreasing maximal VD. The shift in EC50 corresponded to an upregulation in nitric oxide synthase III protein expression in the aorta of the estrogen-treated obese rats. In summary, estrogen treatment improves vascular function in male insulin-resistant, obese rats, partially via an upregulation of nitric oxide synthase III protein expression. These effects are counteracted by adverse factors, such as hyperlipidemia and, potentially, a release of an endothelium-derived contractile agent.

Myasthenia gravis causes weakness and fatigue of the skeletal muscles, including respiratory muscles. When immobile surgical fields are needed, neuromuscular blocking agents (NMBAs) are often administered to block muscle activity, leading to an immobile surgical field and respiratory arrest. Acetylcholinesterase inhibitors are administered to reverse the muscle block, promoting spontaneous respiration for patient recovery. If immobile surgical fields are required in myasthenic patient operations, NMBAs should be administered. However, recovery from NMBAs using acetylcholinesterase inhibitors might be delayed in myasthenic patients due to their intake of medicines that already inhibit cholinesterase, resulting in a delay in spontaneous respiration. Sugammadex is a recently introduced medicine that reverses muscle blocks through a different mechanism from acetylcholinesterase inhibitors and can be administered to facilitate the return of spontaneous respiration in myasthenic patients. Our experience of the rapid return to spontaneous respiration of a myasthenic patient with Sugammadex is reported in this paper.

BackgroundAging causes profound changes of stiffness and compliance in the cardiovascular system, which contributes to decreased cardiovascular reserve. Mechanisms of the underlying endothelial vasodilator dysfunction in vasodilator signaling pathways may occur at multiple sites within any of these pathways.MethodsAge-related changes in the vasculature were investigated in adult young (3-6 months, Y) and old (26-29 month, O) Wistar rats (n = 6). The aortas were carefully dissected from the rat and cut into rings 1.5-2.0 mm in length to measure in vitro isometric tension. Vasorelaxant responses of aortic rings to acetylcholine (ACh), sodium nitroprusside (SNP) and P1075 were examined using Dose Response software (AD Instruments, Mountain View, CA).ResultsEndothelium-dependent vasodilator function was impaired. The endothelium of aging rats impaired endothelial NO dependent vasodilation, but the machinery for vasodilation was not impaired.ConclusionsAge-related NO-mediated vasorelaxation in the aging endothelium was inhibited and appears to be major mechanism of vascular change and impaired vascular regulation.