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)

The presence of sulfhydryl (SH) groups appears to be fundamental to nitrate-induced vasodilation and N-acetylcysteine (NAC), a sulfhydryl (SH)-donor substance, potentiates hemodynamic responsiveness to nitrates. We investigated the effect of simultaneous administration of NAC and isosorbide dinitrate (ISDN) on development of nitrate tolerance. In a double-blind, randomized, placebo-controlled cross-over study, seven patients with stable angina pectoris were treated for two 8-day periods with ISDN (40 mg four times daily, q.i.d.) together with NAC (controlled release 600 mg q.i.d.) or matching placebo. Bicycle exercise tests were performed before treatment was started, 1 h after treatment was started, and at day 8. After 8-day treatment with ISDN + placebo, responses determined by exercise testing were diminished as compared with responses obtained during acute therapy and did not differ from baseline values, suggesting development of tolerance to ISDN. During treatment with ISDN + NAC, time to 1-mm ST depression was significantly prolonged (441 +/- 44 vs. 381 +/- 40 s, mean +/- SEM) and total ST segment depression significantly reduced (1.9 +/- 0.7 vs. 3.5 +/- 0.8 mm) as compared with baseline values. The reduction in ST segment depression was significantly more pronounced during ISDN + NAC (46%) as compared with ISDN + placebo (23%). Although exercise time and time to angina pectoris were unaffected. NAC augmented the antiischemic effects of ISDN as assessed by ECG. This finding may suggest that development of nitrate tolerance is modified by chronic oral high-dose NAC administration.
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PMID:Continuous oral N-acetylcysteine treatment and development of nitrate tolerance in patients with stable angina pectoris. 171 11

We screened the antiischemic, hemodynamic, and inotropic effects of different dosages of the new calcium channel blocker Ro 40-5967 in 65 patients with stable effort-induced angina pectoris. In a double-blind way, patients were randomized to recieve a single oral dose of 50, 100, or 200 mg Ro 40-5967 or placebo, given as a drinking solution. Left ventricular ejection fraction (LVEF), blood pressure (BP), and heart rate (HR) were measured at rest and during a supine bicycle exercise test on day 0 (baseline) and 2 h after drug intake on day 1. Twenty-four hours later, the bicycle exercise test was repeated. Ro 40-5967 improved exercise duration and resting LVEF. After 200 mg, exercise time increased significantly from 8.4 +/- 0.8 min (mean +/- SEM) to 9.6 +/- 0.7 min (p = 0.018), and LVEF at rest increased from 54.5 +/- 2.2 to 58.1 +/- 2.6% (p = 0.045). Time to 0.1 mV ST-segment depression increased significantly from 4.3 +/- 0.8 to 5.5 +/- 0.9 min in the 100-mg group (p = 0.013) and from 4.3 +/- 1.3 to 5.4 +/- 1.5 min in the 200-mg group (p = 0.027). Maximum ST-segment depression decreased significantly at all dose levels (p = 0.01), with the maximum decrease noted in the 200-mg group (from 0.21 +/- 0.03 to 0.15 +/- 0.02 mV, p = 0.004). BP, HR, and rate-pressure product did not change significantly at rest or at maximum exercise. A single dose of Ro 40-5967 has antiischemic properties in patients with stable angina pectoris, with maximum effects obtained after 200 mg. No signs of negative inotropy were noted, and the drug was well tolerated.
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PMID:Lack of negative inotropic effects of the new calcium antagonist Ro 40-5967 in patients with stable angina pectoris. 172 72

The clinical and haemodynamic effects of adrenaline infusion (30 ng kg-1 min-1) producing plasma adrenaline concentrations in the range seen during acute myocardial infarction and of placebo were investigated in a crossover design in 14 patients with stable coronary heart disease. Adrenaline infusion resulted in electrocardiographic evidence of myocardial ischaemia (greater than or equal to 1 mm (0.1 mV) horizontal or downsloping ST segment depression) in 10 patients and angina in four, although the mean (SEM) increase in heart rate was modest (14 (2) beats/min) and mean coronary vascular resistance fell from 1.56 (0.21) to 1.16 (0.14) mm Hg min ml-1 (p less than 0.005). New or increasingly frequent or complex ventricular arrhythmias occurred in five patients. Placebo infusion had no effect on the variables measured. Supine bicycle exercise during infusion of the saline placebo was associated with a similar degree of ST segment depression (0.9 (0.2) mm) as adrenaline infusion at rest (0.9 (0.1) mm) but exercise performed during adrenaline infusion (10 patients) resulted in more pronounced ST segment depression (1.9 (0.3) mm) (p less than 0.005) than either intervention alone. Angina occurred in three of 11 patients during control exercise and in six of 10 during the combination of adrenaline infusion and exercise. Such potentially adverse consequences of low dose adrenaline infusion in patients with stable coronary heart disease are consistent with the suggestion that adrenal activation is detrimental during acute myocardial infarction, being both arrhythmogenic and proischaemic.
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PMID:Myocardial ischaemia and ventricular arrhythmias precipitated by physiological concentrations of adrenaline in patients with coronary heart disease. 138 26

Urethane-anesthetized rats were used to study the mechanism of cocaine-induced death. Continuous recording of the changes in five physiological parameters, including respiratory rate (RR), electroencephalogram (EEG), blood pressure (BP), electrocardiogram (ECG), and body temperature (BT), were conducted after intraperitoneal (IP) administration of a single dose of cocaine HCl (70 mg/kg). In the control group (normothermic with core body temperature 37.7 +/- 0.1 degree C and spontaneously breathing), the death rate was 88% (15/17), and the average time to respiratory arrest was 12.99 +/- 1.40 min (mean +/- SEM). The first set of experiments investigated the contribution of hypothermia to cocaine-induced death. The hypothermic group (core body temperature 33.9 +/- 0.3 degrees C and spontaneously breathing) had a death rate of 81.5% (22/27), and an average time to respiratory arrest of 16.70 +/- 1.24 min, which was significantly (p les than 0.05) prolonged. A substantial decrease in respiratory rate was seen in normothermic group, while all the other measured parameters remained relatively stable until respiratory arrest. Sequential arterial blood gas data in this group showed a decrease in PaO2 from 116.0 +/- 5.7 mmHg to 57.7 +/- 4.6 mmHg, an increase in PaCO2 from 27.7 +/- 2.2 mmHg to 42.7 +/- 3.0 mmHg, and a decrease in pH from 7.467 +/- 0.039 to 7.357 +/- 0.003. To confirm that respiratory depression was an important mechanism of cocaine-induced death in this model, ten normothermic rats underwent mechanical ventilation, and all survived cocaine exposure. This study points to the important role of respiratory depression as a cause of cocaine-induced death.
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PMID:Cocaine-induced respiratory depression in urethane-anesthetized rats: a possible mechanism of cocaine-induced death. 178 91

The pressor response to intubation is known to be exaggerated in patients with gestational proteinuric hypertension (GPH). The effect of pretreatment with lignocaine 1.5 mg kg-1, magnesium sulphate 40 mg kg-1 or alfentanil 10 micrograms kg-1 on this pressor response was studied in 69 patients with moderate to severe GPH. Systolic arterial pressure exceeded baseline values for the first 5 min after tracheal intubation in the lignocaine group, with a peak increase of 31.6 (SEM 3.6) mm Hg at 2 min after intubation, but no mean increase in pressure occurred in the two other groups. Following intubation, six of 24 mothers in the alfentanil group, six of 21 in the lignocaine group and one of 24 in the magnesium group (P less than 0.05) exhibited a systolic arterial pressure (SAP) greater than 180 mm Hg sustained for 2 min or more. Alfentanil caused the least change in heart rate, but resulted in significant fetal depression.
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PMID:Attenuation of the pressor response to tracheal intubation in hypertensive proteinuric pregnant patients by lignocaine, alfentanil and magnesium sulphate. 181 24

The effects of intravenous glucose (1 ml, 40% solution) and insulin (1.5-3.0 U/kg in 0.2-0.4 ml Ringer solution) on the velocity of propagation (VP) of cortical spreading depression (SD) were studied in 36 well-nourished (W) and 25 malnourished (M) adult (90 days old) Wistar rats of both sexes. Blood glucose levels, measured 40-70 min after glucose, were increased by 330% in the W group (N = 18) and by 202.9% in the M rats (N = 12), when compared to the pre-injection levels. Insulin decreased it by 43.5% and 61.2% in W and M rats, respectively (N = 13). In the W rats, SD VP decreased after glucose and increased after insulin. The effect of glucose could not be attributed to increases in blood osmolarity, since iv mannitol (1 ml, 20% solution, N = 5) failed to decrease SD VP. The mean +/- SEM VP before and after the treatments were as follows (in mm/min): W rats, glucose 3.31 +/- 0.16 and 3.11 +/- 0.13; insulin 3.50 +/- 0.12 and 3.81 +/- 0.11; mannitol 3.53 +/- 0.46 and 3.92 +/- 0.48. In the M rats, the above effects on SD were not seen (SD VP: glucose 3.89 +/- 0.20 and 4.13 +/- 0.24; insulin 3.51 +/- 0.19 and 3.63 +/- 0.17). The results suggest that changes in the production of brain energy influence SD propagation.
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PMID:Differential effect of changes in blood glucose levels on the velocity of propagation of cortical spreading depression in normal and malnourished rats. 184 79

To study the effects of succinylcholine on subsequent pharmacodynamics of nondepolarizing muscle relaxants, a comparative pharmacodynamic study was carried out in patients having balanced anesthesia (thiopental, fentanyl, nitrous oxide/oxygen) in whom equipotent doses of pipecuronium (80 micrograms/kg) and pancuronium (100 micrograms/kg) were given with or without prior administration of succinylcholine (1 mg/kg). Fifty-two patients were randomly assigned to one of the following four groups: 1, pancuronium (100 micrograms/kg); 2, pipecuronium (80 micrograms/kg); 3, succinylcholine (1 mg/kg) plus pancuronium (100 micrograms/kg); and 4, succinylcholine (1 mg/kg) plus pipecuronium (80 micrograms/kg). In groups 3 and 4, the nondepolarizing relaxant was given after succinylcholine when the twitch height recovered to 75% of its control value. For maintenance of neuromuscular blockade, additional increments of pancuronium (20 micrograms/kg) or pipecuronium (15 micrograms/kg) were given. Neuromuscular function was monitored throughout induction, maintenance, spontaneous recovery, and pharmacologic reversal of the neuromuscular block. Mean onset times for pancuronium (group 1) and pipecuronium (group 2) given without succinylcholine were (mean +/- SEM) 2.5 +/- 0.3 and 2.8 +/- 0.2 min, respectively. Mean onset times (times to maximum twitch depression) of the two drugs given after succinylcholine (groups 3 and 4) were significantly shorter (1.4 +/- 0.4 and 1.6 +/- 0.1 min, respectively). Clinical durations (i.e., until 25% twitch recovery of pancuronium and pipecuronium) were not significantly different among the four groups, varying from 81.1 +/- 5.4 (group 4) to 107.0 +/- 17.0 (group 2) min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of succinylcholine on the pharmacodynamics of pipecuronium and pancuronium. 183 Jan 95

In an effort to determine the incidence of respiratory depression and other side effects of subarachnoid morphine, we conducted the following prospective study in a large number (856) of young female patients undergoing cesarean delivery in one hospital. During the period from July 1987 to January 1989, patients receiving subarachnoid hyperbaric bupivacaine combined with 0.2 mg preservative-free morphine were included. They were continuously monitored for 24 hours using a pulse oximeter. For 24 hours, the vital signs, including respiratory rate every hour, and the side effects, including pruritus, nausea, and vomiting, were recorded. The need for analgesia and the total dose of opioids during the first 24 hours were documented. Our results showed that respiratory depression (SaO2 less than or equal to 85% and/or respiratory rate ten breaths per minute or less) occurred in eight patients, all of whom were markedly obese. Fifty-eight percent of the patients did not require analgesics for 24 hours. In those requiring an added opioid, the dose was (9.1 +/- 0.5 mg morphine, mean +/- SEM). Eighty-five percent of the patients were satisfied with the postoperative analgesia. Six percent were dissatisfied due to the side effects, i.e., pruritus, nausea and/or vomiting. Nine percent were dissatisfied with the pulse oximeter because it caused false alarms and limited their mobility.
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PMID:The addition of 0.2 mg subarachnoid morphine to hyperbaric bupivacaine for cesarean delivery: a prospective study of 856 cases. 188 70

The authors conducted a randomized, prospective study comparing epidural morphine with patient-controlled intravenous (iv) morphine in 30 patients recovering from total hip or total knee arthroplasty. Six, 18, and 24 hr postoperatively, patients used a 10 cm visual-analogue scale to indicate both their current degree of discomfort and the maximum discomfort they had experienced since the previous evaluation. Pain at the time of evaluation did not differ between patients receiving epidural (2.6 +/- 0.4 cm, mean +/- SEM) and patient-controlled iv morphine (3.4 +/- 0.3 cm). However, patients who received epidural morphine recalled less pain during the period preceding evaluation (4.2 +/- 0.5 cm) than did those receiving patient-controlled analgesia (5.5 +/- 0.4 cm, P less than 0.05). Patients receiving epidural morphine were more likely to require treatment for pruritus (4 of 15) than patients who received patient-controlled iv morphine (none of 15, P less than 0.05). Minimum respiratory rates were lower in patients receiving epidural morphine (15.0 +/- 0.3) than in those receiving patient-controlled analgesia (16.5 +/- 0.4, P less than 0.05), but no patients required treatment for respiratory depression. The authors conclude that epidural morphine may provide more consistent analgesia following joint replacement surgery than patient-controlled morphine; however, there is a higher incidence of side-effects with the epidural technique.
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PMID:Comparison of epidural and patient-controlled intravenous morphine following joint replacement surgery. 193 5

After unilateral uterine artery ligation in midpregnancy twelve guinea-pig does were anesthetized at 63 days of gestation. The ST waveform of the fetal electrocardiogram and the short term heart rate variability were studied during normoxia and in response to acute hypoxia in growth retarded fetuses (n = 12, mean +/- SEM, 58.5 +/- 3.9 g) and their normal sized littermates (n = 12, 94.3 +/- 3.5 g). Hypoxia was induced by letting the doe breathe a low-oxygen gas mixture. After 10 min of hypoxia fetal blood was sampled by decapitation and blood gases, acid-base status and catecholamine concentrations were analyzed. The does responded to decrease in inspired oxygen concentration with changes in oxygen tension (13.8 +/- 0.8 to 4.3 +/- 0.2 kPa) and oxygen saturation (99.9 +/- 0.1% to 70.5 +/- 1.8%). Fetal blood gases and plasma catecholamine concentrations did not differ between the groups. In the growth retarded group standard bicarbonate was significantly lower compared to controls. The T/QRS ratio (the quotient between T wave height and QRS peak to peak amplitude) was normal and similar in both groups prior to the hypoxic period. In response to hypoxia T/QRS ratio increased in the normal sized group and T/QRS was correlated to carbon dioxide tension, oxygen saturation, pH, lactate, standard bicarbonate concentration, standard base excess and plasma noradrenaline concentration, respectively. The growth retarded fetuses presented a completely different pattern where 7 out of 12 fetuses showed a biphasic ST waveform during hypoxia with depression and downward sloping of the ST segment and negative T wave.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ECG waveform, short term heart rate variability and plasma catecholamine concentrations in response to hypoxia in intrauterine growth retarded guinea-pig fetuses. 194 Jan 43


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