Coronary Artery Occlusion with Sharp Blood Pressure Drop during General Anesthesia Induction: A Case Report.

Most anesthetics reduce cardiac functions and lower blood pressure (BP), potentially causing excessive BP reduction in dehydrated patients or those with heart conditions, such as coronary artery disease (CAD). Considering the increased prevalence of cardiovascular disease with age, anesthesiologists must be cautious about BP reduction during general anesthesia in older adults. In the present case, a 76-year-old male patient with undiagnosed CAD in a hypovolemic state experienced a significant drop in systolic BP to the fifties during propofol and sevoflurane anesthesia. Despite the use of vasopressors, excessive hypotension persisted, leading to anesthesia suspension. Subsequent cardiac examinations, including computed tomography heart angio and calcium score, and coronary angiogram, revealed a near total occlusion of the proximal left anterior descending coronary artery (pLAD) and the formation of collateral circulation. After 5 days of hydration and anticoagulation medications and confirmation of normovolemic state, general anesthesia was attempted again and successfully induced; a normal BP was maintained throughout the surgery. Thus, it is important to conduct a thorough cardiac evaluation and maintain normovolemia for general anesthesia in older adults.

7,8-Dihydroxyflavone Attenuates Inflammatory Response and Insulin Resistance Induced by the Paracrine Interaction between Adipocytes and Macrophages.

Obesity-induced inflammation and insulin resistance are mediated by macrophage infiltration into adipose tissue. We investigated the effects of 7,8-dihydroxyflavone (7,8-DHF), a flavone found in plants, on the inflammatory response and insulin resistance induced by the interaction between adipocytes and macrophages. Hypertrophied 3T3-L1 adipocytes were cocultured with RAW 264.7 macrophages and treated with 7,8-DHF (3.12, 12.5, and 50 µM). The inflammatory cytokines and free fatty acid (FFA) release were evaluated by assay kits, and signaling pathways were determined by immunoblotting. Coculture of adipocytes and macrophages increased inflammatory mediators, such as nitric oxide (NO), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) and FFA secretion but suppressed the production of anti-inflammatory adiponectin. 7,8-DHF counteracted the coculture-induced changes (p < 0.001). 7,8-DHF also inhibited c-Jun N-terminal kinase (JNK) activation and blocked nuclear factor kappa B (NF-κB) nuclear translocation in the coculture system (p < 0.01). In addition, adipocytes cocultured with macrophages did not increase glucose uptake and Akt phosphorylation in response to insulin. However, 7,8-DHF treatment recovered the impaired responsiveness to insulin (p < 0.01). These findings show that 7,8-DHF alleviates inflammation and adipocyte dysfunction in the coculture of hypertrophied 3T3-L1 adipocytes and RAW 264.7 macrophages, indicating its potential as a therapeutic agent for obesity-induced insulin resistance.

Fucoidan from Undaria pinnatifida has anti-diabetic effects by stimulation of glucose uptake and reduction of basal lipolysis in 3T3-L1 adipocytes.

Fucoidan, a sulfated polysaccharide derived from brown seaweeds, has been shown to reduce blood glucose levels and improve insulin sensitivity in mice. We investigated the effects of fucoidan on lipid accumulation, lipolysis, and glucose uptake in 3T3-L1 cells to test the hypothesis that fucoidan exerts an anti-diabetic function by acting directly on adipocytes. The 3T3-L1 cells were treated with 10, 50, 100, and 200 µg/mL of fucoidan from Undaria pinnatifida. Oil Red O staining and AdipoRed assay were used to determine lipid accumulation during adipocyte differentiation. Fucoidan was shown to reduce lipid accumulation and glycerol-3-phosphate dehydrogenase (GPDH) activity in a dose-dependent manner (P < .01). The expression of peroxisome proliferator-activated receptor γ (PPARγ), a major transcription factor associated with adipocyte differentiation, was also suppressed upon treatment with fucoidan. Treatment with fucoidan stimulated glucose uptake in normal adipocytes and restored insulin-stimulated glucose uptake in obesity-induced insulin resistant adipocytes, which were made by incubating hypertrophied 3T3-L1 cells with the conditioned media of RAW 264.7 macrophages (RAW-CM) (P < .01). In the presence of RAW-CM, fucoidan enhanced epinephrine-stimulated lipolysis but reduced basal lipolysis, as determined by non-esterified fatty acid into the culture medium (P < .001). These results suggest that fucoidan may have anti-diabetic effects by improving insulin-stimulated glucose uptake and inhibiting basal lipolysis in adipocytes without inducing adipogenesis.