Rapid Return of Spontaneous Respiration after General Anesthesia with Sugammadex in a Patient with Myasthenia Gravis.

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.

Ankle-brachial blood pressure differences in the beach-chair position of the shoulder surgery.

BACKGROUND: During shoulder surgery, blood pressure is frequently measured at the ankle. Anesthetic complications may result when ankle blood pressure is higher than brachial blood pressure and anesthesiologists misinterpret ankle blood pressure as brachial blood pressure. Therefore, we investigated whether ankle blood pressure is significantly higher than brachial blood pressure before anesthesia induction, during induction, after tracheal intubation, before beach chair position, and in the beach chair position. METHODS: Thirty patients requiring general anesthesia for shoulder surgery were included in this study. Ankle and brachial blood pressure were simultaneously measured before induction, during induction, after intubation, before beach chair position, and in the beach chair position. RESULTS: Ankle blood pressure was higher than brachial blood pressure before induction, during induction, after intubation, before beach chair position, and in the beach chair position. Ankle-brachial blood pressure differences in the beach chair condition were much higher than in four other conditions. The correlation coefficient between mean ankle-brachial blood pressure differences before the beach chair position and mean ankle-brachial blood pressure differences in the beach chair position was 0.616. Brachial systolic blood pressure could be predicted by regression equations (R(2) = 0.306-0.771). CONCLUSIONS: These results suggest that anesthesiologists should consider these ankle-brachial blood pressure differences when monitoring anesthesia in the beach chair position.

Aging impairs vasodilatory responses in rats.

BACKGROUND: Aging 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. METHODS: Age-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). RESULTS: Endothelium-dependent vasodilator function was impaired. The endothelium of aging rats impaired endothelial NO dependent vasodilation, but the machinery for vasodilation was not impaired. CONCLUSIONS: Age-related NO-mediated vasorelaxation in the aging endothelium was inhibited and appears to be major mechanism of vascular change and impaired vascular regulation.

The vasorelaxatory effect of the milrinone on the preconstricted rat aorta.

BACKGROUND: Milrinone, phosphodiesterase III inhibitor, has been used effectively in patients with right heart failure, especially resulted from pulmonary hypertension. However, milrinone is often used with alpha- and beta-adrenergic receptor agonist to prevent severe systemic vasodilation and unfavorable hypotension. Furthermore, structural and functional vasacular changes are associated with aging and are greatest in the aorta. We evaluated the vasodilatory effects of milrinone and sodium nitroprusside (SNP) on young and old rat aortic rings preconstricted with various catecholamines. METHODS: Aortic rings of young and old rat were placed in 25 ml organ chamber and preconstricted with epinephrine (EPI, 10(-6) M), norepinephrine (NE, 10(-7) M) , phenylephrine 10(-7) M) , and U46619 (10(-8) M). Cummulative dose-responses to milrinone (10(-9)-10(-5) M) and SNP (10(-9)-10(-5) M) were obtained to characterize vasodilatory effects. RESULTS: Relaxation response to milrinone was markedly enhanced in both young and old aortic rings preconstricted with U46619 compared with other vasoconstrictors. The maximal response of the young rat aortic rings preconstricted with NE is significantly reduced, compared with that of EPI. The maximal vasorelaxant response of SNP in young and old aortic rings are nearly identical. CONCLUSIONS: We conclude that combined use of milrinone and epinephrine may be more useful in prevention and treatment of systemic hypotension.

Different brain activation patterns to pain and pain-related unpleasantness during the menstrual cycle.

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.

The effect of pretreatment with thiopental on reducing pain induced by rocuronium injection.

We examined whether pretreatment with a small dose of thiopental was effective in reducing pain induced by the intravenous injection of rocuronium. Withdrawal movement was used to assess pain reduction. Ninety patients were randomly assigned to one of two groups: patients in the control group were pretreated with 2 mL saline, and those in the thiopental group were pretreated with 2 mL (50 mg) thiopental. Thiopental 5 mg/kg was injected intravenously. After a loss of consciousness, the upper arm was compressed with a rubber tourniquet, and the pretreatment drugs were administered. Thirty seconds later the tourniquet was removed and 0.6 mg/kg rocuronium was administered. Withdrawal movement was assessed using a four-grade scale: no movement, movement limited to the wrist, to the elbow or to the shoulder. The frequency of withdrawal movement in the group pretreated with thiopental was lower than in the control group (34 vs. 13, p < 0.05). We concluded that pretreatment with 2 mL (50 mg) thiopental is effective in reducing pain caused by the intravenous injection of rocuronium.

Estrogen has opposing effects on vascular reactivity in obese, insulin-resistant male Zucker rats.

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.