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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.

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.

Hypotensive anesthesia induced by trimethaphan was maintained at 70-79 mmHg of the systolic radial artery pressure for two hours in 35 patients undergoing spherical acetabul osteotomy. The creatinine clearance, free water clearance, fractional sodium excretion, urine volume, urinary excretion of NAG and levels of gamma-GTP, serum GOT and GPT were measured perioperatively. The creatinine clearance, free water clearance and urine volume decreased by 50% during surgery but recovered to normal values on the third day after surgery. The fractional sodium excretion remained unchanged during and after surgery. The urinary NAG activity increased from 3 +/- a (SD) to 10 +/- 5 U.g-1 and gamma-GTP activity increased from 23 +/- 7 to 33 +/- 13 U.g-1 during surgery, and these remained at high levels for three days after surgery. The serum GOT and GPT levels were within normal ranges for 21 postoperative days. The increase in urinary enzyme activities during and after surgery indicates that mild damage of renal tubular cells has occurred during hypotensive anesthesia.

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.

We performed hypotensive anesthesia using trimetaphan, prostaglandin E1, or nicardipine for eighteen patients undergoing cerebral aneurysm clipping. We measured the hemodynamic parameters (systolic arterial pressure, diastolic arterial pressure, and heart rates), concentration of catecholamines in blood (epinephrine, norepinephrine), blood platelet counts, and aggregation of blood platelets, before induction of anesthesia, before induced hypotension, during hypotension, after hypotension, and at the end of operation. Hypotension was produced rapidly, and hemodynamics was stable with any of the three drugs. In trimetaphan group, however, recovery time of arterial pressure was longer than in other two groups. There was no significant change of catecholamine during induced hypotension in prostaglandin E1 and nicardipine groups. However, in trimetaphan group, concentration of norepinephrine in blood decreased significantly during hypotension. No significant change was observed in either platelet count or platelet aggregation. These results suggest that trimetaphan has an effect to suppress excretion of stress hormones, and prostaglandin E1 and nicardipine have no influence on blood catecholamine levels and aggregation of platelet. We consider that nicardipine is useful as a hypotensive drug for neurosurgery.

Plasma and red blood cells cyanide concentrations during hypotension induced by sodium nitroprusside and a nitroprusside-trimetaphan mixture were studied in 29 male rabbits under halothane anesthesia. They were randomly divided into three groups; Nitroprusside (group N; n = 10), A nitroprusside-trimetaphan mixture (group M; n = 10), Controls (group C; n = 9). No changes were noted in plasma and red blood cells cyanide concentrations in group C throughout the experiment. During and after induced hypotension, in group N, plasma cyanide concentration was significantly higher than the control value. The maximum increase occurred 60min after induction of hypotension and the highest concentration of plasma cyanide was six times the control value. In contrast, in group M, plasma cyanide concentration was unchanged from the control value. However, during and after induced hypotension, red blood cells cyanide concentrations of group N and group M were significantly higher compared with the control values. Red blood cells concentrations of cyanide increased for 30 and 60 min during induced hypotension in group N (27.11 +/- 3.9 micrograms.ml-1, P less than 0.001, 46, 73 +/- 4.7 micrograms.ml-1, P less than 0.001, respectively) and in group M (0.31 +/- 0.05 micrograms.ml-1, P less than 0.05, 0.29 +/- 0.03 micrograms.ml-1, P less than 0.05, respectively). In conclusion, the data suggest that a nitroprusside-trimetaphan mixture is a safe method for hypotensive anesthesia.

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.

Arterial blood ketone body ratio (AKBR; acetoacetate/beta-hydroxybutyrate) is known as a parameter to indicate the function of the liver cells. We evaluated the effects of induced hypotension with prostaglandin E1 (PGE1) or trimetaphan (TMP) on AKBR in patients without liver disease undergoing mastectomy. Almost no change was observed in AKBR before, during and after hypotension with PGE1, but slight diminution was observed during hypotension with TMP. No hepatic dysfunction, however, developed in these patients postoperatively. These findings suggest that usual hypotension with TMP may provoke no postoperative hepatic dysfunction in patients without liver disease. For the patient who required either hypotension of long duration or hypotension with other factors affecting function of liver (surgical procedures, drugs and others), we prefer PGE1 to TMP as a hypotensive drug. We should also adopt PGE1 when cardiovascular control with hypotensive drug is necessary in patients with liver disease.