Abdominal blood flow in anesthetized dogs during plus G sub x acceleration.
Abdominal blood flow changes in anesthetized dogs during transverse acceleration
ABDOMEN↗
SEARCH · Engineering Papers
Results for “ANESTHETICS”
Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Middle-ear characteristics of anesthetized cats.
Stapes motion and transfer characteristics in anesthetized cat middle ear from 30 to 10,000 Hz
Guinan, J. J., Jr.↗
Abdominal blood flow changes during acceleration stress in anesthetized dogs.
Abdominal blood flow changes in anesthetized dogs during acceleration stress measured by hydrogen electrode technique
Alexander, W. C.↗
Brain temperature and cutaneous blood flow in the anesthetized pig
Cutaneous blood flow in anesthetized pig forelimb modified by brain temperature changes
Ingram, D. L.↗
Dynamic respiratory and circulatory responses to hypoxia in the anesthetized dog
Dynamic respiratory and circulatory responses to hypoxia in anesthetized dogs, recording oxygen partial pressures, heart rate, blood pressure, blood flows, respiratory rate, etc
Carrell, D. E.↗
Operating Room Environment Control. Part A: a Valve Cannister System for Anesthetic Gas Adsorption. Part B: a State-of-the-art Survey of Laminar Flow Operating Rooms. Part C: Three Laminar Flow Experiments
An anesthetic gas flow pop-off valve canister is described that is airtight and permits the patient to breath freely. Once its release mechanism is activated, the exhaust gases are collected at a hose adapter and passed through activated coal for adsorption. A survey of laminar air flow clean rooms is presented and the installation of laminar cross flow air systems in operating rooms is recommended. Laminar flow ventilation experiments determine drying period evaporation rates for chicken intestines, sponges, and sections of pig stomach.
Meyer, J. S.↗
Comparative study of choleretic agents in anesthetized rats as well as in restrained and and unrestrained rats, with or without compensation for biliary loss
Tests were conducted on Wistar rats by using 3 control choleretic agents: 1-phenyl-1-hydroxy n-pentane, dehydrocholic acid, and phenyl-dimethylacetic acid. The effects of these agents were compared in different experimental conditions. The comparative study of choleretic agents in anesthetized rats, in restrained and unrestrained rats, with or without compensation for biliary loss by the biliary secretion of restrained or unrestrained rats does not show, in systematic pharmecodynamic investigations, an obvious superiority over the methods based on the simple technique.
Labrid, C.↗
Cardiopulmonary responses to acute hypoxia, head-down tilt and fluid loading in anesthetized dogs
Cardiopulmonary responses to acute hypoxia (HY), fluid loading by saline infusion (FL), and head-down tilt (HD) of mechanically ventilated anesthetized dogs were investigated by measuring thermodynamics and pulmonary gas exchange. It was found that HD decreased the total respiratory compliance both during HY and normoxia (NO) and that the reduction in compliance by FL was twice as large as by HD. Superimposing HD on HY doubled the increase in vascular resistance due to HY alone. In the systemic circulation, HD lowered the resistance to below NO levels. There was a significant positive correlation between the changes in blood volume and in pulmonary artery pressure for experimental transitions, suggesting that a shift in blood volume from systemic to pulmonary circulations and changes in the total blood volume may contribute substantially to these apparent changes in resistance.
Loeppky, J. A.↗
Anteroventral Third Ventricle Lesions Attenuate Pressor Responses to Serotonin in Anesthetized Rats
When administered intravenously, serotonin (5-hydroxytryptamine; 5-HT) evokes a triphasic blood pressure response, consisting of the Bezold-Jarisch-associated depressor response, a pressor action, and long-lasting depressor response. Because the pressor response may, in part, be caused by central nervous system (CNS) activation by 5-HT, we predicted that destruction of the anteroventral third ventricle (AV3V) region, an area rich in 5-HT receptors, would attenuate increases in blood pressure to intravenous 5-HT. In anesthetized sham-lesioned and AV3V-lesioned Sprague-Dawley rats. we measured mean arterial pressure (MAP), heart rate (HR), and lumbar sympathetic nerve activity (SNA) to increasing bolus doses of intravenous 5-HT (1, 2.5, 5, 10, 25 microg/kg), before and after blockade of bradycardia using methylatropine (200 microg/kg). In all rats, bolus injections of 5-HT elicited bradycardia accompanied by a fall in lumbar SNA and an initial hypotension followed by a pressor response and a longer lasting hypotensive response. The bradycardia, reduction in lumbar SNA, and both depressor responses were equivalent in sham-lesioned and AV3V-lesioned groups. Importantly, AV3V lesions attenuated pressor responses to increasing doses of 5-HT (3 +/- 1, 6 +/- 4, 6 +/- 4, 17 +/- 4, 35 +/- 3 mmHg) compared to sham-lesioned controls (6 +/- 3, 16 +/- 7, 33 +/- 5, 54 +/- 4, 51 +/- 6 mmHg; P < 0.0001). This attenuation was conserved following blockade of bradycardia with methylatropine (P < 0.01). In summary, pressor responses to intravenous 5-HT are diminished by AV3V lesions. These data indicate that the pressor component of the blood pressure response to intravenous 5-HT is partly dependent upon interaction with the CNS.
Muntzel, Martin S.↗
Mechanisms for vasopressin effects on intraocular pressure in anesthetized rats
Continuous intracameral infusions of a balanced salt solution (0.175 microliter min-1) have been reported to raise intraocular pressure (IOP) in anesthetized rats. Palm et al. (1995) previously reported that this effect was attenuated significantly by inclusion of arginine-vasopressin (AVP, 10 ng 0.175 microliter-1) in the infusate. This study used experimental and computer simulation methods to investigate factors underlying these changes in IOP. First, constant intracameral infusions of artificial cerebrospinal fluid (aCSF) at different fixed rates (0.049-0.35 microliter min-1) were used to estimate the outflow resistance. Secondly, IOP responses were measured during an 2 hr intracameral infusion of either aCSF or AVP that was the sum of a small constant component (0.05 microliter min-1) and a larger periodic component (0.25 microliter min-1, cycling for 4 min on, then 4 min off); the mean infusion rate was 0.175 microliter min-1. As shown previously for 0.175 microliter min-1 constant infusions, the periodic aCSF infusion induced a significant rise in IOP that was attenuated by AVP administration. Complex demodulation analysis and the estimated gain parameter of a second order transfer function fit to the periodic responses indicated that outflow resistance increased significantly during the infusions in both aCSF and AVP groups, but that the indices of resistance did not differ significantly between aCSF and AVP infused eyes. This finding implies that changes in outflow resistance do not explain the difference in IOP responses to intracameral aCSF and AVP. The two responses differed significantly, though, in damping factors, such that the aCSF responses were considerably more underdamped than the AVP responses. It is hypothesized that aCSF-induced increase in IOP reflects both (1) a small component reflecting increased outflow resistance and (2) a larger non-resistive component. Since the non-resistive component is insensitive to pretreatment with acetazolamide, it is suggested that the aCSF-induced elevation in IOP reflects primarily vascular perfusion changes that are reduced by local vasoconstrictor actions of AVP. The latter mechanism likely maintains vascular perfusion of the globe when intraocular hypertension develops.
NASA Discipline Cardiopulmonary↗
Effects of angiotensin, vasopressin and atrial natriuretic peptide on intraocular pressure in anesthetized rats
The effects of atrial natriuretic peptide (ANP), vasopressin (AVP) and angiotensin (ANG) on blood and intraocular pressures of pentobarbital anesthetized rats were evaluated following intravenous, intracerebroventricular or anterior chamber routes of administration. Central injections did not affect intraocular pressure. Equipressor intravenous infusions of ANG raised, whereas AVP decreased, intraocular pressure. Direct infusions of a balanced salt solution (0.175 microliter/min) raised intraocular pressure between 30 and 60 min. Adding ANG or ANP slightly reduced this solvent effect but AVP was markedly inhibitory. An AVP-V1 receptor antagonist reversed the blunting of the solvent-induced rise by the peptide, indicating receptor specificity. Acetazolamide pretreatment lowered intraocular pressure, but the solvent-induced rise in intraocular pressure and inhibition by AVP still occurred without altering the temporal pattern. Thus, these effects appear unrelated to aqueous humor synthesis rate. The data support the possibility of intraocular pressure regulation by peptides acting from the blood and aqueous humor.
NASA Discipline Number 14-10↗
Acute Cor Pulmonale and Right Heat Failure Complicating Ethanol Ablative Therapy: Anesthetic and Radiologic Considerations and Management
Ethanol is an effective ablative agent used for the treatment of certain solid organ tumors and vascular malformations (VMs). The egress of ethanol beyond the target tissue can be associated with significant changes to the cardiopulmonary system that can lead to cardiac arrest. This article reviews the contemporary role of ethanol in tumor and VM treatment and discusses the physiological mechanisms of acute pulmonary hypertension and cardiovascular collapse. The importance of periprocedural recognition of the hemodynamic changes that can occur with the use of ethanol and the treatment of this condition are discussed.
62 RADIOLOGY AND NUCLEAR MEDICINE↗
Probing the dynamics of complexed local anesthetics via neutron scattering spectroscopy and DFT calculations
Not Available
60 APPLIED LIFE SCIENCES↗
Anesthetic propofol overdose causes endothelial cytotoxicity in vitro and endothelial barrier dysfunction in vivo
An overdose and a prolonged treatment of propofol may cause cellular cytotoxicity in multiple organs and tissues such as brain, heart, kidney, skeletal muscle, and immune cells; however, the underlying mechanism remains undocumented, particularly in vascular endothelial cells. Our previous studies showed that the activation of glycogen synthase kinase (GSK)-3 is pro-apoptotic in phagocytes during overdose of propofol treatment. Regarding the intravascular administration of propofol, we therefore hypothesized that propofol overdose also induces endothelial cytotoxicity via GSK-3. Propofol overdose (100 μg/ml) inhibited growth in human arterial and microvascular endothelial cells. After treatment, most of the endothelial cells experienced caspase-independent necrosis-like cell death. The activation of cathepsin D following lysosomal membrane permeabilization (LMP) determined necrosis-like cell death. Furthermore, propofol overdose also induced caspase-dependent apoptosis, at least in part. Caspase-3 was activated and acted downstream of mitochondrial transmembrane potential (MTP) loss; however, lysosomal cathepsins were not required for endothelial cell apoptosis. Notably, activation of GSK-3 was essential for propofol overdose-induced mitochondrial damage and apoptosis, but not necrosis-like cell death. Intraperitoneal administration of a propofol overdose in BALB/c mice caused an increase in peritoneal vascular permeability. These results demonstrate the cytotoxic effects of propofol overdose, including cathepsin D-regulated necrosis-like cell death and GSK-3-regulated mitochondrial apoptosis, on endothelial cells in vitro and the endothelial barrier dysfunction by propofol in vivo. Highlights: ► Propofol overdose causes apoptosis and necrosis in endothelial cells. ► Propofol overdose triggers lysosomal dysfunction independent of autophagy. ► Glycogen synthase kinase-3 facilitates propofol overdose-induced apoptosis. ► Propofol overdose causes an increase in peritoneal vascular permeability.
60 APPLIED LIFE SCIENCES↗
A Time-Out Checklist for Pediatric Regional Anesthetics
Although pediatric regional anesthesia has a demonstrated record of safety, adverse events, especially those related to block performance issues, still may occur. To reduce the frequency of those events, we developed a Regional Anesthesia Time-Out Checklist using expert opinion and the Delphi method.
Anesthesia, Conduction/methods/standards↗