Comment on "Carnot efficiency at divergent power output" (and additional discussion)

In a recent Letter [EPL, 118 (2017) 40003], Polettini and Esposito claimed that it is theoretically possible for a thermodynamic machine to achieve Carnot efficiency at divergent power output through the use of infinitely-fast processes. It appears however that this assertion is misleading as it is not supported by their derivations as demonstrated below. In this Comment, we first show that there is a confusion regarding the notion of optimal efficiency. We then analyze the quantum dot engine described in Ref. [EPL, 118 (2017) 40003] and demonstrate that Carnot efficiency is recovered only for vanishing output power. Moreover, a discussion on the use of infinite thermodynamical forces to reach Carnot efficiency is also presented in the appendix.Comment: Modified version compared to the manuscript submitted to EP

Nissl and immunostaining of NeuN for brain morphology and hippocampal CA1 region at five weeks after hypoxia ischemia.

<p><b>(A)</b> All groups except sham showed brain atrophy with loss of brain tissue in the hypoxia ischemia (HI) injured hemisphere. Delayed remote ischemic Postconditioning (dRIPC) did not attenuate or worsen the atrophy. <b>(B) Nissl and (C) NeuN</b> Higher magnification of the hippocampus CA1 region (depicted within boxes in <b>(A)</b>) showed a decrease of the CA1 cells after HI compared to sham group. dRIPC treatment did not show improvement microscopically. <b>(D)</b> Nissl quantification of brain atrophy shows significant brain volume loss in HI. dRIPC groups did not show significant improvement but a trend is seen. Data expressed as mean ± SEM. #<i>p</i><0.05 compared with sham.</p

Neurobehavioral tests for cognitive function at five weeks after hypoxia ischemia.

<p>All animals in hypoxia ischemia (HI) group exhibited significant cognitive impairment. However, following delayed remote ischemic postconditioning (dRIPC) treatment, a statistical significance was not reached. Nevertheless treatment groups showed improvement, indicated by a consistent trend to reverse the neurobehavioral deficits caused by HI. Morris Water Maze test shows, three day treatment group had improved performance <b>(A, C)</b> and a trend of improvement <b>(B)</b>, and also one day treatment group shows an improvement in performance <b>(C)</b>. The T Maze test <b>(D)</b> demonstrates improved functional outcome following dRIPC in both treatment groups. Data expressed as mean ± SEM. #<i>p</i><0.05 compared with sham. <i>p</i> = 0.13 vs. HI and 3days and <i>p</i> = 0.3 vs. HI and 1day.</p

Neurobehavioral tests for sensory motor function at five weeks after hypoxia ischemia.

<p>All animals in hypoxia ischemia (HI) group exhibited significant sensory motor impairment. The three day delayed remote ischemic postconditioning treatment group showed a trend to decrease the number of left foot faults after HI <b>(A)</b>, and the number of total foot faults was significantly less in the three day treatment group compared to the non-treated HI group <b>(B)</b>. The Beam Balance test did not show significant difference between the groups <b>(C)</b>. The Wire Hang test did not show significant difference between the treated and non-treated groups <b>(D)</b>. Data expressed as mean ± SEM. #<i>p</i><0.05 compared with sham, §<i>p</i><0.05 compared with non-treated HI group.</p

Brain Weight (A), Body Weight (B), and Organ Weights (C), (D), and (E) at five weeks after hypoxia ischemia.

<p><b>(A)</b> A significant loss of right-to-left hemispheric (RH: LH) weight ratio was evident after hypoxia ischemia. Although a slight preservation of the injured hemisphere was observed grossly in the delayed remote ischemic postconditioning (dRIPC) treatment groups, there was no significant improvement or worsening of brain weights in both one day and three day treatment groups. Representative pictures of brain samples shown. <b>(B)</b> All treated and non-treated groups had a significant loss in body weight compared to sham. dRIPC did not aggravate weight loss. <b>(C)</b> Lung, <b>(D)</b> Liver, and <b>(E)</b> Spleen, the organ: body weight ratios, showed no significant difference between the groups. dRIPC did not adversely affect organ: body weight ratios. The treatment groups showed a slight decrease in pulmonary haemorrhage <b>(C)</b>. Representative pictures of lung samples shown. Data expressed as mean ± SEM. #<i>p</i><0.05 compared with sham. <i>p</i> = 0.98 vs. RIPC groups and HI in <b>(B)</b>.</p

Effects of Isoflurane Preconditioning on MAP, HR, and CBF Changes During and Post-sGVS.

<p><b>(A)</b> MAP is significantly reduced by sGVS in unconditioned and isoflurane preconditioned rats subjected to sGVS compared to Sham (p<0.1 Sham vs sGVS, p<0.05 Sham vs sGVS + Isoflurane PC). MAP recovers immediately upon stopping sGVS, but prolonged anesthesia has a tendency to steadily decrease MAP (Sham: p<0.1 Baseline vs 20–30 Min Post-S-Stimulation; sGVS: p<0.1 Baseline vs 20–30 Min Post-Stimulation). <b>(B)</b> During sGVS, HR is significantly lowered by sGVS in unconditioned and isoflurane preconditioned rats compared to Sham (p<0.05 for Sham vs sGVS and sGVS + Isoflurane PC). HR in unconditioned animals remains decreased for up to 10 minutes post-sGVS, while the HR of isoflurane preconditioned rats recovers after sGVS stops. Prolonged anesthesia causes continued decreased in HR for sham and unconditioned sGVS animals (Sham: p<0.1 between Baseline and 20–30 Min Post-Stimulation; sGVS: p<0.05 for Baseline vs 10–20 and 20–30 Min Post-Stimulation). <b>(C)</b> CBF is reduced by sGVS in unconditioned and isoflurane preconditioned animals compared to Sham (p<0.05 for Sham vs sGVS and sGVS + Isoflurane PC), yet isoflurane preconditioning attenuates the CBF reduction caused by sGVS (p<0.05 sGVS vs sGVS + Isoflurane PC). The CBF reduction caused by sGVS remains for up to 30 minutes post-stimulation (p<0.05 for Sham vs sGVS and sGVS + Isoflurane PC for each time frame Post-Stimulation). * p<0.05 for Sham vs sGVS for the given time variable, <b>#</b> p<0.05 for Sham vs sGVS + Isoflurane PC, <b>&</b> p<0.05 for sGVS vs sGVS + Isoflurane PC.</p

An Experimental Model of Vasovagal Syncope Induces Cerebral Hypoperfusion and Fainting-Like Behavior in Awake Rats

<div><p>Vasovagal syncope, a contributing factor to elderly falls, is the transient loss of consciousness caused by decreased cerebral perfusion. Vasovagal syncope is characterized by hypotension, bradycardia, and reduced cerebral blood flow, resulting in fatigue, altered coordination, and fainting. The purpose of this study is to develop an animal model which is similar to human vasovagal syncope and establish an awake animal model of vasovagal syncope. Male Sprague-Dawley rats were subjected to sinusoidal galvanic vestibular stimulation (sGVS). Blood pressure, heart rate, and cerebral blood flow were monitored before, during, and post-stimulation. sGVS resulted in hypotension, bradycardia, and decreased cerebral blood flow. One cohort of animals was subjected to sGVS while freely moving. sGVS in awake animals produced vasovagal syncope-like symptoms, including fatigue and uncoordinated movements; two animals experienced spontaneous falling. Another cohort of animals was preconditioned with isoflurane for several days before being subjected to sGVS. Isoflurane preconditioning before sGVS did not prevent sGVS-induced hypotension or bradycardia, yet isoflurane preconditioning attenuated sGVS-induced cerebral blood flow reduction. The sGVS rat model mimics elements of human vasovagal syncope pathophysiology (hypotension, bradycardia, and decreased cerebral perfusion), including behavioral symptoms such as fatigue and altered balance. This study indicates that the sGVS rat model is similar to human vasovagal syncope and that therapies directed at preventing cerebral hypoperfusion may decrease syncopal episodes and reduce injuries from syncopal falls.</p></div

sGVS Causes CBF Reduction.

<p>Representative plot of CBF (bottom, blue plot) changes during sGVS (top, red plot). Baseline CBF (~1780 perfusion units) was collected for 4 minutes before beginning sGVS (at minute 4). Approximately 1 minute after starting sGVS a significant drop in CBF was observed, which was maintained throughout stimulation. After sGVS, CBF recovers, but does not return to baseline values.</p

MAP, HR, and CBF Changes Induced by sGVS.

<p><b>(A)</b> MAP tends to decrease during sGVS (p<0.1). After sGVS, MAP recovers. Prolonged anesthesia causes a steady MAP drop in all rats (Sham: p<0.05 for Baseline vs 10–20 and 20–30 Min Post-Stimulation, p<0.1 for 0–5 Min Post-Stimulation vs 20–30 Min Post-Stimulation; sGVS: p<0.1 between Baseline and 20–30 Min Post-Stimulation). <b>(B)</b> HR is significantly reduced for sGVS rats compared to Sham during sGVS (p<0.05), and for up to 10 Min Post-Stimulation (p<0.05). Prolonged anesthesia causes steady decline of HR in all rats (Sham: p<0.05 for Baseline vs 10–20 and 20–30 Min Post-Stimulation, p<0.05 for 0–5 and 5–10 Min Post-Stimulation vs 10–20 and 20–30 Min Post-Stimulation; sGVS: p<0.05 for Baseline vs each time range post-sGVS, p<0.05 for 0–5 and 5–10 Min Post-Stimulation vs 20–30 Min Post-Stimulation). <b>(C)</b> CBF is significantly reduced during sGVS compared to Sham (p<0.05) and remains depressed for up to 30 minutes post-sGVS (p<0.05). Prolonged anesthesia does not significantly lower CBF in either sham or sGVS rats. * p<0.05 for Sham vs sGVS for the given time variable.</p

Behavioral Changes during sGVS in Awake Rats.

<p>Representative images of the changes in behavior observed during sGVS in awake rats. Sinusoidal galvanic vestibular stimulation in the awake animal induces similar symptoms as that experienced by VVS patients. Awake animals during stimulation exhibit signs of fatigue-like behavior (reduced responsiveness and lethargy), labored breathing, altered coordination, and even faint-like behavior (<i>i</i>.<i>e</i>. falling). Representative images from fainting-like behavior in two animals are shown (<b>A</b>, <b>B</b>) with pre-faint-like stance (<b>i</b>), stance during the faint-like behavior (<b>ii</b>), and spontaneous recovery within 1–2 seconds after the onset of the faint-like behavior (<b>iii</b>). <b>(C)</b> Representative images of altered coordination and head swaying.</p