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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↗
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↗
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↗
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↗
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↗
PubMed1992

Treatment of stress response during balanced anesthesia. Comparative effects of isoflurane, alfentanil, and trimethaphan.

Acute hypertensive responses during nitrous oxide-opioid-relaxant anesthesia are a common clinical problem. In adult men undergoing radical prostatectomy procedures and anesthetized with a standardized technique, we evaluated the effectiveness of alfentanil, isoflurane, and trimethaphan in treating acute hemodynamic and stress hormone responses to surgical stimulation. Stress hormone concentrations were measured 1 min before skin incision, after the onset of an acute hypertensive response, and after returning the mean arterial pressure to within 10% of the preincision values with one of the three treatment modalities. Pretreatment plasma alfentanil concentrations (151 +/- 47 to 156 +/- 47 ng.ml-1) and end-tidal nitrous oxide concentrations (66 +/- 2 to 68 +/- 2%) were similar in all three groups. Acute hypertensive events were associated with significantly increased concentrations of catecholamines and vasopressin (antidiuretic hormone [ADH]). Whereas intravenous alfentanil returned all hormone concentrations to preincision values, norepinephrine and glucose concentrations were significantly increased after adjunctive isoflurane administration. Although trimethaphan decreased the norepinephrine concentration, the epinephrine, beta-endorphin, cortisol, ADH, and glucose concentrations were significantly increased compared to preincision values. However, the persistent elevation in the posttreatment ADH concentration in the trimethaphan group was the only significant difference between the three groups. Mean (+/- standard deviation) times to awakening (2.8 +/- 3.3 to 3.8 +/- 4.2 min), extubation (8.1 +/- 4.8 to 10.3 +/- 8.5 min), and orientation (19.6 +/- 20.4 to 24.6 +/- 19.1 min) were similar in all three groups. Naloxone was required more frequently in patients in the alfentanil (35%) and isoflurane (24%) groups than in the trimethaphan group (4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

[Effects of hypotensive anesthesia with prostaglandin E1 or trimethaphan on renal microstructure].

A study was made on the presence or absence and the degree of histopathological renal cell damage, in hypotensive anesthesia models with prostaglandin E1 (PGE1) or trimethaphan. Cell damage was most noticeable in the S3 segment, the straight and second half part of the proximal renal tubule. The lesion was evaluated and semiquantified. The trimethaphan group in this area exhibited degeneration--including cell vacuolation and granule increase in this site, as well as cytoclasis such as cell fragments in the lumen, luminal extension, flattening of epithelial cell and damage of distal renal tubular columns. In the PGE1 group, cell degeneration was milder than in the trimethaphan group, and there were no cytoclasis findings. Renal cell damage in the PGE1 group was slighter than in the trimethaphan group.

Alprostadil↗
PubMed1976

Changes in serum potassium and blood glucose concentrations after trimethaphan administration in man.

Blood glucose and serum potassium (K+) concentrations were measured before, during, and 60 minutes after operation in two groups of 10 patients during nitrous oxide/halothane/d-tubocurarine anesthesia for major orthopedic surgery. In the control group, arterial blood pressure was maintained within normal range, while in the study group trimethaphan camsylate was administered as an intravenous infusion (average, 218 mg.) to maintain a systolic blood pressure of 60 to 65 torr. In the normotensive group, blood glucose rose significantly during operation and early postoperatively and serum K+ was essentially unchanged. In the hypotensive group, trimethaphan caused a striking modification of surgically induced hyperglycemia, together with a small significant decrease in serum K+ intraoperatively. The observed increase in blood glucose is part of the autonomic response to surgical stress. Hormonal factors (growth hormone, cortisol and glucagon) may conceivably be involved. The decrease in serum K+ is probably caused by decreased hepatic glycogenolysis and attenuation of the suppressive effect of catecholamines on insulin release, both effects being secondary to the ganglionic blocking property of trimethaphan. These results indicate that trimethaphan, in contrast to other ganglionic blocking drugs, does not cause hypoglycemia and suggest that serum K+ concentration should be monitored whenever these drugs are used.

Adolescent↗
PubMed1986

The influence of trimethaphan (Arfonad)-induced hypotension with and without spine distraction on canine spinal cord blood flow.

Controlled hypotension is used in scoliosis surgery to reduce the need for transfusion and to improve operating conditions, but there is concern that deliberate hypotension may decrease spinal cord blood flow (SCBF) and predispose the spinal cord to injury, particularly when it is distracted during Harrington instrumentation. To study the effect of deliberate hypotension on SCBF, the mean arterial pressure (MAP) was reduced to 50% of its normotensive value with trimethaphan (Arfonad) in dogs and the SCBF measured using the hydrogen washout technique with and without spine distraction. The SCBF was significantly reduced to half its normotensive value of 23.2 ml/min/100 gm to 11.4 ml/min/100 gm after hypotension was established. The SCBF remained significantly decreased compared with controls when measured at 30, 45, and 60 minutes following the induction of hypotension and also when hypotension was terminated. SCBF was not further reduced when 2 cm of spine distraction was added. These results show that induction of hypotension with trimethaphan is associated with a similar decrease in SCBF, which is maintained as long as the drug is used and that this effect continues after the drug is terminated and the MAP increases. Cautiously extrapolating these findings clinically would suggest that trimethaphan may not be the drug of choice for controlled hypotension during scoliosis surgery, despite its apparently favorable hemodynamic and hormonal responses.

Animals↗
PubMed1988

The effect of trimethaphan-induced hypotension on canine spinal cord blood flow. Measurement at different cord levels using radiolabelled microspheres.

Controlled hypotension which is used during scoliosis surgery to improve operating conditions and minimize transfusion requirements may decrease spinal cord blood flow (SCBF). Previous studies using hydrogen washout, an invasive technique, have shown that trimethaphan-induced hypotension is associated with a decrease in SCBF, whereas hypotension induced with sodium nitroprusside or nitroglycerin is not. To determine whether the decrease seen with trimethaphan represented a generalized rather than regional spinal cord phenomenon, SCBF was measured at three separate cord levels (T2-3, 7-8, L2-3) using a noninvasive radionuclide-labelled microsphere technique. When the mean arterial pressure was reduced by 50%, SCBF decreased 35 to 45% at all levels of the cord examined, and remained at this reduced level during the period of hypotension. The results confirm that trimethaphan-induced hypotension is associated with a significant reduction in SCBF and that this occurs throughout the spinal cord during the period of hypotension.

Animals↗
PubMedDate not supplied

Prolonged neuromuscular blockade associated with trimethaphan: a case report.

A case of prolonged neuromuscular blockade associated with the administration of trimethaphan to a neurosurgical patient aged 29 is believed to be the possible result of interaction between trimethaphan, a ganglionic-blocking drug, and muscle relaxant. This possibility should be kept in mind when the administration of trimethaphan is being considered.

Adult↗
PubMed1975

Comparative hemodynamic responses to chlorpromazine, nitroprusside, nitroglycerin, and trimethaphan immediately after open-heart operations.

The hemodynamic effects of intravenous chlorpormazine, nitroprusside, nitroglycerin, and trimethaphan camsylate were studied in 51 patients with high mean arterial pressures immediately after open-heart operations. Chlorpromazine was given by bolus intravenous injection to 24 patients (average dose 10.3 mg); nitroprusside (17 patients), nitroglycerin (8 patients), and trimethaphan (12 patients) were administered by constant intravenous infusion at average doses of 77 mug/min, 59 mug/min, and .097 mg/min, respectively. Measured or derived variables included right atrial pressure, pulmonary artery pressure, left atrial pressure, systemic arterial pressure, heart rate (HR), cardiac index (CI), stroke index (SI), stroke work index (SWI), and systemic vascular resistance index (SVRI). All four vasodilators significantly reduced systemic and intracardiac pressures and SWI (P less than 0.01). Associated changes in left ventricular pumping performance, however, differed importantly between groups. Chlorpromazine caused a significant rise (+19%) in HR with preservation of SI; thus, CI rose significantly (P less than 0.01). Only nitroprusside, however, resulted in enhancement of SI (P less than 0.05) at the lowered left atrial pressure; CI increased by 19% (P less than 0.01), HR rose minimally (6.5%), and calculated SVRI diminished 33% (P less than 0.01). Both nitroglycerin and trimethaphan caused decreases in SI and CI. These results indicate that in general, among the vasodilators studied, nitroprusside is associated with the most favorable hemodynamic responses in early postoperative cardiac surgical patients.

Blood Pressure↗