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Kitahara H muscle relaxant in spanish generic mefenamic 500 mg fast delivery, Nozaki J muscle relaxant whiplash mefenamic 500 mg on-line, Kawahito S, et al: Low-dose sevoflurane inhalation enhances late cardioprotection resulting from antiulcer drug geranylgeranylacetone, Anesth Analg 107:755-761, 2008. Zhao P, Peng L, Li L, et al: Isoflurane preconditioning improves long-term neurologic outcome after hypoxic-ischemic brain injury in neonatal rats, Anesthesiology 107:963-970, 2007. Kuzuya T, Hoshida S, Yamashita N, et al: Delayed effects of sublethal ischemia on the acquisition of tolerance to ischemia, Circ Res 72:1293-1299, 1993. Mullenheim J, Ebel D, Bauer M, et al: Sevoflurane confers additional cardioprotection after ischemic late preconditioning in rabbits, Anesthesiology 99:624-631, 2003. Stumpner J, Lange M, Beck A, et al: Desflurane-induced postconditioning against myocardial infarction is mediated by calcium-activated potassium channels: role of the mitochondrial permeability transition pore, Br J Anaesth 108:594-601, 2012. Lutz M, Liu H: Inhaled sevoflurane produces better delayed myocardial protection at 48 versus 24 hours after exposure, Anesth Analg 102:984-990, 2006. Wakeno-Takahashi M, Otani H, Nakao S, et al: Isoflurane induces second window of preconditioning through upregulation of inducible nitric oxide synthase in rat heart, Am J Physiol Heart Circ Physiol 289:H2585-H2591, 2005. Bolli R: Cardioprotective function of inducible nitric oxide synthase and role of nitric oxide in myocardial ischemia and preconditioning: an overview of a decade of research, J Mol Cell Cardiol 33:1897-1918, 2001. Zhong C, Zhou Y, Liu H: Nuclear factor kappaB and anesthetic preconditioning during myocardial ischemia-reperfusion, Anesthesiology 100:540-546, 2004. Wang C, Xie H, Liu X, et al: Role of nuclear factor-kB in volatile anaesthetic preconditioning with sevoflurane during myocardial ischaemia/reperfusion, Eur J Anaesthesiol 27:7477-7556, 2010. Wang Y, Ahmad N, Kudo M, Ashraf M: Contribution of Akt and endothelial nitric oxide synthase to diazoxide-induced late preconditioning, Am J Physiol 287:H1125-H1131, 2004. Shi Y, Hutchins W, Ogawa H, et al: Increased resistance to myocardial ischemia in the Brown Norway vs. Dahl S rat: role of nitric oxide synthase and Hsp90, J Mol Cell Cardiol 38:6256-6335, 2005. Lotz C, Lange M, Redel A, et al: Peroxisome-proliferator-activated receptor gamma mediates the second window of anaestheticinduced preconditioning, Exp Physiol 96:317-324, 2011. Dransfeld O, Rakatzi I, Sasson S, et al: Eicosanoids participate in the regulation of cardiac glucose transport by contribution to a rearrangement of actin cytoskeletal elements, Biochem J 359: 47-54, 2001. Lucchinetti E, Aguire J, Feng J, et al: Molecular evidence of late preconditioning after sevoflurane inhalation in healthy volunteers, Anesth Analg 105:629-640, 2007. Hausenloy D, Yellon D: Survival kinases in ischemic preconditioning and postconditioning, Cardiovasc Res 70:240-253, 2006. Staat P, Rioufol G, Piot C, et al: Postconditioning the human heart, Circulation 112:2143-2148, 2005. Redel A, Stumpner J, Tischer-Zeitz T, et al: Comparison of isoflurane-, sevoflurane-, and desflurane-induced pre- and postconditioning against myocardial infarction in mice in vivo, Exp Biol Med (Maywood) 234:1186-1191, 2009. Zhu L, Lemoine S, Babatasi G, et al: Sevoflurane- and desfluraneinduced human myocardial post-conditioning through phosphatidylinositol-3-kinase/Akt signaling, Acta Anaesthesiol Scand 53:949-956, 2009. Feng J, Fischer G, Lucchinetti E, et al: Infarct-remodeled myocardium is receptive to protection by isoflurane postconditioning: role of protein kinase B/Akt signaling, Anesthesiology 104: 1004-1014, 2006. Eefting F, Rensing B, Wigman J, et al: Role of apoptosis in reperfusion injury, Cardiovasc Res 61:414-426, 2004. Inamura Y, Miyamae M, Sugioka S, et al: Sevoflurane postconditioning prevents activation of caspase 3 and 9 through antiapoptotic signaling after myocardial ischemia-reperfusion, J Anesth 24:215-224, 2010. Lemoine S, Beauchef G, Zhu L, et al: Signaling pathways involved in desflurane-induced postconditioning in human atrial myocardium in vitro, Anesthesiology 109:1036-1044, 2008. Argaud L, Gateau-Roesch O, Muntean D, et al: Specific inhibition of mitochondrial permability transition prevents lethal reperfusion injury, J Mol Cell Cardiol 38:367-374, 2005. Feng J, Lucchinetti E, Ahuja P, et al: Isoflurane postconditioning prevents opening of the mitochondrial permeability transition pore through inhibition of glycogen synthase kinase 3beta, Anesthesiology 103:987-995, 2005. Pravdic D, Mio Y, Sedlic F, et al: Isoflurane protects cardiomyocytes and mitochondria by immediate and cytosol-independent action at reperfusion, Br J Pharmacol 160:220-232, 2010. Tong H, Imahashi K, Steenbergen C, Murphy E: Phosphorylation of glycogen synthase kinase-3beta during preconditioning through phosphatidylinositol-3-kinase-dependent pathway is cardioprotective, Circ Res 90:377-379, 2002. Inamura Y, Miyamae M, Sugioka S, et al: Aprotinin abolishes sevoflurane postconditioning by inhibiting nitric oxide production and phosphorylation of protein kinase C-delta and glycogen synthase kinase 3beta, Anesthesiology 111:1036-1043, 2009. Mihara M, Erster S, Zaika A, et al: p53 has a direct apoptogenic role at the mitochondria, Mol Cell 11:577-590, 2003. Alarcon-Vargas D, Ronai Z: p53-Mdm2-the affair that never ends, Carcinogenesis 23:541-547, 2002. Ogawara Y, Kishishita S, Obata T, et al: Akt enhances Mdm2mediated ubiquitination and degradation of p53, J Biol Chem 277:21843-21850, 2002. Culmsee C, Zhu X, Yu Q-S, et al: A synthetic inhibitor of p53 protects neurons against death induced by ischemic and excitotoxic insults, and amyloid b-peptide, J Neurochem 77:220-228, 2001. Matsusaka H, Ide T, Matsushima S, et al: Targeted deletion of p53 prevents cardiac rupture after myocardial infarction in mice, Cardiovasc Res 70:457-465, 2006. Fischer U, Schulze-Osthoff K: New approaches and therapeutics targeting apoptosis in disease, Pharmacol Rev 57:187-215, 2005. Reiz S: Nitrous oxide augments the systemic and coronary haemodynamic effects of isoflurane in patients with ischaemic heart disease, Acta Anaesthesiol Scand 27:464-469, 1983. Cromheecke S, Pepermans V, Hendrickx E, et al: Cardioprotective properties of sevoflurane in patients undergoing aortic valve replacement with cardiopulmonary bypass, Anesth Analg 103:289296, 2006. Yildirim V, Doganci S, Aydin A, et al: Cardioprotective effects of sevoflurane, isoflurane, and propofol in coronary surgery patients: a randomized controlled study, Heart Surg Forum 12:E1-E9, 2009. Meco M, Cirri S, Gallazzi C, et al: Desflurane preconditioning in coronary artery bypass graft surgery: a double-blind, randomised and placebo-controlled study, Eur J Cardiothorac Surg 32:319-325, 2007.

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On the other hand muscle relaxant and alcohol buy generic mefenamic on line, neurocrine regulation transmits information over long distances muscle relaxant non sedating purchase mefenamic 500 mg otc, but the communication is narrow and precise, traveling from the end of the nerve fiber to release neurotransmitters that activate the appropriate receptor and then affects the effector. For its specificity, neurocrine communication has been compared with the telephone rather than the radio. In paracrine communication, certain substances are released from cells other than nerves. Juxtacrine or immune communications are achieved with the release of substances from the mucosal immune system. These immune cells are activated by pathogenic microorganisms during invasion of the mucosa by pathogens or antigenic substances and release chemical mediators that include histamines, prostaglandins, and cytokines. Mast cells are particularly important in these processes, and their density is high in the lamina propria. The mucosal immune system is composed of mucosa-associated lymphoid tissues and is one of the most powerful barriers to invasion by pathogens. The system includes nonimmunologic barriers such as acid in the stomach and other digestive secretions and enzymes. The immune host defense barriers include innate and adaptive or acquired immune systems. The innate mucosal immune system responds quickly to pathogens by expressing pattern recognition receptors that detect molecules in pathogenic microbes. For example, lipopolysaccharide and peptidoglycan are often present within pathogenic microbes. The innate system senses these chemicals, activating and releasing chemotactic molecules that stimulate the influx of other inflammatory cells, including microphages and neutrophils. These activated cells facilitate microbial killing by releasing a variety of toxic products such as oxygen free radicals. These inflammatory mediators are important in host-defense mechanisms against microbes, but they also may traumatize nearby uninfected tissues. The innate immune system generates cytokines that facilitate the response and activation of the adaptive immune system, which recognizes components of microorganisms, antigens within microorganisms, as well as abnormal host cells. Such recognition is mediated by specific receptors expressed on lymphoid cells and T and B cells. Transport of antigens and microbes through epithelial cells to lymphoid cells for destruction by the immune system is accomplished by epithelial M cells; they provide an opening in the epithelial barrier through vesicular transport. The functions of the glycocalyx include protection of the cellular membrane from chemical injury. The glycocalyx also enables the immune system to recognize and selectively attack foreign organisms. It coats the endothelial cells within blood vessels and prevents leukocytes from rolling. When the glycocalyx is damaged by inflammation, its permeability increases, leading to loss of water, electrolytes, and proteins during many inflammatory conditions, including the perioperative period. The ganglionic presynaptic fibers leave the spinal cord, enter the sympathetic chain of ganglia (celiac ganglion and a few mesenteric ganglia), synapse with postganglionic neurons, and travel to the gut, terminating at the neurons of the enteric nervous system. The multiple afferent nerves that travel within the vagus and pelvic nerves provide information to the brain and spinal cord for integration. Vagus fibers provide innervation to the esophagus, stomach, pancreas, small intestine, and the first half of the large intestine. The sacral parasympathetic nerves originate in the sacral segments of the spinal cord and within the pelvic nerves, innervating the lower part of the large intestine, sigmoid, rectal, and anal regions. This information is also transmitted to the central nervous system, which modulates it with the adaptive plasticity of mostly vagal brainstem circuits and sends signals back to the enteric nervous system, modifying the functional result. This process ensures that extrinsic factors such as stress or the time of day are incorporated as well. Chapter 21: Gastrointestinal Physiology and Pathophysiology 495 the longitudinal and circular muscular layers and is called the myenteric plexus, or Auerbach plexus. The inner plexus is located within submucosa and is called the submucosal plexus, or Meissner plexus. The submucosal plexus controls mainly absorption, secretion, and mucosal blood flow. Stimulation of the myenteric plexus mainly increases the tone or tonic contraction of the intestinal wall, mediated by neurotransmitters within the enteric nervous system. Distention of the distal ileum or the colon leads to inhibition of motility within the proximal ileum, slowing down gastric emptying to protect the duodenum from excessive exposure to the highly acid gastric contents. Sympathetic inhibitory effects within the enteric nervous system are achieved by norepinephrine. Sphincter muscles (unlike nonsphincter muscles) have excitatory and inhibitory -adrenergic receptors. The distention of intestinal segments is the most important stimulus of peristalsis. Muscles in the nasopharynx prevent food from moving into the nasal passages during swallowing. The hypopharynx is located between the base of the tongue and the cricoid cartilage; it contains the upper esophageal sphincter. The functional coordination between muscles during swallowing is regulated by the swallowing center in the brain. There are two phases of swallowing, the first of which is the initiatory voluntary stage.

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Thus spasms icd 9 code purchase mefenamic 250 mg without a prescription, the first phenomenon that might be seen with anesthesia is loss of muscle tone with a subsequent change in the balance between outward forces zma muscle relaxant cheap mefenamic 500 mg. This causes or is paralleled by an increase in the elastic behavior of the lung (reduced compliance) and an increase in respiratory resistance. This alters the distribution of ventilation and matching of ventilation and blood flow and impedes oxygenation of blood and removal of carbon dioxide. In a healthy subject, there is a rapid equilibration (<30% capillary length) of the oxygen tension in capillary blood with that in alveolar gas; however, during exercise, the flow rate is greater. If diffusion is impaired, equilibration takes longer, and it might not occur with exercise. At rest, equilibrium is usually reached within 25% to 30% of the capillary length, and almost no gas transfer occurs in the remaining capillary. Thickened alveolar-capillary membranes will also prolong the equilibration process and, if severe, can prevent equilibration occurring and increasing the propensity to hypoxemia. The driving pressure is expressed: P = (PaO2 - Pmv O2) mm Hg Most of the oxygen that dissolves in plasma diffuses into the red cell and binds to hemoglobin; therefore, 1 L of blood (Hb 150 g/L) with a saturation of 98%-normal in arterial blood-carries 200 mL of Hb-bound O2, compared with 3 mL that is dissolved (PaO2 100 mm Hg). The Hb-bound oxygen creates no pressure in plasma, which is important because it allows much more oxygen to diffuse over the membranes before a pressure equilibration is reached. Chapter 19: Respiratory Physiology and Pathophysiology 457 and paralysis, was responsible. Raw Compliance and Resistance of the Respiratory System Static compliance of the total respiratory system (lungs and chest wall) is reduced on average from 95 to 60 mL/ cm H2O during anesthesia. Although most studies suggest that anesthesia increases respiratory resistance, especially during mechanical ventilation,95 no studies have corrected for lung volume and flow rates (both affect resistance considerably), and it is possible that changes in resistance occur merely because of volume. Anesthesia induces cranial shift of the diaphragm and a decrease of transverse diameter of the thorax. However, others noticed an abrupt decrease in compliance and PaO2 during induction of anesthesia, and yet atelectasis could not be shown on conventional chest radiography. Morphologic studies of these densities in various animals supported the diagnosis of atelectasis. Computed tomography with transverse exposures of the chest when the subject is awake (upper panel) and anesthetized (lower panel). In the awake condition, the lung is well aerated (radiations from a pulmonary artery catheter are seen in the heart). During anesthesia, atelectasis has developed in the dependent regions (grey/white irregular areas). The large grey/white area in the middle of the right lung field is caused by a cranial shift of the diaphragm and the underlying liver. The amount of lung tissue that is collapsed is larger, because the atelectatic area consists mostly of lung tissue, whereas normal aerated lung consists of 20% to 40% tissue (the rest being air). Thus, 15% to 20% of the lung is atelectatic during uneventful anesthesia, before surgery has commenced; it decreases toward the apex, which usually remains aerated. However, this degree of atelectasis is larger (upwards of 50% of lung volume) after thoracic surgery or cardiopulmonary bypass, and can last for several hours. Alternatively, the greater loss of lung (elastic recoil) versus chest wall tissue may serve to protect against atelectasis. A three-dimensional reconstruction of the thorax of an anesthetized patient with atelectasis in the dependent regions of both lungs. There is a slight decrease in the degree of atelectasis toward the apex (distal in this image). The left panel is a cross-sectional slice of a computed tomographic image of the chest of an anesthetized patient, illustrating atelectasis in the basal (dorsal) regions. The right panel illustrates the distribution of ventilation and perfusion throughout that slice. The bulk of the ventilation is to the upper lung region (zone A), in contrast to the awake subject without atelectasis, and it exceeds the level of local perfusion; this results in wasted ventilation. In the next lowest region (zone C), there is complete cessation of ventilation because of atelectasis, but some perfusion exists and causes a shunt. The farther from the top of the lung, the higher the perfusion; however, in the lowermost regions perfusion decreases (see text). In the presence of an intrapulmonary shunt, such as with atelectasis, the mixed venous blood is shunted directly into pulmonary venous blood causing arterial desaturation. Atelectasis formation in anesthetized subjects following preoxygenation with different inspired oxygen concentrations. Increasing the Fio2 during preoxygenation increases the propensity to subsequent atelectasis (closed symbols), although there is much variability. The open circle at around an expired oxygen concentration (FeO2) of 25% represents data from anesthesia being induced while breathing 30% O2. Gamma camera images of lung blood flow in an anesthetized subject in the lateral position. Of course, the image presented is perfused tissue (not total anatomic lung tissue; in the right lateral position the upper-right lung would be larger). Although the SaO2 is usually well maintained with this approach, atelectasis inevitably forms. The use of 30% versus 100% O2 during induction was demonstrated in a clinical study to eliminate the formation of atelectasis.

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They also found that both indices were more sensitive to propofol than remifentanil muscle relaxant football commercial buy mefenamic 250 mg free shipping. They found spasms bladder purchase mefenamic 500 mg overnight delivery, based on these models, that the propofol and remifentanil effect-site concentration pairs provide a Ramsay Sedation Score of 4 ranging from (1. Definition of the optimal concentrations range for the combined administration of drugs A and B, in the case of zero interactions. The optimal concentrations range results from the intersection between the well-being surface and the plane representing a wellbeing value of 0. Interaction between alfentanil and propofol on three different endpoints: response to intubation (blue line), maintenance of anesthesia (gold line), and concentrations associated with emergence from anesthesia (green line). The curve shows the concentrations associated with a 50% probability of the respective endpoint. Bouillon and associates and Nieuwenhuijs and associates investigated the effects of hypnotic-opioid combinations on cardiorespiratory control. When combined, their effect on respiration is strikingly synergistic, resulting in severe respiratory depression. Surface models were also used to optimize drug administration in challenging situations such as shortduration procedures in spontaneous breathing patients. LaPierre and co-workers90 explored remifentanil-propofol combinations that led to a loss of response to esophageal instrumentation, a loss of responsiveness, and/or an onset of ventilatory depression requiring intervention. They found that the combinations that allowed esophageal instrumentation and avoided intolerable ventilatory depression and/or loss of responsiveness primarily clustered around remifentanil-propofol effect-site concentrations ranging from 0. However, blocking the response to esophageal instrumentation and avoiding both intolerable ventilatory depression and/or a loss of responsiveness is difficult. It may be necessary to accept some discomfort and blunt, rather than block, the response to esophageal instrumentation to consistently avoid intolerable ventilatory depression and/or loss of responsiveness. The interactions between hypnotics such as propofol and sevoflurane should be understood, because these drugs are frequently used sequentially. The definition of concentration can be rearranged to find the amount of drug required to produce any desired concentration for a known volume. This formula is often used to calculate the initial (loading) bolus dose required to achieve a given concentration. The problem with applying this concept to anesthetic drugs is that there are several volumes of distribution: V1 (central compartment), V2 and V3 (the peripheral compartments), and Vdss (the sum of the individual volumes). Consideration should be given to the dose of fentanyl required to attenuate the hemodynamic response to endotracheal intubation when combined with thiopental. The C50 for fentanyl, combined with thiopental for intubation, is approximately 3 ng/mL. Downward deflection of the surface represents synergy, in units of fractional reduction in C50. The three edges represent relative amounts of propofol to midazolam (Mid-prop), alfentanil to midazolam (Mid-alf), and alfentanil to propofol (Alf-prop). The surface between the edges represents the relative synergy of all three drugs taken together. Response surface for each of the paired interactions between propofol and midazolam (A), alfentanil and midazolam (B), and alfentanil and propofol (C) on the probability of opening eyes to a verbal command. The isoboles for a 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, and 90% response are shown. A fentanyl bolus of 39 g achieves the desired concentration in plasma for an initial instant, but plasma levels almost instantly decrease below the desired target. Levels at the effect site will never be close to the desired target concentration of 3 ng/mL. A fentanyl bolus of 1080 g, not surprisingly, produces a significant overshoot in plasma levels that persists for hours. Additionally, using equations to calculate the fentanyl dose if the resulting recommendation is to "use a fentanyl dose between 39 and 1080 g" is absurd. The usual dosing guidelines for a bolus dose, presented earlier, are designed to produce a specific plasma concentration. Because plasma is not the site of drug effect, calculating the initial bolus on the basis of a desired plasma concentration is irrational. Pharmacokinetic simulation demonstrating the limitations of infusion regimens based on simple pharmacokinetic parameters with fentanyl used as an example. These infusion schemes were designed to achieve a fentanyl plasma concentration (Cp) of 3 ng/mL. The upper blue curve shows that a regimen using a loading dose based on the volume of distribution followed by a constant infusion based on clearance results in a transient period of very high plasma concentrations. If the same maintenance infusion is given but the loading dose is based on the volume of the central compartment, then the distribution of drug to the peripheral compartments causes the plasma concentration to fall below the desired level until the compartments reach steady-state concentrations as shown in the lower gold curve. This dosing guideline is more reasonable, compared with the previous recommendation of a dose between 39 and 1080 g. Table 33-4 lists V1 and Vdpe for fentanyl, alfentanil, sufentanil, remifentanil, propofol, thiopental, and midazolam. Table 33-1 lists the time to peak effect and the t1/2 ke0 of the commonly used intravenous anesthetics. Cls of an intravenous anesthetic, a dosing regimen can be designed that yields the desired concentration at the site of drug effect. To avoid an overdose for the patient, a bolus should be selected that produces the desired peak concentration at the effect site. The decline in plasma concentration between the initial concentration after the bolus (amount/V1) and the concentration at the time of peak effect can be thought of as dilution of the bolus into a larger anatomic volume than the volume of the central compartment.

Usage: q._h.

Some investigators have suggested a greater incidence of propofol abuse by health care providers spasms under ribs order 250 mg mefenamic overnight delivery,75 muscle relaxant 2265 mefenamic 250 mg buy free shipping,76 and these investigators support stricter propofol regulation. Propofol has no direct preconditioning effect but may attenuate glutamate-mediated excitotoxicity. Compared with thiopental, propofol produces a larger decrease in intraocular pressure and is more effective in preventing an increase in intraocular pressure secondary to succinylcholine and endotracheal intubation. Normal cerebral reactivity to carbon dioxide and autoregulation are maintained during a propofol infusion. These should be used as guidelines and be adjusted to the individual needs of the patient. Current evidence indicates that propofol can protect neurons against ischemic injury caused by excitotoxicity, but neuroprotection may be sustained only if the ischemic insult is relatively mild and is not sustained after a prolonged recovery period. Prolonged propofol sedation in children is associated with adverse neurologic sequelae. The "required dose" is usually directly related to the required concentration for a given effect. The propofol Cp50 (blood concentration needed for 50% of subjects to not respond to a defined stimulus) for loss of response to verbal command in the absence of any other drug is 2. The propofol Cp50 for skin incision when combined with benzodiazepine premedication (lorazepam, 1 to 2 mg) and 66% nitrous oxide is 2. The concentration of propofol (when combined with 66% nitrous oxide) required during minor surgical procedures is 1. Not surprisingly, awakening is postponed in the presence of high blood concentrations of opioids. Optimal propofol blood concentrations have been defined when the drug is combined with several opioids, including remifentanil, alfentanil, sufentanil, and fentanyl, that ensure adequate anesthesia and the most rapid return to consciousness postoperatively (Table 30-2). In the presence of remifentanil, a relatively large-dose opioid anesthetic regimen is recommended, whereas with fentanyl, an accompanying large dose of propofol should be used to ensure rapid return to recovery postoperatively. When equilibration between blood and effect site is allowed, awakening concentrations (2. However, the duration of apnea occurring with propofol may be prolonged to more than 30 seconds. The incidence of prolonged apnea (>30 seconds) is increased further by addition of an opiate, either as premedication or just before induction of anesthesia. Computer simulation of effect-site propofol and fentanyl (A) or remifentanil (B) concentrations versus time during the first 40 minutes after termination of target-controlled infusions of propofol and fentanyl or remifentanil that had been maintained for 300 minutes at constant target blood or plasma concentration combinations associated with a 50% probability of no response to surgical stimuli. These concentration combinations are represented by the curved line on the bottom of the figure in the x-y plane. The decrease in concentrations following the intraoperative propofol-fentanyl and propofol-remifentanil combinations is represented by the curves running upward from the x-y plane. The curved lines parallel to the x-y plane represent consecutive 1-minute time intervals. The bold blue curves within the two figures represent the propofol-fentanyl-time and propofol-remifentanil-time relationships at which consciousness was regained in 50% of the patients. Doubling the infusion rate from 100 to 200 g/kg/minute causes a further moderate decrease in tidal volume but no change in respiratory frequency. Propofol (50 to 120 g/kg/minute) also depresses the ventilatory response to hypoxia, presumably by a direct action on carotid body chemoreceptors. Propofol attenuates vagal (at low concentrations) and methacholine-induced (at high concentrations) bronchoconstriction, and it seems to have a direct action on muscarinic receptors. Propofol inhibits the receptorcoupled signal transduction pathway through inositol phosphate generation and inhibition of calcium mobilization. The preservative used with propofol is important because of its bronchodilator activity. Propofol with metabisulfite (compared with propofol without metabisulfite) does not inhibit vagal or methacholine-induced bronchoconstriction. Propofol has an impact on the pulmonary pathophysiology of adult respiratory distress syndrome. In an animal model of septic endotoxemia, propofol (10 mg/kg/hour) significantly reduced free radical­mediated and cyclooxygenase-catalyzed lipid peroxidation. In addition, the partial pressure of arterial oxygen (Pao2) and hemodynamics were maintained closer to baseline. Independent of the presence of cardiovascular disease, an induction dose of 2 to 2. The decrease in arterial blood pressure is associated with a decrease in cardiac output and cardiac index (± 15%), stroke volume index (± 20%), and systemic vascular resistance (15% to 25%). When right ventricular function is considered specifically, propofol produces a marked reduction in the slope of the right ventricular end-systolic pressure-volume relationship. In patients with valvular heart disease, pulmonary artery and pulmonary capillary wedge pressure also are reduced, a finding that implies the resultant decrease in pressure reflects a decrease in preload and afterload. Although the decrease in systemic pressure after an induction dose of propofol is caused by vasodilation, the direct myocardial depressant effects of propofol are more controversial. The decrease in cardiac output after propofol administration may result from its action on sympathetic drive to the heart. The hemodynamic response to propofol lags significantly behind that of the hypnotic effect. The effect-site equilibration half-life of propofol is on the order of 2 to 3 minutes for the hypnotic effect and approximately 7 minutes for the hemodynamic depressant effect. Clinically, the myocardial depressant effect and the vasodilation depend on the dose and on the plasma concentration. The stimulation of nitric oxide may be modulated by any intralipid rather than propofol itself.

References

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