Caloric restriction-mimetics for the reduction of heart failure risk in aging heart: with consideration of gender-related differences.

The literature is full of claims regarding the consumption of polyphenol or polyamine-rich foods that offer some protection from developing cardiovascular disease (CVD). This is achieved by preventing cardiac hypertrophy and protecting blood vessels through improving the function of endothelium. However, do these interventions work in the aged human hearts? Cardiac aging is accompanied by an increase in left ventricular hypertrophy, along with diastolic and systolic dysfunction. It also confers significant cardiovascular risks for both sexes. The incidence and prevalence of CVD increase sharply at an earlier age in men than women. Furthermore, the patterns of heart failure differ between sexes, as do the lifetime risk factors. Do caloric restriction (CR)-mimetics, rich in polyphenol or polyamine, delay or reverse cardiac aging equally in both men and women? This review will discuss three areas: (1) mechanisms underlying age-related cardiac remodeling; (2) gender-related differences and potential mechanisms underlying diminished cardiac response in older men and women; (3) we select a few polyphenol or polyamine rich compounds as the CR-mimetics, such as resveratrol, quercetin, curcumin, epigallocatechin gallate and spermidine, due to their capability to extend health-span and induce autophagy. We outline their abilities and issues on retarding aging in animal hearts and preventing CVD in humans. We discuss the confounding factors that should be considered for developing therapeutic strategies against cardiac aging in humans.

Folic acid and RAAS blockers in ischemia/reperfusion-induced hepatic injury: A current mechanistic concept for understanding the incidence, significance & outcome.

Hepatic ischemia-reperfusion injury (IRI) is not only one of the pathophysiological process involving the liver, but also a complex systemic process affecting multiple tissues and organs. IRI after liver transplant occurs due to in major resections and occlusion of vessels, or during the perioperative period, leads to acute liver failure which shows the dynamic process that involves two interrelated phases of local ischemic insult and inflammation-mediated reperfusion injury and has an impact on morbidity and mortality. The renin-angiotensin-aldosterone system (RAAS) is activated locally in the injured cells by the occurrence of I/R, which plays an essential role in the fate of the damaged tissue. However, a preclinical study explores the protective role of RAAS inhibitor in acute liver injury in a model of inflammation caused by ischemia and reperfusion. In-addition to RAAS blockers in monotherapy does not effectively block the complete pathway. Thus, the present study is designed to explore the effect of combined folic acid with RAAS blockers in combination, produce a synergistic effect. Moreover, in this review, we will describe the understanding of the possible incidence of downregulatory molecular mechanisms associated with renin-angiotensin-aldosterone system and the significance & outcome of the combination of folic acid and RAAS blockers in liver injury due to ischemia/reperfusion.

A review on the physiological and pathophysiological role of endothelial glycocalyx.

The glycocalyx is a gel-like layer covering the luminal surface of vascular endothelial cells. It comprises of membrane-attached proteoglycans, glycosaminoglycan chains, glycoproteins, and adherent plasma proteins. The glycocalyx maintains homeostasis of the vasculature, which includes controlling vascular permeability and microvascular tone, preventing microvascular thrombosis, and regulating leukocyte adhesion. In the past decades, the number of studies on endothelial glycocalyx has steadily grown. Glycocalyx emerged as an essential part of blood vessels involved in multiple physiological functions. Damage to glycocalyx is associated with many types of diseases. The structure and physiology and pathophysiology of the glycocalyx, as well as the clinical effects of glycocalyx degradation, are addressed throughout this study. We strive in particular to define therapeutic approaches for the survival or reparation of the glycocalyx.

Laparoscopic gynecological surgery in an adult woman with Becker muscular dystrophy performed with sevoflurane with cisatracurium anesthesia: A case report.

RATIONALE: Becker muscular dystrophy (BMD) and Duchenne muscular dystrophy (DMD) are progressive neuromuscular disorders caused by mutations in the dystrophin gene. The management of anesthesia in patients with BMD is complicated because they are highly sensitive to the conventional anesthetics such as volatile anesthetics and muscle relaxants. It is reported that anesthesia in patients with DMD is associated with several complications. However, a few case reports have been published on adult patients with BMD undergoing surgery with general anesthesia. Reports indicate that children with BMD may experience some serious complications with flurane-inhaled anesthesia. However, no study has yet shown that the use of flurane-induced anesthesia in adults with DMD carries high risks. PATIENT CONCERNS: We describe a 56-year-old woman with BMD who was scheduled for laparoscopic hysterectomy and bilateral adnexectomy under general anesthesia due to a mass in the uterus. The patient was diagnosed with BMD 20 years back and reported that during this period, she was able to walk slowly with help during her daily life. Additionally, she also had a history of hypertension since 4 years and type 2 diabetes mellitus since 2 years. DIAGNOSIS: The patient was postmenopausal and presented with abnormal uterine bleeding and elevated CA125. Abdominal ultrasonography revealed diffuse enlargement of the uterus and hypoechoic internal echoes. These findings were suggestive of diffuse adenomyosis with multiple uterine leiomyomas, which would have adverse effects later in her life. Therefore, the patient required surgery to address the symptoms and further confirm the diagnosis. The final diagnosis was confirmed by histopathological analysis. INTERVENTIONS: The patient was scheduled for laparoscopic hysterectomy and bilateral adnexectomy. Anesthesia was induced and maintained by a combination of intravenous and inhalation anesthetic agents, particularly cisatracurium besilate and inhaled. sevoflurane. OUTCOMES: The duration of anesthesia and postoperative period were uneventful. At the end of the operation, the patient had normal vital signs and was fully conscious. The patient was followed up for 8 months and no complications were noted during this period. LESSONS: The combination of sevoflurane and cisatracurium besilate is a safe and effective method for the anesthetic management of adult patients with BMD scheduled for laparoscopic gynecological surgery. On the other hand, it is important to be aware of even rare complications of procedures, so that necessary precautions can be undertaken. Further investigations are necessary to determine the safe dosage of volatile anesthetics specifically for this clinical scenario so that anesthesiologists can use this combination method more accurately and precisely.

Effect of penehyclidine hydrochloride on heart rate variability in hysteroscopy.

In order to evaluate the effect of different doses of penehyclidine hydrochloride (penehyclidine) on heart rate (HR) and HR variability (HRV) in hysteroscopy, 180 patients (American Society of Anesthesiologists grade I-II) were randomized equally to three groups: 0.5 mg penehyclidine and intravenous anesthesia (group I), 1.0 mg penehyclidine and intravenous anesthesia (group II) and saddle anesthesia combined with intravenous anesthesia (control group). HR and HRV, including total power (TP), low-frequency power (LF), high-frequency power (HF) and the LF to HF ratio (LF/HF), were recorded prior and subsequent to the induction of anesthesia (T0 and T1, respectively), following the start of surgery (T2) and following completion of surgery (T3). HR was lower at T2 than at T0 in the control patients, but no differences were observed in groups I and II. The HR at T2 was increased in group II compared with that in group I. TP in group II was significantly higher compared with that in group I at T2. At T1 and at T2, the LF and HF values were lower in group I than those in the controls. Patients in group II also had higher LF and HF at T2 than patients in group I. The HF was higher at T2 than that at T0 in the controls; however, the HF and LF did not change significantly within groups I and II. No significant differences were observed in the LF/HF ratio among the three groups. At a dose of 0.5 mg, penehyclidine stabilized HRV and did not alter the autonomic nervous modulation of HR. A penehyclidine dose of 1.0 mg may be superior to a dose of 0.5 mg in maintaining HR, but is less effective at balancing sympathetic and parasympathetic activity.

Fiberoptic bronchoscopy-assisted endotracheal intubation in a patient with a large tracheal tumor.

In the event of a high degree of airway obstruction, endotracheal intubation can be impossible and even dangerous, because it can cause complete airway obstruction, especially in patients with high tracheal lesions. However, a smaller endotracheal tube under the guidance of a bronchoscope can be insinuated past obstructive tumor in most noncircumferential cases. Here we report a case of successful fiberoptic bronchoscopy-assisted endotracheal intubation in a patient undergoing surgical resection of a large, high tracheal tumor causing severe tracheal stenosis. A 42-year-old Chinese man presented with dyspnea, intermittent irritable cough, and sleep deprivation for one and a half years. X-rays and computed tomography scan of the chest revealed an irregular pedunculated soft tissue mass within the tracheal lumen. The mass occupied over 90% of the lumen and caused severe tracheal stenosis. Endotracheal intubation was done to perform tracheal tumor resection under general anesthesia. After several failed conventional endotracheal intubation attempts, fiberoptic bronchoscopy-assisted intubation was successful. The patient received mechanical ventilation and then underwent tumor resection and a permanent tracheostomy. This case provides evidence of the usefulness of the fiberoptic bronchoscopy-assisted intubation technique in management of an anticipated difficult airway and suggests that tracheal intubation can be performed directly in patients with a tracheal tumor who can sleep in the supine position, even if they have occasional sleep deprivation and severe tracheal obstruction as revealed by imaging techniques.

[Role of central neuronal nicotinic receptor in the inhibitory effect of isoflurane on synaptic long-term potentiation in hippocampal slices of rats].

OBJECTIVE: To determine effect of central neuronal nicotinic receptor on synaptic long-term potentiation (LTP) in the CA1 area of rats hippocampal slices. METHODS: Brain slice preparation transverse hippocampal slices were obtained from male Sprague-Dawley rats that were ether-anesthetized and decapitated. The hippocampus was rapidly removed, and slices were prepared in ice-cold artificial cerebrospinal fluid (ACSF), oxygenated with 95% O2 - 5% CO2. Seventy-seven slices were randomly divided into 11 equal groups (n = 7 each): group LTP; group isoflurane 0.125; group isoflurane 0.25; group isoflurane 0.5; group nicotine 0.1; group nicotine 1.0; group nicotine 10.0; group nicotine 1.0 + isoflurane 0.25; group nicotine 10.0 + isoflurane 0.25; group mecamylamine; group mecamylamine + isoflurane 0.125. One recording electrode was positioned in the pyramidal cell layer of the CA1 area of rats hippocampal slices to simultaneously record evoked population spikes (PS). For LTP induction, high-frequency stimulation (HFS) conditioning pulses (100 Hz/s) were applied to the Schaffer collateral-commissural pathway of hippocampus using a bipolar stimulating electrode. The changes of PS amplitude after HFS were analyzed in each group. RESULTS: The PS amplitude of the rats hippocampal slices in group LTP after HFS was significantly increased by (52 +/- 12)% compared with that of pre-HFS indicating the successful induction of LTP. Compared with group LTP, the PS amplitudes decreased significantly in group isoflurane 0.125, 0.25 and 0.5 after HFS (P < 0.01) and increased significantly in group nicotine 1.0 and 10.0 (P < 0.01), but the PS amplitudes in group nicotine 0.1 was not significantly changed after HFS (P > 0.05). The PS amplitudes after HFS in group nicotine 1.0 + isoflurane 0.25 and group nicotine 10.0 + isoflurane 0.25 was dramatically increased compared with the value of group isoflurane 0.25 (P < 0.01), but did not differ significantly from group LTP (P > 0.05). The PS amplitudes after HFS in group mecamylamine has no significant difference compared with the value of group isoflurane 0.125, but it was significantly lower than that in group LTP (P < 0.01). The PS amplitudes after HFS in group mecamylamine + isoflurane 0.125 significantly decreased compared with the value of group isoflurane 0.125 and group LTP (P < 0.05 or P < 0.01). CONCLUSION: The inhibition of LTP induction may contribute to isoflurane-induced deficits in memory, and the underlying mechanism is involved in the inhibition of nicotinic acetylcholine receptor activation in hippocampus of rats.

[Effect of propofol on synaptic long-term potentiation in hippocampal slices of rats].

OBJECTIVE: To investigate the effect of propofol on the synaptic long-term potentiation (LTP) in the CA(1) area of rats hippocampal slices and the possible mechanisms of its effect, and to elucidate the mechanisms underlying the effect of propofol on memory. METHODS: Hippocampal slices (400 microm thick) were obtained from male Sprague-Dawley rats (2 month old) that were ether-anesthetized and decapitated. The slices were prepared in artificial cerebrospinal fluid (ACSF), oxygenated with 95% O2 and 5% CO2. One glass electrode filled with superfusion solution was positioned in the pyramidal cell layer of the CA(1) area of rats hippocampal slices to simultaneously record evoked population spikes (PS). For LTP induction, high-frequency stimulation (HFS) conditioning pulses (100 Hz/1 s) were applied to the Schaffer collateral-commissural pathway of hippocampus using a bipolar stimulating electrode. The present study was performed to determine the effect of propofol at concentrations of 1 - 100 micromol/L on the LTP induction in rats hippocampal slices and to explore the functional importance of gamma-aminobutyric acid (GABA) type receptors in the effect of propofol on LTP induction. RESULTS: The amplitude of the PS in hippocampal slices of rats was significantly increased by 52% +/- 12% after HFS compared with that of pre-HFS. The amplitude of the PS was not significantly changed after HFS by perfusion of propofol at concentrations of 1, 5 micromol/L, when compared with the value in control group. The amplitude of the PS after HFS in the presence of propofol at 10, 30, 50 and 100 micromol/L was 124% +/- 9%, 112% +/- 8%, 106% +/- 7%, 102% +/- 6% respectively, which was significantly decreased compared with the control (all P < 0.01). The amplitude of the PS under perfusion with 50 micromol/L propofol after HFS in the presence of 50 micromol/L picrotoxin or 10 micromol/L bicuculline was 150% +/- 11%, 147% +/- 11% respectively, which was dramatically increased compared with the value of pre-HSF and 50 micromol/L propofol (all P < 0.01), but did not differ significantly from the control group. The amplitude of the PS under perfusion with 50 micromol/L propofol after HFS in the presence of 5 micromol/L CGP35348 has no significant difference compared with the value of pre-HSF and 50 micromol/L propofol, but it was significantly lower than that in the control group (P < 0.01). CONCLUSION: The inhibition of LTP induction in hippocampus of rats may contribute to propofol-induced deficits in memory, and the underlying mechanism is involved in the activation of GABA(A) receptor other than GABA(B) receptor.

Effects of adenosine agonist R-phenylisopropyl-adenosine on halothane anesthesia and antinociception in rats.

AIM: To investigate the antinociceptive effect of adenosine agonist R-phenylisopropyl-adenosine (R-PIA) given to conscious rats by intracerebroventricular (ICV) and intrathecal (IT), and identify the effect of R-PIA on minimum alveolar concentration (MAC) of halothane with pretreatment of A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) or K+ channel blocker 4-aminopyridine (4-AP). METHODS: Sprague-Dawley rats were implanted with 24-gauge stainless steel guide cannula using stereotaxic apparatus and ICV method, and an IT catheter (PE-10, 8.5 cm) was inserted into the lumbar subarachnoid space, while the rats were under pentobarbital anesthesia. After one week of recovery from surgery, rats were randomly assigned to one of the following protocols: MAC of halothane, or tail-flick latency. All measurements were performed after R-PIA (0.8-2.0 microg) microinjection into ICV and IT with or without pretreatment of DPCPX or 4-AP. RESULTS: Microinjection of adenosine agonist R-PIA in doses of 0.8-2.0 microg into ICV and IT produced a significant dose- and time-dependent antinociceptive action as reflected by increasing latency times and ICV administration of adenosine agonist R-PIA (0.8 microg) reducing halothane anesthetic requirements (by 29%). The antinociception and reducing halothane requirements effected by adenosine agonist R-PIA was abolished by DPCPX and 4-AP. CONCLUSION: ICV and IT administration of adenosine agonist R-PIA produced an antinociceptive effect in a dose-dependent manner and decreased halothane MAC with painful stimulation through activation of A1 receptor subtype, and the underlying mechanism involves K+ channel activation.

[Effect of propofol on the activation of nuclear factor-kappa B and expression of inflammatory cytokines in cerebral cortex during transient focal cerebral ischemia-reperfusion: experiment with rats].

OBJECTIVE: To investigate the effect of propofol on the activation of nuclear factor-kappa B (NF-kappa B) and the expression of inflammatory cytokines, such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule-1 (ICAM-1) in cerebral cortex during transient focal cerebral ischemia-reperfusion, and to discuss the probable mechanism of its protective effect. METHODS: Ninety male Wistar rats were randomly divided into 3 equal groups: sham operation group undergoing sham operation; ischemia/reperfusion (I/R) group undergoing thread embolism of the left middle cerebral artery occlusion (MCAO) to cause focal ischemia for 2 hours and then undergoing reperfusion; and propofol group undergoing peritoneal injection of propofol 2 hours before the ischemia-reperfusion of MCAO. Then the rats in the 3 groups were re-divided into subgroups of 5 rats, totally 18 subgroups, to be decapitated 2, 3, 6, 12, 24, and 72 hours after reperfusion for the latter 2 groups, and their brains were taken out and fixed. Immunohistochemistry was used to detect the translocation of NF-kappaB in the neurons and the expression of IL-1, TNF-alpha, and ICAM-1 in the brain. Western blotting was used to detect the expression of NF-kappa B. The opposite non-ischemic cortexes were used as controls. RESULTS: Two to 24 hours after the reperfusion NF-kappaB was significantly translocated from the cytoplasm into the nucleus; however, NF-kappa B remained in the cytoplasm of bilateral cortexes in the sham operation groups, and the nonischemic cortexes in the I/R and protofol groups. The translocation of NF-kappa B from cytoplasm into nucleus was significantly inhibited in the ischemic cortex of the propofol group. The expression values of NF-kappa B in the nuclei of ischemic cortexes in the I/R group 2 to 24 hours after reperfusion were significantly higher than those in the sham operation group and the nonischemic cortexes of the I/R and propofol groups (all P < 0.01). The expression values of NF-kappa B in the ischemic cortex of the propofol group 2 to 24 hours after reperfusion was significantly lower than that of the I/R group (all P < 0.05). The expression values of IL-1, TNF-alpha, and ICAM-1 in the ischemic cortexes were significantly higher than that in the cortex of the sham operation group and those in the nonischemic cortexes of the I/R group and propofol group (P < 0.01 or P < 0.05) and the expression values of IL-1, TNF-alpha, and ICAM-1 in the propofol group were all significantly lower than those in the I/R group (all P < 0.05). CONCLUSION: Propofol inhibits the inflammatory reaction by inhibiting the NF-kappa B activation during focal ischemia-reperfusion which may be one of the mechanisms of its neuroprotective function.