Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ophthalmic preparations are frequently instilled topically to protect the eye during general anesthesia. The purpose of this study was to determine if such prophylactic precautions are warranted, as determined by the effect of general surgical anesthesia on basal tear production by the Schrimer I test. As general surgical anesthesia produced a marked depression of basal tear production, both mechanical protection and topical medications are recommended for the ocular care of patients undergoing general surgical anesthesia.
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PMID:Implications of the effects of general anesthesia on basal tear production. 55 8

The cardiovascular effects of 3 preparations of atropine sulfate were studied acutely in open-chest, vagotomized dogs under endotracheal halothane anesthesia. Indices of myocardial performance (LVdp/dt/CPIP and maximum ascending aortic blood acceleration) showed insignificant changes when varying doses of IV atropine (0.04 mg/kg and 0.04 mg/kg) were given. However, mean ascending aortic pressure fell by 20 percent following the larger doses of 2 commercial preparations containing antibacterial preservatives, and only 9 percent following a "pure" (USP) atropine preparation. Calculated changes in systemic vascular resistance closely followed actual pressure values. These results indicate that atropine, even in large doses, causes little or no depression of ventricular function independently of its chronotropic action. However, atropine does cause a fall in blood pressure, seemingly due to peripheral vasodilation, particularly in commercial preparations containing preservatives.
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PMID:Cardiovascular effects of atropine sulfate preparations in vagotomized dogs under halothane anesthesia. 55 29

By simultaneous rapid-strip recordings of the electrocardiogram, phonocardiogram, and carotid pulse wave, systolic time intervals (STI) can be calculated and used to assess cardiac activity during general anesthesia. The principal advantage of this methodology over more conventional technics of determining anesthetic effects on the heart is that it is noninvasive. One anesthetic agent, halothane, was chosen to illustrate the usefulness of the technic. Results obtained by using STI supported the well-documented effect of myocardial depression produced by halothane. Becuase the equipment and technic are relatively simple, this procedure has definite clinical applications.
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PMID:Effect of halothane on systolic time intervals. 56 Jan 39

The theoretical implications of anesthetizing patients with Eisenmenger's syndrome are discussed and the anesthetic management of 16 such patients is described. A variety of technics were chosen which caused minimal depression of the cardiovascular system. These patients tolerate general anesthesia well and do not present the risks that have been suggested on theoretical grounds.
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PMID:General anesthesia in the presence of Eisenmenger's syndrome. 56 Jan 42

The cardiovascular effects of 2 and 3 mg/kg of meperidine plus 60 to 67% N2O in O2 on cardiovascular dynamics in man were measured before and after the administration of 0.08 mg/kg of IV pancuronium. N2O and 2 mg/kg of meperidine did not change heart rate (HR) but produced a marked reduction (-49%) in cardiac output (QT) plus significant decreases in stroke volume (SV) and blood pressure (BP) and an increase in peripheral arterial resistance (PVR). Additional meperidine did not further alter any of the variables; however, surgical stimulation caused significant increases in HR, BP, and PVR. SV and QT were not significantly changed by surgical stimulation and were still markedly depressed when compared to control values. Pancuronium produced marked increases in HR, SV, QT, and BP and a reduction in PVR. These changes were maximal 4 to 8 minutes after pancuronium and returned toward pre-pancuronium values thereafter. These data demonstrate that N2O-meperidine anesthesia results in a moderate reduction in BP but a marked depression in QT. The findings also indicate that pancuronium reverses the cardiovascular depression produced by N2O-meperidine and is therefore, a desirable muscle relaxant when the above technic is employed.
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PMID:Cardiovascular effects of meperidine-N2O anesthesia before and after pancuronium. 56 91

The effect of Innovar on ventilatory response to CO2 was studied in 35 patients undergoing peripheral surgery with regional anesthesia. The dosage schedule (per 70 kg body weight) was 2 ml intramuscularly, prior to the block, and 1 ml intravenously, after the block. The decrease in mean CO2 response slope (15 percent decrease from control 30 minutes after the first dose) was not statistically significant. Control slope varied inversely with age (r = 0.41, p less than 0.05), and (in 22 patients) directly with the FEV1/FVC ratio (r = 0.54, p less than 0.02) and with the combined variables (FEV1/FVC)/age (r = 0.58, p less than 0.01). Depression of CO2 response slope following Innovar did not vary with age or FEV1. We conclude that, in otherwise normal patients, these doses of innovar cause only minor depression of ventilatory response to CO2. However, in those patients who already have a depressed response (the elderly and those with a decreased FEV1/FVC ratio), this additional depression occasionally may be clinically important.
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PMID:Age, chronic obstructive pulmonary disease, and Innovar induced ventilatory depression during regional anesthesia. 56 87

Six mongrel dogs were used to investigate the mechanism of action of fentanyl-induced bradycardia. With controlled acid-base balance and temperature, and under 1.0 to 1.2 percent endtidal halothane anesthesia, 5 and microgram/kg of IV fentanyl citrate were given sequentially 1 hour apart and heart rate (HR) followed for 60 minutes. A dose-related depression of HR followed both injections. One week later the same dogs were studied similarly, except that bilateral cervical vagotomies were performed before fentanyl was given. The decrease in HR was at most 10 percent of the decrease in HR observed in the innervated dogs. Serum fentanyl levels were comparable. The data indicate the majority of the chronotropic action of fentanyl involves vagal efferent impulses from the central nervous system.
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PMID:Central vagal control of fentanyl-induced bradycardia during halothane anesthesia. 56 41

To investigate the effect of physostigmine on central nervous system (CNS) depression produced by halothane, control halothan minimum alveolar concentration (MAC) measured over 1 hour in 7 dogs was compared to MAC 30 minutes after each sequential IV dose of 0.04, 0.4, and 4 mg/kg physostigmine. MAC decreased 6.8, 11.1 (p less than 0.05), and 35.9 (p less than 0.01) percent, respectively. Six dogs were observed for an acute increase in halothane requirement in the first 30 minutes after administration of physostigmine. All 6 showed such a response at 1 or more dose levels, beginning within 1 to 5 minutes after administration and lasting 2 to 30 minutes (p less than 0.05). Five other dogs were tested with neostigmine in the same doses and showed respective decreases in MAC of 7.9, 16.6 (p less than 0.01), and 17.5 ( less than 0.01) percent. No dog showed an acute increase in anesthetic requirement. Intravenous atropine 0.5 mg/kg failed to further alter MAC after 4 mg/kg neostigmine. Physostigmine transiently antagonizes halothane anesthesia, presumably by facilitating cholinergic transmission in the CNS; neostigmine does not. After this initial response, both drugs decrease anesthetic requirement. If these data may be extrapolated to patients, they suggest that physostigmine is not an effective antagonist to postoperative somnolence due to halothane.
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PMID:Physostigmine and anesthetic requirement for halothane in dogs. 56 55

We studied the effect of ethanol on glucose and water absorption in vivo. In preliminary experiments, using sodium amytal anesthesia, we found that control animals, whose jejunal segment was perfused without ethanol, required more anesthetic agent than those perfused with ethanol. Thus, to allow for unbiased comparison of the absorption data between the two groups of animals, all absorption studies were carried out on conscious restrained hamsters. We found that ethanol did not influence the permeability of the jejunum to polyethylene glycol (PEG) and meglumine diatrizoate. In addition, ethanol did not influence the time required for the onset of steady-state absorption. Using both the gravimetric and the electrical methods, we were unable to show any measurable osmotic pressure exerted by ethanol (150-1050 mM) on the hamster jejunum. In the absorption studies we found that perfusion of the hamster jejunum with five increasing concentration of ethanol (450-1050 mM) appeared to cause a concentration-dependent depression in steady-state glucose transport. Water transport was depressed only when 4.8% (1050 mM) ethanol was perfused.
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PMID:Effect of ethanol on glucose and water absorption in hamster jejunum in vivo. Methodological problems: anesthesia, nonabsorbable markers, and osmotic effect. 56 12

The cardiovascular effects of three doses of intravenous fentanyl (50, 100, and 200 microgram) were determined in 42 adult patients undergoing intraabdominal surgical procedures with enflurane (2--3%) and nitrous oxide (50%) in oxygen. Fentanyl was administered a minimum of 40 minutes after induction of anesthesia and 30 minutes after initiation of the surgical procedure. Stroke volume, heart rate, cardiac output, mean arterial and central venous blood pressures, and peripheral arterial resistance were determined by computer analysis of the central aortic pulse-pressure curve according to the method of Warner. Measurements were made before and 2, 4, 6, 8, and 10 minutes after fentanyl. Fentanyl (50 microgram) produced increases in stroke volume and cardiac output as well as a decrease in peripheral arterial resistance but did not alter heart rate or mean arterial blood pressure. Fentanyl (100 microgram) did not significantly change any variable at any time. Fentanyl (1l (200 microgram) produced sustained decreases in stroke volume, cardiac output and mean arterial blood pressure and increased central venous pressure but did not alter heart rate or peripheral arterial resistance. The data indicate that fentanyl (50--100 microgram) stimulates or has no effect on cardiovascular dynamics during enflurane-nitrous oxide anesthesia but fentanyl (200 microgram) produces significant cardiovascular depression. Our findings suggest that small doses of intravenous fentanyl may be of benefit during enflurane-nitrous oxide but larger doses should probably be avoided.
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PMID:Cardiovascular effects of fentanyl during enflurane anesthesia in man. 57 55


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