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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↗
PubMed1993

Epidural blood flow during prostaglandin E1 or trimethaphan induced hypotension.

To evaluate the effect of prostaglandin E1 (PGE1) or trimethaphan (TMP) induced hypotension on epidural blood flow (EBF) during spinal surgery, EBF was measured using the heat clearance method in 30 patients who underwent postero-lateral interbody fusion under isoflurane anaesthesia. An initial dose of 0.1 microgram.kg-1.min-1 of PGE1 (15 patients), or 10 micrograms.kg-1.min-1 of TMP (15 patients) was administered intravenously after the dural opening and the dose was adjusted to maintain the mean arterial blood pressure (MAP) at about 60 mmHg. The hypotensive drug was discontinued at the completion of the operative procedure. After starting PGE1 or TMP, MAP and rate pressure product (RPP) decreased significantly compared with preinfusion values (P < 0.01), and the degree of hypotension due to PGE1 remained constant until 60 min after its discontinuation. Heart rate (HR) did not change in either group. EBFF did not change during PGE1 infusion whereas in the TMP group, EBF decreased significantly at 30 and 60 min after the start of TMP (preinfusion: 45.9 +/- 13.9 ml/100g/min. 30 min: 32.3 +/- 9.9 ml/100 g/min (P < 0.05). 60 min: 30 +/- 7.5 ml/100 g/min (P < 0.05)). These results suggest that PGE1 may be preferable to TMP for hypotensive anaesthesia in spinal surgery because TMP decreased EBF.

Adult↗
PubMed1994

Epidural blood flow during prostaglandin E1 or trimethaphan induced hypotension.

To evaluate the effect of prostaglandin E1 (PGE1) or trimethaphan (TMP) induced hypotension on epidural blood flow (EBF) during spinal surgery, EBF was measured using the heat clearance method in 30 patients who underwent postero-lateral interbody fusion under isoflurane anaesthesia. An initial dose of 0.1 microgram.kg-1.min-1 of PGE1 (15 patients), or 10 micrograms.kg-1.min-1 of TMP (15 patients) was administered intravenously after the dural opening and the dose was adjusted to maintain the mean arterial blood pressure (MAP) at about 60 mmHg. The hypotensive drug was discontinued at the completion of the operative procedure. After starting PGE1 or TMP, MAP and rate pressure product (RPP) decreased significantly compared with preinfusion values (P < 0.01), and the degree of hypotension due to PGE1 remained constant until 60 min after its discontinuation. Heart rate (HR) did not change in either group. EBF did not change during PGE1 infusion whereas in the TMP group, EBF decreased significantly at 30 min and 60 min after the start of TMP (preinfusion: 45.9 +/- 13.9 ml/100 g/min. 30 min: 32.3 +/- 9.9 ml/100 g/min (P < 0.05). 60 min: 30 +/- 7.5 ml/100 g/min (P < 0.05). These results suggest that PGE1 may be preferable to TMP for hypotensive anaesthesia in spinal surgery because TMP decreased EBF.

Aged↗
PubMed1996

Intravenous trimethaphan during epidural plus general anesthesia decreases the direct radial artery pressure lower than the brachial artery pressure.

STUDY OBJECTIVE: To determine whether vasodilators such as sodium nitroprusside (SNP) and trimethaphan (TMP) produce a pressure difference between the radial artery and the brachial artery during epidural plus general anesthesia or simple general anesthesia. DESIGN: Randomized study and prospective study. SETTING: Operating rooms of two hospitals. PATIENTS: 36 and 6 adult patients in the first and second studies, respectively, who received spherical acetabular osteotomy with induced hypotensive anesthesia. INTERVENTIONS: In the first study, 18 patients received epidural plus general anesthesia (epidural group) and 18 patients received general anesthesia alone (general group). All patients received the hypotensive drugs for more than 50 minutes each. In the second study, 6 patients received TMP-induced hypotension for 20 minutes under epidural plus general anesthesia. MEASUREMENTS AND MAIN RESULTS: In the first study, radial intra-arterial blood pressure (RIBP) and tonometric blood pressure (TBP) calibrated with oscillometric blood pressure of the arm were compared. In the second study, RIBP and the brachial intra-arterial blood pressure (BIBP) were compared. In the first study, the bias between RIBP and TBP for systolic, mean and diastolic blood pressure were significantly less during TMP-induced hypotension in the epidural group (-11.5 +/- 2.5 (mean +/- SD), -6.0 +/- 3.1, and -2.8 +/- 3.7 mmHg, respectively] than during SNP-induced hypotension in the epidural group and SNP- and TMP-induced hypotension in the general group (p < 0.01). The precision of systolic and mean pressures were significantly greater during TMP-induced hypotension in the epidural group (11.8 +/- 2.3 and 7.1 +/- 1.9 mmHg, respectively) than the other three hypotension groups (p < 0.01). In the second study, the bias between RIBP and BIBP for systolic, mean, and diastolic pressures were significantly less (p < 0.01), and precision was significantly greater during hypotension than during normotension (p < 0.01). CONCLUSIONS: Our results demonstrate that TMP decreases the direct radial artery systolic and mean pressures to levels below the brachial artery systolic and mean pressures in patients who received epidural plus general anesthesia.

Adult↗
PubMed1993

Effects of prostaglandin E1 or trimethaphan on local cerebral blood flow and carbon dioxide reactivity during cerebral aneurysm surgery.

Effects of prostaglandin E1 (PGE1) or trimethaphan (TMP) on local cerebral blood flow (LCBF) and carbon dioxide (CO2) reactivity were studied in 26 patient undergoing cerebral aneurysm surgery for subarachnoid hemorrhage (SAH) under isoflurane anesthesia. Measurement of LCBF was made using a thermal gradient blood-flow meter. Hypotension was induced with a continuous i.v. infusion of PGE1 or TMP. The dose of PGE1 or TMP was adjusted to maintain the MAP at about 70 mm Hg, and CO2 reactivity was studied during and after PGE1 or TMP administration. PaCO2 was changed by the controlled hyperventilation. CO2 reactivity was evaluated by the following formula: % delta LCBF/delta PaCO2% mm Hg. Hypotensive drugs were discontinued at the completion of aneurysm clipping. Mean arterial pressure (MAP) decreased immediately after the start of either PGE1 or TMP. Heart rate (HR) did not change significantly in either group. LCBF decrease at 30 min after start of TMP administration (p < 0.05 compared with preinfusion value), whereas LCBF was unchanged during PGE1 administration. Neither PGE1 nor TMP affected CO2 reactivity during cerebral aneurysm surgery, whereas CO2 reactivity showed a close correlation with presurgical neurological status: before, rs = -0.523, p < 0.01; during, rs = -0.794, p < 0.01; after, rs = -0.643, p < 0.01. Comparison of the outcomes after aneurysm surgery demonstrated no significant difference between groups; however, there was a close correlation between presurgical neurological status and outcome in both groups (rs = 0.829, p < 0.01). These results suggest that PGE1 is preferable to TMP in inducing hypotension for cerebral aneurysm surgery because this drug maintains both LCBF and CO2 reactivity.

Adult↗
PubMed1986

Cerebral metabolism and the electroencephalogram during hypocapnia plus hypotension induced by sodium nitroprusside or trimethaphan in dogs.

The effects on cerebral metabolism and the electroencephalogram (EEG) of combining hypocapnia with hypotension have been only incompletely examined. The present study examined the possibility that hypocapnia may worsen the cerebral metabolic and EEG disturbances caused by hypotension. Cerebral metabolism and the EEG were studied at three levels of hypotension during hypocapnia (PaCO2 = 20 mm Hg) in dogs under light halothane anesthesia. A sequential decrease of the mean arterial pressure (MAP) to 60, 50, and 40 mm Hg (30 minutes at each level) was achieved with sodium nitroprusside (SNP) (n = 12) or trimethaphan (TMP) (n = 12). With SNP-induced hypotension plus hypocapnia, the power of the alpha and beta 2 spectra of the EEG decreased at MAP less than or equal to 60 mm Hg. Cerebral metabolic values were unchanged at a MAP of 60 or 50 mm Hg. Brain tissue phosphocreatine and the cerebral energy charge decreased, and the lactate/pyruvate ratio increased at a MAP of 40 mm Hg. With TMP-induced hypotension plus hypocapnia, power decreased in the alpha and beta 2 spectra of the EEG at MAP less than or equal to 60 mm Hg. Cerebral metabolic values were unchanged at a MAP of 60 mm Hg. At MAP less than or equal to 50 mm Hg, power in the beta 1 spectrum, brain tissue phosphocreatine, and the cerebral energy charge all decreased. At a MAP of 40 mm Hg, the cerebral glucose value decreased and the lactate/pyruvate ratio increased.(ABSTRACT TRUNCATED AT 250 WORDS)

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↗
PubMed1990

[Baroreceptor reflex response to acute blood loss during induced hypotension--a comparison of sodium nitroprusside, prostaglandin E1 and trimethaphan].

This experiment was designed to evaluate the reflexive heart rate (HR) response to acute blood loss during sodium nitroprusside (SNP), prostaglandin E1 (PGE1) and trimethaphan (TM) induced-hypotension in isoflurane anesthetized dogs. Reflexive increase in HR to acute blood loss was significantly greater during PGE1 induced-hypotension than during that with SNP. TM inhibited the reflexive HR response to acute blood loss. These results suggest that PGE1 induced-hypotension provides a safer margin than that with SNP and TM when rapid bleeding occurs during anesthesia and surgery.

Alprostadil↗
PubMed1978

Trimethaphan camsylate (Arfonad) and human plasma cholinesterase.

These results for the first time document that the brief duration of action of the ganglionic blocker, Arfonad (trimethaphan camsylate), is not due to inactivation by plasma cholinesterase. Inhibition of the enzyme in vitro by Arfonad was not altered by prior incubation of the drug in plasma at 37 degrees C for up to 16 hours nor by treatment with NaOH at 100 degrees C for 10 minutes. Both procedures inactivated succinylcholine. These results in vitro were confirmed in vivo by finding that the toxicity of Arfonad in mice was not significantly altered by these procedures whereas they rendered succinylcholine inocuous. Arfonad is a noncompetitive whereas succinylcholine is a competitive inhibitor of plasma cholinesterase using benzoylcholine as the substrate. The camphorsulfonate moiety of Arfonad was inactive in vitro but caused mild tremors in mice at relatively high doses.

Binding, Competitive↗
PubMed1994

[Effect of deliberate hypotension on renal functions during epidural block plus inhalation anesthesia: a comparison of prostaglandin E1 and trimethaphan].

To clarify the effect of prostaglandin E1 (PGE1) or trimethaphan (TMP) on the kidney during deliberate hypotension induced with epidural block plus inhalation anesthesia, we compared renal functions and renal tubular injury between the patient with PGE1-induced hypotension (n = 22) and those with TMP-induced hypotension (n = 18) undergoing spherical acetabular osteotomy. Hypotension was maintained at 75-80 mmHg of the systolic radial artery pressure for two hours. The urine volume, creatinine clearance, fractional sodium excretion and free water clearance were maintained within normal limits and they were not different between the two groups. The mean NAG index increased significantly to normal upper limits during hypotension in the PGE1 group but did not increase in the TMP group. However, there was no difference in the NAG index between the two groups. The changes in serum ADH level were not different between the two groups perioperatively. These results suggest that renal functions are not influenced by controlled hypotension induced with PGE1 or TMP during epidural plus general anesthesia.

Adult↗
PubMed1996

[Effect of intra-operative fluid on renal function during hypotensive anesthesia with trimethaphan].

During induced hypotensive anesthesia in 26 cases with trimethaphan, either Ringer's lactate solution (LR group) or 2/3 lactate-saline solution (2/3 LS group) was infused at the same rate. Urine volume, creatinine clearance (Ccr), FENa, urinary gamma-GTP index and urinary Na/K ratio were determined before hypotension, during hypotension and after the operation. During hypotension, FENa and urine Na/K ratio decreased in both groups. In 2/3 LS group, these remained low after the operation compared with the values before hypotension and in LR group. These results suggest that LR solution might depress an endocrine response which is induced by hypotensive anesthesia. As urine volume and Ccr were unchanged by hypotension, and infusion of colloid solution (Hespander) could not increase these figures, circulating blood volume might not be decreased during hypotensive anesthesia. Since urinary gamma-GTP index increased slightly during hypotension or after the operation, there might have been a slight epithelial cell damage of tubules with hypotensive anesthesia.

Adult↗
PubMed1979

Cerebral energy levels during trimethaphan-induced hypotension in the rat: effects of light versus deep halothane anesthesia.

Hypotension may be expected to produce less perturbation of metabolism in the brain when cerebral metabolic rate is lowered by deep anesthesia. Male Wistar rats having unilateral carotidartery ligation were exposed to mean arterial pressure (MAP) of 40 torr for 22 min by an intravenous infusion of trimethaphan during anesthesia with halothane, 0.6 or 2 per cent, in oxygen. Cortical tissue metabolite levels on the side of the ligated carotid artery were more abnormal in rats receiving halothane, 0.6 per cent, than in those receiving halothane, 2 per cent. Values at halothane, 0.6 per cent, were adenosine triphosphate (ATP), 1.71 +/- 0.05 (+/-SEM) mumol/g, phosphocreatine (PCr) 1.97 +/- 0.07 mumol/g. and lactate 16.5 +/- 5.1 mumol/g; corresponding values at halothane, 2 per cent, were ATP 2.27 +/- 0.02, PCr 4.02 +/- 0.23, and lactate 4.75 +/- 0.9 mumol/g. ATP and PCr values were significiantly lower (P less than 0.05) and the lactate value was significantly higher with halothane, 0.6 per cent, than with halothane 2 per cent. Cerebral oxygen consumption decreased 47 per cent in rats anesthetized with halothane, 2 per cent. Preservation of cortical metabolite levels in deeply anesthetized animals suggests a protective effect of cerebral metabolic depression.

Adenosine Triphosphate↗