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At least 19 recordsLinked to original sources
PubMed1991

Mixtures of sodium nitroprusside and trimethaphan for induction of hypotension.

A mixture of sodium nitroprusside (SNP) and trimethaphan, empirical 1:10 weight ratio, has been advocated to decrease untoward side effects of SNP when used to induce hypotension during anesthesia and operation. The purpose of this study was to investigate the effects of various ratios of mixtures of SNP and trimethaphan on heart rate (HR), renal sympathetic nerve activity (RSNA), and renal artery blood flow to find the best ratio of SNP and trimethaphan for producing induced hypotension. Five mixtures with different ratios of SNP and trimethaphan, as well as each drug alone, were given intravenously to mongrel dogs in amounts adequate to achieve a stable mean arterial blood pressure of 75 +/- 5 mm Hg. Sodium nitroprusside alone significantly increased HR (163% +/- 14.5%) and RSNA (222% +/- 24%). Trimethaphan alone significantly decreased RSNA (11.6% +/- 4.5%). There were significant positive correlations between SNP-to-trimethaphan ratios and percent changes in HR (r2 = 0.301, P less than 0.01) and in RSNA (r2 = 0.648, P less than 0.01). Renal artery blood flow was well maintained with all ratios. Sodium nitroprusside and trimethaphan interacted synergistically to produce hypotension. However, they antagonize each other in their effects on arterial baroreflex-mediated changes in HR and RSNA. According to linear regression lines, HR changed least with a SNP-to-trimethaphan ratio of 1:5, and RSNA changed least with SNP-to-trimethaphan ratios of 1:2.5 and 1:5. Our results indicate that mixtures of SNP and trimethaphan in ratios of approximately 1:2.5 to 1:5 may produce induced hypotension with stable reflex sympathetic nerve activity.

Animals↗
PubMed1977

A comparison of the cardiovascular effects of sodium nitroprusside and trimethaphan.

In dogs anesthetized with pentobarbital-chloralose, cardiac output and blood flows of four regional vascular beds (superior mesenteric, left renal, left circumflex coronary and left femoral) were continuously monitered with electromagnetic flowmeters. Arterial blood pressure and heart rate were also measured. Hypotension was induced with intravenous infusions of sodium nitroprusside and trimethaphan for 5-16 min to produce comparable reductions of mean arterial pressure (32 mm Hg or 26 per cent with nitroprusside and 37 mm Hg or 31 per cent with trimethaphan). Cardiac output also decreased, but to a lesser extent (11.5 per cent with nitroprusside and 12.5 per cent with trimethaphan). Thus, total peripheral resistance was consistently decreased. Nitroprusside caused slight tachycardia, while trimethaphan produced bradycardia. Both drugs decreased mesenteric blood flow and increased mesenteric vascular resistance. Renal blood flow was maintained or increased with nitroprusside; thus, renal vascular resistance decreased; with trimethaphan, renal blood flow decreased and renal vascular resistance did not change. Both nitroprusside and trimethaphan reduced coronary blood flow; the reduction was more pronounced with the latter. Nitroprusside affected femoral blood flow minimally, with a slight reduction of femoral vascular resistance. In contrast, trimethaphan increased femoral blood flow and markedly decreased femoral vascular resistance. Redistribution of cardiac output favoring the dilated skin and muscle vascular beds appears to be an important undesirable effect of trimethaphan.

Animals↗
PubMed1988

The site of action of trimethaphan-induced neuromuscular blockade in isolated rat and frog muscle.

The present study was undertaken to determine the site of action of trimethaphan in causing neuromuscular blockade using isolated rat and frog muscle. Trimethaphan and d-tubocurarine attenuated the twitch tension developed by nerve stimulation, trimethaphan being 1/100 to 1/200 as potent as d-tubocurarine. Neostigmine potentiated the inhibitory effect of trimethaphan but reversed the effect of d-tubocurarine. Trimethaphan shifted the dose response curve of frog rectus abdominis muscle for carbachol downwards, while d-tubocurarine shifted the curve parallel to the right. Treatment with d-tubocurarine or succinylcholine protected acetylcholine receptors from persistent blockade by alpha-bungarotoxin while, in contrast, trimethaphan failed to protect the receptors. The findings indicate that trimethaphan acts on the motor endplate but, unlike d-tubocurarine, does not interact with the recognition site of acetylcholine receptors; the action of trimethaphan appears to be associated with the blockade of endplate ionic channels.

Animals↗
PubMed1984

Trimethaphan is a direct arterial vasodilator and an alpha-adrenoceptor antagonist.

In helically cut strips of dog cerebral, mesenteric, and femoral arteries contracted with prostaglandin(PG)F2 alpha, trimethaphan (10(-5)-10(-3)M) caused a dose-related relaxation that was not influenced by atropine, propranolol, diphenhydramine, cimetidine, aminophylline, or indomethacin. Trimethaphan-induced relaxation was greater in extracerebral than in cerebral arteries. The relaxation was greater in phenylephrine-contracted arteries than in PGF2 alpha-contracted arteries. On the other hand, hexamethonium did not relax the arteries. Trimethaphan (10(-4)-10(-3)M) shifted the dose-response curve for norepinephrine in mesenteric arteries to the right, but failed to influence the contractile response to 25 mM KCl. Treatment with trimethaphan (10(-4)-10(-3)M) protected alpha-adrenergic receptors from persistent blockade by phenoxybenzamine. Trimethaphan (10(-7)-3 X 10(-6)M) and hexamethonium (3 X 10(-8)-10(-6)M) significantly attenuated the contractile response of mesenteric arteries to nicotine in a dose-dependent manner, but did not alter the response to transmural electrical stimulation. The antinicotinic potency of trimethaphan was approximately one-fourth that of hexamethonium. It is concluded that, unlike hexamethonium, trimethaphan acts directly on vascular smooth muscle to induce vasodilation, more prominently in extracerebral arteries than in cerebral arteries. In high concentrations, trimethaphan appears to possess an alpha-adrenergic blocking action.

Adrenergic alpha-Antagonists↗
PubMed1983

Trimethaphan as a glutamate inhibitor at the crayfish neuromuscular junction.

At the crayfish neuromuscular junction trimethaphan reduced the amplitude of both the glutamate-induced synaptic current and the excitatory junctional current in a dose-dependent manner at concentrations greater than 5 microM. These effects were dependent on membrane potential. Trimethaphan did not affect the inhibitory junctional potential and the input resistance of the opener muscle. The dose-response curves for inhibition of glutamate responses by trimethaphan suggest that trimethaphan is not a competitive glutamate antagonist. A quantum analysis of extracellularly recorded excitatory junctional potentials showed that trimethaphan decreased both quantum content and average unit size. Trimethaphan also prolonged the glutamate currents evoked by both short and prolonged ionophoretic currents, but the decay of nerve-evoked synaptic currents was accelerated by the drug. Three explanations worthy of consideration to explain the action of trimethaphan are the responses of extra-junctional receptors, the sudden release and short actions of the neurotransmitter in contrast with the progressive application and long exposure of exogenous agonists to receptors, and discrimination of glutamate and excitatory transmitter in the crayfish neuromuscular junction. The second of these possibilities is mainly discussed at length.

Animals↗
PubMed1996

Trimethaphan versus sodium nitroprusside for the control of proximal hypertension during thoracic aortic cross-clamping: the effects on spinal cord ischemia.

Sodium nitroprusside (SNP) has been used to control the proximal hypertension associated with thoracic aortic cross-clamping (TACC) during thoracic aortic surgery. It worsens neurologic outcome, presumably by further decreasing distal arterial pressure and increasing cerebrospinal fluid (CSF) pressure, thereby worsening the spinal cord perfusion pressure (SCPP). Trimethaphan does not increase CSF pressure. Therefore, the present study investigates the effect of trimethaphan versus SNP to control proximal hypertension during TACC on neurologic outcome. Two groups, each with eight mongrel dogs, were studied. All animals underwent descending TACC for 45 min. The mean proximal aortic blood pressure was maintained at 95-100 mm Hg by the use of SNP or trimethaphan. Distal aortic pressure was allowed to vary. The dogs were neurologically evaluated 24 and 48 h later by a blinded observer. During cross-clamping, there was no difference in mean proximal aortic pressure between groups. After 10 min of cross-clamping, distal aortic pressure was higher (P < 0.01), CSF pressure was lower (P < 0.01), and SCPP was higher (P < 0.005) in the trimethaphan group as compared with the SNP group (group effect). Neurologic outcome as assessed by Tarlov's score was better at 24 and 48 h in the trimethaphan group (P < 0.05). Histopathologic injury trended with worsened neurologic outcome. We conclude that 1) trimethaphan produced higher SCPP than SNP, and 2) neurologic outcome was better in the trimethaphan group.

Animals↗
PubMed1990

Preservation of platelet function during trimethaphan infusion.

The effect of trimethaphan (Arfonad) infusion on platelet function was prospectively evaluated in 38 (n = 38) patients (28 patients receiving trimethaphan, ten control patients) undergoing elective cardiac surgery. Any patient with a positive history for the ingestion of medication known to interfere with platelet function was excluded from the study. Following induction of anesthesia with fentanyl (and prior to cardiopulmonary bypass) 28 patients (n = 28) received trimethaphan as clinically indicated to maintain a mean blood pressure of 80 mmHg. The infusion rate and total dose of trimethaphan delivered was recorded for each patient. The evaluation of platelet function was performed via adenosine diphosphate (ADP) and epinephrine-induced platelet aggregation tests. The administration of trimethaphan failed to result in any detrimental effect on platelet function as assessed via these aggregation studies. Template bleeding times were also performed on all study patients. Bleeding time measurements performed in patients following trimethaphan administration were unchanged from baseline values. Platelet aggregation studies and bleeding time performed in control group following the administration of fentanyl (30 micrograms/kg) plus enflurane (inspired concentration 0.5-1%) did not reveal any deviation from baseline values. These results are in contrast to a previous study that demonstrated a negative effect upon platelet function following sodium nitroprusside administration (at clinically acceptable doses). These data demonstrate that trimethaphan provides control of arterial pressure with preservation of platelet function.

Aged↗
PubMed1995

Haemodynamic changes during induced hypotension--comparison of trimethaphan with prostaglandin E1 assessed using transoesophageal echocardiography.

Haemodynamic changes during induced hypotension depend upon the hypotensive agent used. We investigated if, using transoesophageal echocardiography (TEE), we could identify the haemodynamic differences between trimethaphan and prostaglandin E1. Twenty-nine patients undergoing total hip replacement were selected for study. Hypotension was induced to a mean arterial pressure of 8.0-9.3 kPa with either trimethaphan (5-20 micrograms.kg-1.min-1) or prostaglandin E1 (0.5-2.0 micrograms.kg-1.min-1). The left atrial dimension, cardiac output, fractional shortening, pulmonary venous flow and mitral valve flow were evaluated using TEE. During induced hypotension, left atrial dimension decreased in both trimethaphan and prostaglandin E1 groups (P < 0.05). In the trimethaphan-treated patients systolic velocity in pulmonary venous flow decreased from 41.9 +/- 4.8 cm.sec-1 before induced hypotension to 27.8 +/- 4.2 cm.sec-1 by 30 min after stable hypotension had been established (P < 0.01). The late/early ratio of peak velocity in mitral blood flow decreased in prostaglandin E1 treated patients. Cardiac output increased from 4.2 +/- 0.5 L.min-1 to 5.3 +/- 0.4 L.min-1 during 30 min hypotension with prostaglandin E1 administration (P < 0.05), but cardiac output decreased from 5.0 +/- 0.5 to 3.5 +/- 0.4 L.min-1 with trimethaphan (P < 0.01). The differences in haemodynamic variables could be attributed to the venule dilatation effect of trimethaphan. We conclude that it was possible to detect the haemodynamic differences between trimethephan and prostaglandin E1 using TEE.

Adult↗
PubMed1985

Effects of trimethaphan on arterial blood histamine and systemic hemodynamics in humans.

Because of lack of direct evidence of histamine release by trimethaphan, the authors determined serum histamine levels and hemodynamic responses to trimethaphan administration in 19 consecutive patients. Group 1 patients (n = 7) received a single intravenous injection of trimethaphan, 0.5 mg X kg-1, while awake and again during stable halothane-nitrous oxide anesthesia. Group 2 patients (n = 6) were pretreated with intravenous H1 (chlorpheniramine, 0.1 mg X kg-1) and H2 (cimetidine, 4 mg X kg-1) receptor antagonists administered 15 min before trimethaphan, 0.5 mg X kg-1, in the awake and anesthetized states. In Group 3 (n = 6), the effects of infusion of trimethaphan, 3 mg X min-1 for 15 min, were studied during halothane-nitrous oxide anesthesia. In Group 1, bolus doses of trimethaphan were associated with maximal increases in serum histamine from 0.56 +/- 0.14 to 2.56 +/- 0.35 ng X ml-1 (P less than 0.01) and from 0.60 +/- 0.11 to 2.58 +/- 0.33 ng X ml-1 (P less than 0.01) 2 min after drug administration in the awake and anesthetized states, respectively; there were also clinical manifestations of histamine release. Mean arterial pressure decreased maximally after 5 min in the awake (from 92.0 +/- 3.4 to 69.9 +/- 2.2 mmHg; P less than 0.01) and anesthetized (from 82.6 +/- 3.7 to 57.3 +/- 2.5 mmHg; P less than 0.01) states, and was associated with increases in cardiac output and heart rate; stroke volume increased in the awake state only.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Lack of CNS depression from large doses of trimethaphan in sheep.

It is not uncommon to observe prolonged CNS depression for several hours following controlled hypotension and halothane anesthesia for neurosurgery. The present study evaluates possible contribution of large doses of trimethaphan to CNS depression. Four adult sheep were placed on transapical left ventricular bypass (TALVB) withdrawing blood from the apex of the left ventricle through a roller pump, Pall Ultipor filter, and returning the blood to a carotid artery. In the awake and unanesthetized animals, 1 to 2 gm of trimethaphan were administered IV during each experiment while maintaining mean arterial pressure at 60 to 75 torr. Two sheep stood up and knelt down without obvious correlation with dose of trimethaphan administered at the time; two remained standing and continued eating during the trimethaphan infusion. Cardiovascular recovery from these large doses of trimethaphan was within 15 to 30 minutes after the conclusion of drug infusion. The data strongly suggest that large doses of trimethaphan have no significant CNS depression in the awake and unanesthetized sheep.

Animals↗
PubMed1987

Aminoglycoside antibiotics: interaction with trimethaphan at the neuromuscular junctions.

Trimethaphan, a ganglionic blocking agent which is administered by intravenous drip to produce controlled hypotension during surgery, produces a complete neuromuscular blockade at the isolated phrenic nerve-hemidiaphragm preparation of the rat at a concentration of 0.3 mmol X l-1. This blockade is not reversed by neostigmine, a cholinesterase inhibitor, nor by calcium chloride, and this action is attributed to the local anaesthetic activity of the drug. Trimethaphan (1.5 X 10(-2) mmol X l-1) interacts with the following aminoglycoside antibiotics: gentamicin (0.04), streptomycin (0.05), netilmicin (0.06), amikacin (0.11), sisomicin (0.14), kanamycin (0.17), tobramycin (0.18) and dibekacin (0.21 mmol X l-1) to produce a complete neuromuscular blockade. These pharmacodynamic interactions of trimethaphan and aminoglycoside antibiotics occur at significantly reduced concentrations of the interacting drugs which are very close to the ones obtained after administration of therapeutic doses. When trimethaphan or aminoglycoside antibiotics are used alone at the above reduced concentrations they do not exert any neuromuscular blocking activity. The neuromuscular blockade which is obtained after the interaction of trimethaphan with aminoglycoside antibiotics is not reversed by either neostigmine or calcium chloride, although the neuromuscular blockade which is produced by aminoglycoside antibiotics alone is reversed by calcium chloride. It is concluded that the local anaesthetic effect of trimethaphan is the predominant factor of the mechanism of the above interactions. These interactions may produce severe respiratory disturbances (respiratory depression or apnoea) to the patients, during the perioperative period, which can be reversed only with artificial ventilation.

Aminoglycosides↗
PubMed1985

Regional blood flows during induced hypotension produced by nitroprusside or trimethaphan in the rhesus monkey.

In monkeys anesthetized with 70% nitrous oxide and 0.5% inspired halothane in oxygen, we measured changes in systemic hemodynamics and regional blood flows produced by nitroprusside and trimethaphan. Regional blood flow measurements were made using the radioactive microsphere technique. Control measurements were made before infusion of nitroprusside and trimethaphan into each animal in sequence in amounts adequate to reduce mean arterial pressure to approximately 55 +/- 5 mm Hg. Measurements were made during each drug infusion after a stable period of hypotension lasting at least 30 min. During nitroprusside infusion, cerebral blood flow remained unchanged, but myocardial blood flow increased significantly. However, pressure-rate product, an indirect measure of myocardial oxygen consumption, was unchanged, implying that myocardial blood flow exceeded myocardial oxygen requirement. During trimethaphan infusion, cerebral blood flow decreased, although cerebral metabolic rate for oxygen was unchanged due to increased oxygen extraction by the brain. Trimethaphan also produced a decrease in myocardial blood flow that was in proportion to the decrease in myocardial oxygen requirement as indicated by pressure-rate product. Neither drug produced changes in renal or total hepatic blood flows. We conclude that brain oxygen reserve is decreased during hypotension induced by trimethaphan. Blood flows to other organs are not significantly impaired in monkeys during hypotension to a mean arterial pressure of approximately 55 mm Hg induced by either nitroprusside or trimethaphan.

Animals↗
PubMed1994

Functional heterogeneity of nicotinic receptors in the avian lateral spiriform nucleus detected with trimethaphan.

We have examined an excitatory response mediated by nicotinic acetylcholine receptors located on the somata and/or dendrites of chick lateral spiriform neurons. On the basis of pharmacological and anatomical studies, these receptors belong to a subgroup of nicotinic receptors termed high affinity nicotine receptors, because they exhibit a high affinity for nicotinic agonists but little or no sensitivity to alpha- or kappa-bungarotoxin. We now report physiological evidence that high affinity nicotine receptors in the lateral spiriform nucleus are heterogeneous. Intracellular recording in brain slices was used to examine the pharmacological characteristics of nicotinic responses in individual lateral spiriform neurons. Nicotinic responses to brief applications of carbachol were inhibited by trimethaphan, dihydro-beta-erythroidine, or d-tubocurarine. Trimethaphan was unusual, in that a wide range of concentrations (< or = 50 microM to > 500 microM) were required to block this nicotinic response in different neurons. To quantitate the inhibition observed with trimethaphan and dihydro-beta-erythroidine, dose-response curves were generated in superfusion studies using a wide range of concentrations of both agonist (3-3000 microM carbachol in the presence of 1 microM atropine and 0.25 microM tetrodotoxin) and antagonists (10-500 microM trimethaphan or 0.1-3 microM dihydro-beta-erythroidine). The data yielded an EC50 of 25 +/- 5 microM for carbachol, with a Hill coefficient of 1.4 +/- 0.1 (mean +/- standard error; n = 8). In the case of dihydro-beta-erythroidine, a narrow range of Ki values was obtained (0.09-0.16 microM; n = 5). In contrast, Ki values for trimethaphan varied over a 15-fold concentration range (4-66 microM; n = 17), demonstrating that trimethaphan showed selectivity for different receptor subtypes found in the lateral spiriform nucleus. For both antagonists, the data indicate a competitive mode of inhibition.

Animals↗
PubMed1982

Trimethaphan-induced hypotension: effect on renal function.

This study was designed to evaluate the effects of trimethaphan-induced hypotension on renal function in healthy young patients undergoing maxillofacial surgery. Anaesthesia was induced with thiopentone and was maintained with halothane 1.5-2.0 per cent in oxygen. Each patient served as his own control, and data were analyzed using the paired t-test. Trimethaphan was infused at a rate of 45-52 microgram.kg-1.min-1 for an average hypotensive period of 53 +/- 4 (mean +/- SEM) minutes to reduce the mean arterial pressure (MAP) to 49 +/- 2 torr. Endogenous creatinine clearance, urinary Po2, sodium reabsorption rate (Tna), and serum and urine osmolalities were determined before, during and after arterial hypotension with trimethaphan. Urine flow averaged 2.9 +/- 1 ml/min during the period of hypotension. Endogenous creatinine clearance and Tna were significantly decreased (p less than 0.05) in the hypotensive period. These values returned to normal levels within one hour upon discontinuation of trimethaphan and restoration of blood pressure. We found no statistical difference in urine Po2, and serum and urine osmolalities during control, hypotensive and recovery periods. These results suggest that medullary renal tissue oxygenation, an index of tissue viability, may have remained adequate despite a significant reduction in endogenous creatinine clearance during the hypotensive period. Furthermore, it appears that the effect of trimethaphan-induced hypotension on renal function is similar to the sodium nitroprusside-induced hypotension in man which we have reported previously.

Anesthesia↗
PubMed1977

Canine systemic and cerebral effects of hypotension induced by hemorrhage, trimethaphan, halothane, or nitroprusside.

In 62 dogs, hypotension to a mean arterial pressure of either 40 or 50 torr (equivalent to a cerebral perfusion pressure of 30 or 40 torr, respectively) for one hour was induced by hemorrhage (oligemia), trimethaphan, halothane, or sodium nitroprusside. Before and during the period of hypotension, the following were measured: mean arterial blood pressure, cardiac output, whole-body O2 consumption, cerebral blood flow, cerebral O2 consumption, arterial blood gases, blood O2 content, and lactate, pyruvate, glucose, epinephrine, and norepinephrine concentrations. At the end of the period of hypotension, brain biopsies were taken for determination of adenosine triphosphate, phosphocreatine, lactate, and pyruvate concentrations. In an additional eight dogs following one hour of hypotension (at 40 torr) induced by one of the four techniques, the brains were perfused with carbon black, removed, and examined. In another ten dogs following hypotension (at 40 torr) induced with either halothane or trimethaphan, the animals were observed for three days and then killed for examination of the brain. Dogs maintained at a mean arterial pressure of 40 torr, despite differences in cerebral blood flow, demonstrated metabolic disturbances compatible with systemic and cerebral hypoxia. These were greatest in those dogs given nitroprusside in excess of 1.0 mg/kg, presumably due to cyanide toxicity. In dogs maintained at 50 torr, metabolic disturbances were minimal or absent in the halothane- and nitroprusside-treated dogs but were still apparent in the oligemic and trimethaphan-treated dogs. Carbon black infusions revealed no evidence of non-homogeneous flow. Three of the ten dogs observed for three days had persistent post-hypotension neurologic dysfunction. Two of these were given trimethaphan. The results suggest that the systemic and cerebral effects of halothane and nitroprusside (at doses less than 1.0 mg/kg) are similar and at a mean arterial pressure of 50 torr are of little consequence. By contrast, hypotension induced by trimethaphan or oligemia results in detectable metabolic alterations even at a pressure of 50 torr.

Adenosine Triphosphate↗
PubMed1976

[The effects of sodiumnitroprusside and trimethaphan induced hypotension on haemodynamics and myocardial oxygen consumption (author's transl)].

The influence of controlled hypotension (mean arterial pressure 60 mmHg) induced by sodium nitroprusside and trimethaphan on systemic circulation and myocardial oxygen consumption was studied in 7 anaesthetized closed chest dogs. The hypotensive effect of both drugs was primarily mediated by a reduction in total peripheral resistance. No change in cardiac output was observed. Stroke volume decreased in the presence of tachycardia. Left ventricular max dp/dt remained unaffected during sodium nitroprusside hypotension and was reduced by trimethaphan. Max dp/dt, load data and heart rate indicated that trimetaphan possesses negative inotropic properties. Sodium nitroprusside induced a hyperperfusion of the heart with a marked decrease in myocardial arteriovenous difference in oxygen. Myocardial oxygen consumption remained unchanged. Trimethaphan, on the other hand, induced only small increments in coronary blood flow and a rise in the arteriovenous difference in oxygen of the heart. This resulted in a higher myocardial oxygen consumption (+16%). Cardiac efficiency was lessened by trimethaphan and remained unaffected in the presence of sodium nitroprusside. As sodium nitroprusside neither affects myocardial oxygen consumption nor alters myocardial contractility, we conclude that sodium nitroprusside has advantages over trimethaphan in the management of controlled hypotension and in the therapy of hypertensive crisis and cardiogenic shock.

Animals↗
PubMed1996

Trimethaphan (Arfonad) control of hypertension and tachycardia during electroconvulsive therapy: a double-blind study.

STUDY OBJECTIVE: To ascertain the optimal dose of trimethaphan camsylate administered by intravenous (i.v.) bolus injection for the control of hypertension and tachycardia during electroconvulsive therapy (ECT). DESIGN: Prospective, double blind, within-subject study. SETTING: Treating room of the psychiatric unit of the University Hospital at Stony Brook, NY. SUBJECTS: Patients undergoing ECT for major psychiatric illnesses. MEASUREMENTS AND MAIN RESULTS: Fifteen ASA status I or II patients received in a random sequence placebo, or 5, 10, or 15 mg boluses of trimethaphan during their second to fifth treatments. Blood pressure (BP) and heart rate (HR) were recorded every 30 seconds by automated oscillometric recorder. Recordings taken before administration, during seizure, 5, and 20 minutes after seizure were examined. All doses ameliorated BP (systolic, diastolic, and mean), HR, and rate pressure product (RPP) increases during the seizure, compared with placebo. The group that received 15 mg exhibited smaller increases in RPP, i.e., 67.7% increase compared with 155.4%, 110.9%, and 98.7% increases for the placebo, 5, and 10 mg, respectively. The 10 mg and 15 mg doses caused a faster return to baseline than did the 5 mg dose or placebo. No rebound hypertension, prolonged hypotension, arrhythmias, or other side effects were noted. Trimethaphan did not alter seizure duration. CONCLUSIONS: Trimethaphan is safe, practical, and effective in the management of the hyperdynamic response to ECT. An i.v. bolus injection of 15 mg is more effective than 10 mg or 5 mg.

Adult↗
PubMed1977

Effects of trimethaphan and sodium nitroprusside on hydrolysis of succinylcholine in vitro.

The use of hypotensive agents in combination with succinylcholine may be necessary. Since trimethaphan has been reported to prolong the action of succinylcholine, the authors studied the abilities of trimethaphan and sodium nitroprusside to inhibit hydrolysis of succinylcholine by pseudocholinesterase in vitro. Trimethaphan was found to be a potent noncompetitive inhibitor of pseudocholinesterase (KI = 0.24 micronM). It could be calculated that a typical dose of trimethaphan would approximately double the duration of paralysis produced by the usual dose of succinylcholine. Nitroprusside had no inhibitory effect in vitro. It is concluded that nitroprusside is preferable when a hypotensive agent must be used in conjunction with succinylcholine.

Butyrylthiocholine↗