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 potential for inducing hypotension during fentanyl anaesthesia by administering either diltiazem (n = 7) or sodium nitroprusside (n = 7) was investigated during total hip arthroplasty. Haemodynamic variables were obtained in the lateral position before, during and after administration of the hypotensive agent. Diltiazem 0.15 mg X kg-1 given as an IV bolus followed by a 12.5 +/- 3 micrograms X kg-1 X min-1 continuous infusion decreased mean arterial pressure (MAP) from 77 +/- 11 mmHg to 63 +/- 16 mmHg (p less than 0.05) while other haemodynamic parameters showed only minor and insignificant changes. Hypotension continued for at least 30 min after the cessation of diltiazem. With sodium nitroprusside MAP decreased immediately from 81 +/- 11 mmHg to 59 +/- 9 mmHg (p less than 0.01) and rapidly returned to its control value after cessation of the infusion. CI and Qs/Qt rose significantly (p less than 0.05) while the systemic vascular resistance index (SVRI) (p less than 0.01) and pulmonary vascular resistance index (PVRI) (p less than 0.05) fell significantly. The haemodynamic profile was significantly different between hypotensive agents for MAP (p less than 0.02), heart rate (HR) (p less than 0.01), SVRI (p less than 0.05), and PVRI (p less than 0.05). HR was lower with diltiazem than with nitroprusside. A bradycardia less than 50 beats/min was observed in five patients in the diltiazem group. MAP, SVRI and PVRI were lower with nitroprusside than with diltiazem. Diltiazem can induce and maintain moderate hypotension without tachycardia and decreased cardiac output in humans during fentanyl anaesthesia but the modulation of the level of arterial pressure and the depression of atrioventricular conduction are unpredictable.
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PMID:Hypotensive actions of diltiazem and nitroprusside compared during fentanyl anaesthesia for total hip arthroplasty. 371 31

Experiments were designed to investigate the effect of two calcium antagonists, diltiazem and nicardipine (concentration range: 10(-7)-10(-4) M), on the contractile responses to transmural nerve stimulation, exogenous noradrenaline and tyramine in isolated canine saphenous vein rings. Both diltiazem and nicardipine inhibited the contractile response to transmural nerve stimulation in a non-competitive, concentration-dependent manner. At a concentration of 10(-4) M, diltiazem and nicardipine inhibited the maximum contractile response to transmural nerve stimulation to 0.8 +/- 0.8% and 20 +/- 10% of control respectively. Effects of diltiazem and nicardipine (up to 10(-4)M) on the contractile response to exogenous noradrenaline were minimal. The only significant difference observed was a 30% depression of the maximum contractile response with a shift in ED50 at high concentrations of nicardipine. Diltiazem (up to 10(-4) M) had no significant effect on concentration-effect curves for tyramine. Nicardipine inhibited the response to tyramine in a non-competitive manner with the maximum response depressed to 46% of control at 10(-4) M-nicardipine. Release of [3H]noradrenaline during transmural nerve stimulation was reduced by both calcium antagonists in a concentration-dependent manner. However, release of [3H]noradrenaline produced by the indirect sympathomimetic agent tyramine was not significantly inhibited by nicardipine. These experiments suggest that the calcium antagonists diltiazem and nicardipine inhibit the contractile response to transmural nerve stimulation in the canine saphenous vein predominantly by inhibiting the release of endogenous noradrenaline. However, nicardipine appears to have an additional post-synaptic inhibitory effect on the responses to exogenous as well as endogenous noradrenaline.
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PMID:Effect of calcium antagonists on adrenergic mechanisms in canine saphenous veins. 372 10

Effects of trapidil on diltiazem-induced changes of myocardial properties were investigated mechanically and electrophysiologically in tissues isolated from rabbit hearts. Application of diltiazem (10(-6) M) on right atria significantly decreased both force development and contraction rate. Additional administration of trapidil (10(-4) M) in the presence of diltiazem significantly restored the magnitude of force development without changes in contraction rate. Electrical stimulation to left atria and papillary muscles with varying frequencies produced a frequency-dependent increase in force developments (Bowditch's staircase). Diltiazem (10(-6) M) caused a depression of contractile force hence inhibited the staircase upon increasing frequency of stimulations. Additional application of trapidil (10(-4) M) partially but significantly restored the staircase. Intracellular recordings with microelectrodes clarified that trapidil increased the amplitude of slow responses which was being depressed by the treatment of diltiazem. Our findings suggest that trapidil, when applied successively to diltiazem, may diminish the inhibitory effects of diltiazem on hearts.
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PMID:Effects of trapidil on diltiazem-induced changes of mechanical and electrical properties in isolated rabbit myocardium. 375 97

Diltiazem retards ischemic arrhythmias and reduces cellular depolarization, as inferred from recordings of T-Q segment depression (delta T-Q). To explore this further, we correlated delta T-Q with the extracellular K+ electrode potential (delta EK) during serial ischemic trials. delta T-Q and delta EK were uniform in control trials, but decreased markedly in trials that immediately followed diltiazem infusion (0.5 mg/kg). delta EK at 2 min of ischemia was reduced from 11.8 +/- 1.3 to 7.4 +/- 1.2 mV; while delta T-Q was reduced from 7.2 +/- 0.5 to 4.4 +/- 0.7 mV. The effect of diltiazem on ischemic depolarization is largely, but not entirely explained by reduction of delta EK.
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PMID:Effect of diltiazem on ischemic myocardial depolarization and extracellular K+ accumulation. 375 82

The effects of the calcium entry blocker diltiazem (iv loading dose 0.4 mg/kg, iv maintenance dose 0.4 mg/min) and subsequent isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right ventricular (RV) and left ventricular (LV) performance (ultrasonic dimension technique), on coronary (electromagnetic flow probes) and systemic hemodynamics, and on electrophysiologic parameters (PR, QRS, QTc intervals) were studied in eight open-chest dogs, anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium. Diltiazem at a plasma concentration of 282 +/- 33 ng/ml (mean +/- SE) caused significant (P less than 0.05) increases in coronary blood flows, and decreases in coronary and systemic vascular resistances with only little effect on global and regional RV and LV function. However, the PR interval increased by 40%, and three animals developed II degrees atrioventricular block type I. At stable diltiazem plasma levels, administration of isoflurane caused dose-dependent decreases in myocardial segment shortening and stroke volume with unchanged LV or increased RV preload, and little changed RV or reduced LV afterload indicating myocardial depression. Coronary and systemic vascular resistances remained unaffected. At the higher concentration of isoflurane (mean inspired 1.3 +/- 0.2%), seven animals developed intermittent sinus node arrests with pauses up to 12 s followed by intermittent junctional escape or sinus rhythms. Similar interactions might develop in patients on diltiazem receiving isoflurane.
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PMID:Cardiovascular and electrophysiologic interactions between diltiazem and isoflurane in the dog. 381 73

Precordial ST-segment depression is typically observed in anterior non-Q-wave acute myocardial infarction (AMI), and is generally not regarded as an indication for acute thrombolytic therapy. Of 544 patients with creatine kinase (CK)-MB-confirmed non-Q-wave AMI randomized to the prospective multicenter Diltiazem Reinfarction Study, 50 patients (9.2%) had isolated precordial ST-segment depression of 1 mm or more in 2 or more contiguous precordial electrocardiographic leads (V1-V4). Serial electrocardiograms recorded at study entry (mean 50.5 hours after onset of chest pain), on study day 2, study day 3 and at predischarge showed that in 23 of 50 patients (40%) electrocardiographic evidence of posterior AMI evolved, defined as an R wave of 0.04 second or more in lead V1 and an R:S greater than or equal to 1 in lead V2. In 18 of these 23 patients (78%), posterior AMI had evolved by study day 3, and none had an abnormal reelevation of CK-MB (every 12-hour sampling) for up to 14 days of hospitalization. Compared with the remaining 27 patients who had electrocardiographic features of anterior non-Q-wave AMI only, the 23 with initial precordial ST segment depression in whom posterior AMI developed had significantly higher mean peak CK values (1,051 +/- 172 vs 663 +/- 89 IU, p less than 0.009) and greater mean precordial ST-segment depression in lead V1 (0.28 vs + 0.19 mm, p = 0.01), in lead V2 (1.3 vs 0.26 mm, p = 0.003) and in lead V3 (2.0 vs 0.93 mm, p = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrocardiographic evolution of posterior acute myocardial infarction: importance of early precordial ST-segment depression. 382 38

Using Holter monitoring the Authors compared the effectiveness of diltiazem 120 mg every 8 hours for three consecutive days with the results of a placebo administered with the same regimen, following a double-blind completely balanced cross-over trial in 20 patients with angina at rest. During treatment with diltiazem the total number of recorded ischemic episodes was 100, during treatment with placebo the total number was 357 (Tab. I); P less than 0.01 at analysis of variance (Tab. II). Ischemic episodes during treatment with diltiazem had a shorter duration (3.9 versus 5.1 min.), less marked ST segment shifts (1.3 versus 2 mm), and were less symptomatic (20% versus 29%) than ischemic episodes during placebo (Tab. III). No significant differences at a paired t test were noted. Diltiazem was more effective in the morning (12 p.m. - 12 a.m.: from 187 to 34 ischemic episodes) than in the evening (12 a.m. - 12 p.m.: from 170 to 66 ischemic episodes) (Fig. 1); P less than 0.01 at the chi-square test (Tab. IV). Diltiazem reduced the number of ischemic episodes with ST segment elevation, peaking of T waves and negative T wave inversion (from 188 to 39) more than the number of episodes with ST segment depression (from 169 to 61) (Tab. V); P less than 0.05 at the chi-square test. In conclusion, in patients with angina at rest, diltiazem reduces the incidence and seems to reduce the severity of ischemic episodes, too.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diltiazem in spontaneous angina: double-blind cross-over study with Holter monitoring]. 383 Jul 64

The electrophysiologic effects of intravenous diltiazem were evaluated in 10 patients with recurrent supraventricular tachycardias. The tachycardia incorporated an accessory pathway in 7 patients and was due to AV nodal reentry in 3 patients. Diltiazem 0.25 mg/kg was administered intravenously over 5 minutes during sustained supraventricular tachycardia. Programmed electrical stimulation was used to restore sinus rhythm if diltiazem failed to terminate the arrhythmia within 10 minutes. Conduction intervals, refractory periods and tachycardia characteristics were evaluated before and immediately after drug administration. Diltiazem did not significantly modify sinus cycle length, AH and HV intervals. Atrial and ventricular effective refractory periods were similar before and after diltiazem. The effective refractory period of the AV node was prolonged by 42 msec after diltiazem (p less than 0.05). Diltiazem increased the tachycardia cycle length from 320 +/- 41 to 353 +/- 36 msec (p less than 0.01) but terminated the arrhythmia in only 2 patients. After diltiazem, supraventricular tachycardia could not be reinitiated in only 2 patients and the tachycardia initiating window was not significantly reduced (56 +/- 26 to 41 +/- 33 msec). The infusion of diltiazem was accomplished without side effects. Thus, 0.25 mg/kg of intravenous diltiazem produces a modest depression of AV nodal function and is not very effective in terminating supraventricular tachycardia or preventing its initiation in this study population. Further studies using higher doses of intravenous diltiazem would be useful to determine its maximal therapeutic benefit in patients with recurrent supraventricular tachycardias.
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PMID:Electrophysiologic effects of intravenous diltiazem in patients with recurrent supraventricular tachycardias. 384 93

In order to assess the long-term efficacy of diltiazem for the treatment of angina pectoris, eight patients with chronic stable exertional angina who were previously entered into a 4-month randomized, double-blind placebo controlled study, were studied for an additional 12-months. The patients continued to take diltiazem, 360 mg/day, and underwent treadmill exercise testing after 10 and 16 months of therapy. A single-blind placebo week was introduced after 16 months and a treadmill test was performed at the end of this week. Diltiazem therapy continued to augment exercise duration until 0.1 mV of ECG ST depression at 10 and 16 months as compared to the final placebo period: 573 +/- 133 (SD) seconds at 10 months; 565 +/- 148 seconds at 16 months; vs 431 +/- 151 seconds at final placebo (both p less than 0.001). Also, the time to angina pectoris was prolonged on diltiazem by 181 seconds at 16 months (p less than 0.01) and the total duration of exercise was increased by 101 seconds (p less than 0.001) as compared to placebo. In addition, angina frequency decreased from 17 +/- 11 attacks/week on placebo to 0.6 +/- 0.6 attacks/week during diltiazem therapy at 16 months. Two of the eight patients noted mild pedal edema, but no other adverse effects were experienced. Thus diltiazem, 360 mg/day, can be an effective single agent for the long-term treatment of chronic stable angina pectoris.
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PMID:Long-term efficacy of high-dose diltiazem for chronic stable angina pectoris: 16-month serial studies with placebo controls. 388 Sep 93

Diltiazem is an orally and intravenously active calcium channel blocking agent shown to be an effective and well-tolerated treatment for stable angina and angina due to coronary artery spasm. Its efficacy in these diseases has generally been similar to that of nifedipine or verapamil - alternative calcium channel blockers with which diltiazem has many electrophysiological, haemodynamic, and antiarrhythmic similarities. The antianginal mechanism of diltiazem cannot be precisely described; however, it appears to increase myocardial oxygen supply and decrease myocardial oxygen demand, mainly by coronary artery dilatation and/or via both direct and indirect haemodynamic alterations. Diltiazem has also shown substantial efficacy in the treatment of unstable angina, hypertension, and supraventricular tachyarrhythmias, but further study is necessary before its place in the treatment of these diseases may be clearly established. Although headache due to peripheral vasodilatation and depression of atrioventricular nodal conduction may be troublesome, side effects occur in only 2 to 10% of patients receiving diltiazem and are generally minor in nature. Thus, diltiazem offers a worthwhile alternative to other agents currently available for the treatment of angina pectoris. Although the infrequency of serious side effects may offer an advantage, its relative place in therapy compared with that of other calcium channel blockers remains to be clarified.
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PMID:Diltiazem. A review of its pharmacological properties and therapeutic efficacy. 389 2


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