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Fentanyl overdose is a survivable condition that commonly resolves without chronic overt changes in phenotype. While the acute physiological effects of fentanyl overdose, such as opioid-induced respiratory depression (OIRD) and Wooden Chest Syndrome, represent immediate risks of lethality, little is known about longer-term systemic or organ-level impacts for survivors. In this study, we investigated the effects of a single, bolus fentanyl overdose on components of the cardiopulmonary system up to one week post. SKH1 mice were administered subcutaneous fentanyl at the highest non-lethal dose (62 mg/kg), LD10 (110 mg/kg), or LD50 (135 mg/kg), before euthanasia at 40 min, 6 h, 24 h, or 7 d post-exposure. The cerebral cortex, heart, lungs, and plasma were assayed using an immune monitoring 48-plex panel. The results showed significantly dysregulated cytokine, chemokine, and growth factor concentrations compared to time-matched controls, principally in hearts, then lungs and plasma to a lesser extent, for the length of the study, with the cortex largely unaffected. Major significant analytes contributing to variance included eotaxin-1, IL-33, and betacellulin, which were generally downregulated across time. The results of this study suggest that cardiopulmonary toxicity may persist from a single fentanyl overdose and have wide implications for the endurance of the expanding population of survivors.

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In this paper, we propose a new mathematical model of cardiovascular system coupled with a respiratory system to study the effects of COVID-19 on global blood circulation parameters using the lumped parameters model. We use the fourth-order Runge-Kutta method for solving the sets of equations of motion. We validate our model by showing that the simulated flows in pulmonary and aortic valves corroborate, respectively, the results established by Smith et al. [IFAC Proceedings Volumes, 39 (2006) 453-458]. Then we examine the effects of the new coronavirus (covid-19) on the cardiopulmonary system through the impact of the high respiratory frequency and the variation of the alveoli volume. To achieve this aim, we propose a new exponential law for the time varying of the pulmonary resistance. It appears that when the respiratory frequency grows, the delay between the systemic artery flow and the flow in the pulmonary artery diminishes. Therefore, the efficiency of the cardiac pump is reduced. Moreover, our results also show that variations of the alveoli volume cause the increment of the pleural pressure in the vascular cavities that induces an exponential growth of the pulmonary resistance. Furthermore, this growth of the pulmonary resistance provokes the augmentation of pressure in some organs and its reduction in others. We found that patient with covid-19 having a prior history of cardiovascular diseases is exposed to a severe case of inflammation/damage of certain organs than those with no history of cardiovascular disease.

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Radiotherapy remains a mainstay of cancer treatment, being used in roughly 50% of patients. The precision with which the radiation dose can be delivered is rapidly improving. This precision allows the more accurate targeting of radiation dose to the tumor and reduces the amount of surrounding normal tissue exposed. Although this often reduces the unwanted side effects of radiotherapy, we still need to further improve patients' quality of life and to escalate radiation doses to tumors when necessary. High-precision radiotherapy forces one to choose which organ or functional organ substructures should be spared. To be able to make such choices, we urgently need to better understand the molecular and physiological mechanisms of normal tissue responses to radiotherapy. Currently, oversimplified approaches using constraints on mean doses, and irradiated volumes of normal tissues are used to plan treatments with minimized risk of radiation side effects. In this review, we discuss the responses of three different normal tissues to radiotherapy: the salivary glands, cardiopulmonary system, and brain. We show that although they may share very similar local cellular processes, they respond very differently through organ-specific, nonlocal mechanisms. We also discuss how a better knowledge of these mechanisms can be used to treat or to prevent the effects of radiotherapy on normal tissue and to optimize radiotherapy delivery.

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Oxygen therapy plays a vital role to recover a patient from severe hypoxia as well as to minimize the risk of hypoxia in a critical situation. Based on this therapeutic technique, this article presents an application of backstepping control for the oxygenation in a cardiopulmonary system. A nonlinear multi-compartment system with unknown hysteresis is used as a human model in this study. With no a priori knowledge of the underlying system dynamics, a radial basis function (RBF) network is integrated into a closed-loop subsystem and trained to identify the unknown nonlinear functions. Consequently, a backstepping controller is designed based on the Lyapunov stability theorem for regulating oxygenation. The theoretical framework and simulation are presented and demonstrated in terms of stability and control performance under the presence of simulated physiological changes, possibly caused by pathophysiological effects in the cardiopulmonary system i.e. critically ill patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

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Pulmonary arterial hypertension (PAH) is a clinical condition characterized by pulmonary arterial remodeling and vasoconstriction, which promote chronic vessel obstruction and elevation of pulmonary vascular resistance. Long-term right ventricular (RV) overload leads to RV dysfunction and failure, which are the main determinants of life expectancy in PAH subjects. Therapeutic options for PAH remain limited, despite the introduction of prostacyclin analogs, endothelin receptor antagonists, phosphodiesterase type 5 inhibitors, and soluble guanylyl cyclase stimulators within the last 15 years. Through addressing the pulmonary endothelial and smooth muscle cell dysfunctions associated with PAH, these interventions delay disease progression but do not offer a cure. Emerging approaches to improve treatment efficacy have focused on beneficial actions to both the pulmonary vasculature and myocardium, and several new targets have been investigated and validated in experimental PAH models. Herein, we review the effects of adenosine and adenosine receptors (A1, A2A, A2B, and A3) on the cardiovascular system, focusing on the A2A receptor as a pharmacological target. This receptor induces pulmonary vascular and heart protection in experimental models, specifically models of PAH. Targeting the A2A receptor could potentially serve as a novel and efficient approach for treating PAH and concomitant RV failure. A2A receptor activation induces pulmonary endothelial nitric oxide synthesis, smooth muscle cell hyperpolarization, and vasodilation, with important antiproliferative activities through the inhibition of collagen deposition and vessel wall remodeling in the pulmonary arterioles. The pleiotropic potential of A2A receptor activation is highlighted by its additional expression in the heart tissue, where it participates in the regulation of intracellular calcium handling and maintenance of heart chamber structure and function. In this way, the activation of A2A receptor could prevent the production of a hypertrophic and dysfunctional phenotype in animal models of cardiovascular diseases.

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Galen (129-c. 216 AD) was a key figure in the early development of Western physiology. His teachings incorporated much of the ancient Greek traditions including the work of Hippocrates and Aristotle. Galen himself was a well-educated Greco-Roman physician and physiologist who at one time was a physician to the gladiators in Pergamon. Later he moved to Rome, where he was associated with the Roman emperors Marcus Aurelius and Lucius Verus. The Galenical school was responsible for voluminous writings, many of which are still extant. One emphasis was on the humors of the body, which were believed to be important in disease. Another was the cardiopulmonary system, including the belief that part of the blood from the right ventricle could enter the left through the interventricular septum. An extraordinary feature of these teachings is that they dominated thinking for some 1,300 years and became accepted as dogma by both the State and Church. One of the first anatomists to challenge the Galenical teachings was Andreas Vesalius, who produced a magnificent atlas of human anatomy in 1543. At about the same time Michael Servetus described the pulmonary transit of blood, but he was burned at the stake for heresy. Finally, with William Harvey and others in the first part of the 17th century, the beginnings of modern physiology emerged with an emphasis on hypotheses and experimental data. Nevertheless, vestiges of Galen's teaching survived into the 19th century.

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This article reviews the existing knowledge about the effects of physical exercise on nitric oxide (NO) production in the cardiopulmonary system. The authors review the sources of NO in the cardiopulmonary system; involvement of three forms of NO synthases (eNOS, nNOS, and iNOS) in exercise physiology; exercise-induced modulation of NO and/or NOS in physiological and pathophysiological conditions in human subjects and animal models in the absence and presence of pharmacological modulators; and significance of exercise-induced NO production in health and disease. The authors suggest that physical activity significantly improves functioning of the cardiovascular system through an increase in NO bioavailability, potentiation of antioxidant defense, and decrease in the expression of reactive oxygen species-forming enzymes. Regular physical exercises are considered a useful approach to treat cardiovascular diseases. Future studies should focus on detailed identification of (i) the exercise-mediated mechanisms of NO exchange; (ii) optimal exercise approaches to improve cardiovascular function in health and disease; and (iii) physical effort thresholds.

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Laparoscopic cholecystectomy is a new surgical procedure which worldwidely applicated gallstone disease and is presenting now anesthetic challenges. The advantages of laparoscopic cholecystectomy are shorter hospital stay, more rapid retum to normal activies and less postoperative ileus, compared with open laparotomy. During the laparoscopic surgery to enable visualization of abdominal structures, pneumoperitoneum is made with CO2 insufflation but insufflation of CO2 into abdominal cavity has been reported several consequences. Hypercarbia, high peak airway pressure, cardiac arrhythmia which were all may result from CO2 insufflation. Also, increased intraabdominal pressure from the induced pneumoperitoneum can cause decreased venous return and may result in hypotension. To ascertain the cardiopulmonary effcts of the increased intraabdominal pressure by CO2 insufflation, a clinical study was performed in 80 patients who divided into four groups likes as control group (open cholecystectomy, number:No=20), group I (15 mmHg of pressure of pneumoperitoneum, No=20), group II (20 mmHg, No=20), group III (25 mmHg, No=20). We investigated the effect of CO2 insufflation to mean arterial pressure, heart rate, end-tidal CO2 partial pressure, mean airway pressure, and arterial blood gas components. The measurements were obtained from the time of skin incision(basic value) to 20 min every 5 min interval in all groups. The results are following, I. Mean arterial pressure significantly began to increase (p<0.05) at post-incision 5 min in control, group IIl & at 10 min in group I, II compared with pre-incision value(basic value), but there were no difference between control and other study groups. II. Heart rate(HR) significantly began to differ (p<0.05) at post-incision 5 min in group II, III. compared with control group. Also HR significantly began to increase (p<0.05) at post-incision 5 min in control, group III & to decrease at post-incision 15 min in group compared with basic value. III. There were significant difference in pH between control and study groups, pH change were in normal ranges clinically. PaCO2 was significantly began to decrease (p<0.05) at post-incision 5 min in study groups compared with basic value, but still in normal acceptable ranges. IV. PaCO2 significantly began to increase (p<0.05) at post-incision 10 min in group II & at 15 min in group IIl compared with control group. Also PaCO2 significantly began to increase (p<0.05) at 5 min in group I, II & at 10 min in group III compared with basic value. V. PETCO2 significantly began to increase (p<0.05) at 10 min in group II & at 15 min in group III compared with control group. Also PETCO2 significantly began to increase (p<0.05) at 10 min in group I,II,III compared with basic value. VI. PAW significantly began to increase (p<0.05) at 10 min in group I,II,III compared with basic value. Conclusively, insufflation of CO2 into abdominal cavity during laparoscopic operation was minimal change in cardiopulmonary system and arterial blood gas value at below 20 mmHg intraabdominal pressure.

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Laparoscopy is a useful procedure for the diagnostic and therapeutic purpose, but it may be associated with many complieations related to large amounts of CO2 insufflation into the peritoneal cavity. To investigste the influence of laparoscopy 15 ASA classification I, II sur- gical patients were selected. We measured the changes in mean arterial pressure(MAP), heart rate(HR), PaO2, PaCO2, end tidal CO2 tension(PETCO2) and stress hormones such as plsma epinephrine, norepinephrine and cortisol. Above parameters were messured 10 minutes after intubation(control value), immediately after CO2 insufflation, 30 minutes after CO2 insufflation and 20 minutes after CO deflation. The results were ss follows 1) Mean arterial pressure was increased at immediately after CO2 insufflation, 30 minutes after CO2 insufflation(p<0.01) and 20 minutes after CO2 deflation(p<0.05). Heart rate was not changed significsntly. 2) PaCO2 was decreased at 30 minutes after CO2 insufflation(p<0.05), but PaCO2 snd PaCO2 were increased at 30 minutes after CO2 insufflation and 20 minutes efter CO2 deflation (p <0.01). 3) The increase of plasma epinephrine at immediately after CO2 insufflation end 30 minutes after CO2 insufflation was not significant, but plasma norepinephrine was increased at immediately after CO2 insufflstion and 30 minutes after CO2 insufflation(p<0.01). Plasme cortisol was increased at immediately after CO2 insufflstion, 30 minutes after CO2 insufflation and 20 minutes after CO2 deflation(p<0.01). We concluded that laparoscopy with CO2 insufflation has some effects on cardiopulmonary and neuroendocrine system and it is recommended to monitor carefully blood pressure, heart rate and PETCO2 for preventing hypercarbia related complications.

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