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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↗

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↗

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↗

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↗

PubMed1976

Respiratory paralysis during treatment of hypertension with trimethaphan camsylate.

Four cases are reported in which respiratory arrest occured coincident with the intravenous administration of large doses of trimethaphan camsylate (Arfonad) to control hypertension. The mechanism of the respiratory depression is unknown, but it may have been related to a direct effect of trimethaphan on the respiratory center or to a curare-like effect of the drug. Close monitoring of ventilatory capacity should be maintained in all patients treated with trimethaphan.

Adult↗

PubMed1991

Local cerebral blood flow with prostaglandin E1 or trimethaphan during cerebral aneurysm clip ligation.

This study was performed to examine changes in local cerebral blood flow during hypotensive anaesthesia with either prostaglandin E1 (PGE1) or trimethaphan (TMP). Local cerebral blood flow (LCBF), mean blood pressure (MBP), heart rate (HR), and hourly urine output (UO) were studied in 51 patients undergoing cerebral aneurysm surgery with neuroleptanalgesia (NLA). The incidence of vasospasm after aneurysm surgery, and outcome (Glasgow Outcome Scale) at discharge were evaluated. Measurements of LCBF were made using a thermal gradient blood flow meter. The dose of PGE1 or TMP was adjusted to maintain MBP at about 70 mmHg, and LCBF was studied during and after PGE1 or TMP administration. Hypotensive drugs were discontinued at the completion of aneurysm clipping. After starting PGE1 or TMP, MBP decreased immediately, but HR did not change in either group. The LCBF decreased 30 min after the start of TMP administration and increased immediately after its discontinuation, whereas PGE1 did not affect LCBF. Urine output increased during PGE1 administration but was unchanged during TMP. Neither drug affected surgical outcome or the incidence of vasospasm. These results suggest that PGE1 may be preferable to trimethaphan for hypotensive anaesthesia in cerebral aneurysm surgery because LCBF is maintained.

Adult↗

PubMedDate not supplied

The effects of sodium nitroprusside and trimethaphan camsylate on cerebral blood flow in rhesus monkeys.

Hemispheric cerebral blood flow was measured in the rhesus monkey before and after infusion of the hypotensive agents sodium nitroprusside and trimethaphan camsylate. The intracarotid injections of 133Xe was utilized, and flow was calculated by the "flow initial" technique. Cerebral blood flow did not change significantly with the administration of trimethaphan camsylate. However, with a small reduction in blood pressure (10.6%) during the administration of sodium nitroprusside, the cerebral blood flow fell significantly (15.4%).

Animals↗

PubMed1979

[The effects of halothane-, nitroprusside- and trimethaphan-induced hypotension on cerebral blood flow and intracranial pressure (author's transl)].

Arterial hypotension to about 50 mm Hg mean pressure was induced in anaesthetized and artificially ventilated dogs by halothane, nitroprusside, and trimethaphan to study their effects on cerebral blood flow and intracranial pressure during hypotension. During nitroprusside induced hypotension there was a 32% increase in cerebral blood flow above control and a marked decrease in cerebral arteriovenous oxygen content difference indicating luxury perfusion of the brain. Cerebral blood flow remained high even 30 min after termination of hypotension. During halothane and trimethaphan hypotension cerebral blood flow remained unchanged. In all groups epidural pressure did not change substantially during hypotension but increased during recovery from nitroprusside hypotension by a maximum of 72% above control. It is concluded that during and after nitroprusside hypotension loss of cerebral autoregulation occurs which may result in a marked rise in intracranial pressure. Special vulnerability seems to exist shortly after termination of induced hypotension when arterial pressure begins to rise and brain perfusion follows a pressure-flow relationship.

Animals↗

PubMed1976

Effects of trimethaphan and sodium nitroprusside on cerebral blood flow in rhesus monkeys.

In tranquilised spontaneously breathing rhesus monkeys we have found that trimethaphan can reduce systemic blood pressure by 20% with little or no change in CBF. This was in marked contrast to those given nitroprusside which showed signs of loss of autoregulation at a 5% MBP reduction. It is our opinion that the divergence of these results from other work might be explained in part by differing anaesthetic techniques and species variations. On this experience we would be hesitant to use sodium nitroprusside or a hypotensive agent in any patient where cerebral blood flow might be already compromised.

Animals↗

PubMed1992

[Effects of induced hypotensive anesthesia on the blood coagulation-fibrinolysis system measured by thrombelastography--comparison between prostaglandin E1 and trimethaphan].

The coagulation-fibrinolysis system has been studied in two groups of 16 patients classified ASA 1 undergoing radical mastectomy during controlled hypotensive anesthesia induced by prostaglandin E1 (PGE1) or by trimethaphan (TMP) under enflurane anesthesia. Thrombelastography (TEG) was used to evaluate both coagulation and fibrinolysis systems, while simultaneously measuring platelet aggregation in response to ADP and collagen, prothrombin time (PT), activated partial thromboplastin time (APTT), serum concentrations of fibrinogen, and platelet counts. In the PGE1 group, APTT was significantly shortened (P less than 0.05) while the drug was being infused, but there was no statistically significant difference between the two groups, which was considered due to the effect of enflurane. Also, no statistically significant changes were noted in the other measured parameters. These results suggest that controlled hypotensive anesthesia using either PGE1 or TMP under enflurane anesthesia produces no significant changes in the blood coagulation-fibrinolysis system and that both are useful for the management of bleeding during surgery. Further, TEG was found to reflect other parameters properly. It is therefore useful for monitoring the blood coagulation-fibrinolysis system during anesthesia.

Adult↗

PubMed1991

[Effects on hemodynamics and myocardial metabolism of prostaglandin E1 and trimethaphan after a descending aorta cross-clamp in experimentally coronary constricted dogs].

We investigated the hemodynamic effects of prostaglandin E1 (PGE1) and trimethaphan (TMP) during cross-clamp of the descending aorta in experimentally coronary constricted dogs. Using 21 mongrel dogs, the blood flow of the left anterior descending coronary artery was reduced to 50% by constricting the artery. After stabilization of hemodynamics, we cross-clamped descending aorta and administered PGE1 (1.0 microgram.kg-1.min-1) or TMP (5.0 micrograms.kg-1.min-1). The drugs were discontinued just before the clamp on the aorta was released. In the PGE1 group, cardiac output (CO) and left ventricular dp/dt (LVdp/dt) increased significantly 5 minutes after clamping, with CO remaining at its high level even after the clamp was released. In the TMP group, CO increased significantly 15 minutes after administration and returned to the preclamping value soon after declamping. LVdp/dt was unchanged during clamping and decreased significantly after declamping. In addition, marked increase of the myocardial blood flow (MBF) in the ischemic areas was seen in the PGE1 group, whereas no changes were seen with the TMP. In the ischemic heart, PGE1 can not only decrease afterload which is elevated by the cross-clamping of the aorta, but also increase the coronary blood flow and MBF in the ischemic areas.

Alprostadil↗