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BACKGROUND: An inhaled anesthetic concentration required to block autonomic hyperreflexia (AHR) is high enough to cause severe hypotension in patients with high spinal cord injury (SCI). We determined the effects of remifentanil on the sevoflurane requirement to block AHR in SCI. METHODS: The study involved 96 patients with chronic, complete SCI scheduled to undergo transurethral litholapaxy during general anesthesia. Anesthesia was induced with thiopental, and sevoflurane concentrations in 50% nitrous oxide were adjusted to maintain a bispectral index of 40 to 50. Whether the patient develops an AHR [an increase of systolic blood pressure (SBP) >20 to 40 mm Hg] was first examined by distending the bladder with glycine solution (the first trial). Patients who developed AHR were then allocated to receive no remifentanil infusion (control, n = 31), a target-controlled plasma concentration of 1 ng/mL (n = 25), or 3 ng/mL remifentanil (n = 24). After baseline hemodynamics had recovered, the target sevoflurane and remifentanil concentrations were maintained for at least 20 minutes and the procedure was resumed (the second trial). Each target sevoflurane concentration was determined by the up-and-down method based on changes (15% increase or more) of SBP in response to the bladder distension. SBP, heart rate, and bispectral index were measured before and during the bladder distension during the trials, and plasma concentrations of catecholamines during the first trial. RESULTS: Eighty-two (85.4%) of 96 patients developed AHR during the first trial, in which 2 were excluded because of hypotension (mean arterial blood pressure

Endotracheal intubation usually causes transient hypertension and tachycardia. We investigated whether the cardiovascular responses to intubation change as a function of the time elapsed in patients with spinal cord injury. One-hundred-six patients with traumatic complete spinal cord injury were grouped into acute and chronic groups according to the time elapsed (less than and more than 4 wk after injury) and into those with quadriplegia and paraplegia according to the level of injury (above C7 and below T5): acute quadriplegia, n = 26; chronic quadriplegia, n = 27; acute paraplegia, n = 24; and chronic paraplegia, n = 29. Twenty-five patients with no spinal cord injury served as controls. Systolic arterial blood pressure (SAP), heart rate, and plasma concentrations of catecholamines were measured. The intubation did not affect SAP in either the acute or chronic quadriplegics, but it significantly increased SAP in both acute and chronic paraplegics. Heart rate was significantly increased in all groups; however, the magnitude of change was less in acute quadriplegics than in the other groups. Plasma concentrations of norepinephrine increased in every group but the acute quadriplegics. The magnitude of increase was attenuated in chronic quadriplegics, accentuated in acute paraplegics, and similar in chronic paraplegics when compared with controls. The incidence of arrhythmias did not differ among groups. We conclude that the cardiovascular and catecholamine responses to endotracheal intubation may change as a function of the time elapsed and the level of spinal cord injury.Cardiovascular and catecholamine responses to endotracheal intubation may differ according to the time elapsed and the level of injury in patients with complete spinal cord injury.

UNLABELLED Nitrous oxide (N(2)O) exerts a sympathomimetic action. We investigated whether N(2)O modifies the cardiovascular responses to tracheal intubation during general anesthesia. One-hundred healthy patients were assigned randomly to receive one of four concentrations (0%, 25%, 50%, or 75%; n = 25 each) of N(2)O in oxygen throughout the study beginning 3 min before tracheal intubation. Anesthesia was induced with IV thiopental (5-7 mg/kg) whereas patients were ventilated with designated concentrations of N(2)O. Tracheal intubation was facilitated with IV vecuronium (0.12 mg/kg). After intubation, all received 2% sevoflurane in oxygen via a semiclosed anesthesia circuit. Systolic arterial blood pressure, heart rate and rhythm, and plasma catecholamine concentrations were measured. The intubation significantly increased arterial blood pressure and heart rate. The maximum pressure changes were 46 +/- 21 and 65 +/- 24 mm Hg in 75% N(2)O and control groups, respectively (P < 0.05), being attenuated by N(2)O without affecting the tachycardiac response. Norepinephrine concentrations were increased at 1 min after the intubation, the magnitude of which was augmented by N(2)O. N(2)O did not affect the incidence of arrhythmias. It was shown that N(2)O suppressed the pressor response to endotracheal intubation, despite the augmented increase of norepinephrine concentrations. IMPLICATIONS We examined whether nitrous oxide modifies the cardiovascular response to endotracheal intubation because it activates the sympathetic nervous system. Nitrous oxide attenuated the pressor response, whereas it augmented the norepinephrine response to laryngoscopy and endotracheal intubation.

We investigated whether sildenafil citrate (Viagra) may reduce the dose of nitrovasodilators to induce deliberate hypotension. Ten mongrel dogs were acutely instrumented with a femoral artery catheter and a pulmonary artery catheter. Sodium nitroprusside (SNP; 1-16 microg. kg(-1). min(-1)) or nitroglycerin (NTG; 2-32 microg. kg(-1). min(-1)) was IV given to induce hypotension. The study consisted of two occasions, in a random order, in each animal: one with sildenafil pretreatment (1 mg/kg IV followed by 0.3 mg. kg(-1). h(-1)) and the other without to serve as a control. Hemodynamic variables were continuously monitored. Plasma cyclic guanosine monophosphate (cGMP) concentrations were measured by radioimmunoassay. Both SNP and NTG produced dose-dependent decreases in mean arterial blood pressure without affecting the heart rate in the presence as well as in the absence of sildenafil. Systemic vascular resistance index and mean pulmonary arterial pressure were also decreased. The magnitude of mean arterial blood pressure and systemic vascular resistance index reductions caused by SNP was augmented by sildenafil, whereas that caused by NTG was not affected. Neither SNP nor NTG alone altered the plasma cGMP concentrations. Sildenafil increased the plasma cGMP concentration, which was further increased by SNP but not affected by NTG. These results indicate that sildenafil may reduce the dose of SNP in producing deliberate hypotension in the dog. The potentiation of SNP-induced hypotension by sildenafil may be related to an augmented accumulation of cGMP.Sildenafil may reduce the dose of sodium nitroprusside required to induce deliberate hypotension and hence the potential for cyanide toxicity.

UNLABELLED: We determined the effects of fentanyl, sufentanil, morphine, and meperidine on the spontaneous contractility of isolated human pregnant uterine muscle strips. Uterine specimens were obtained from normal full-term parturients undergoing elective lower-segment cesarean delivery. Longitudinal muscle strips were prepared and mounted vertically in tissue chambers to record their isometric tension. Opioid concentration-response curves were constructed after rhythmic contractions were established. The responses were also examined in the presence of opioid receptor blocker, nitric oxide synthase inhibitor, beta-adrenoceptor blocker, or cyclooxygenase inhibitor. Fentanyl and meperidine inhibited uterine contractility in a concentration-dependent manner, their concentration that inhibited 50% being 2.3 x 10(-6) and 1.0 x 10(-3)M, respectively. Sufentanil and morphine had no significant effects on uterine contractility. Pretreatment with either naloxone, N(G)-nitro-L-arginine methyl ester, atenolol, or indomethacin did not affect the uterine responses to opioids. These results demonstrate that fentanyl and meperidine may have direct inhibitory effects on the contractility of the human uterus, though at supraclinical concentrations. IMPLICATIONS: Opioids do not have a significant effect on spontaneous contractions of gravid human uterine muscle at their clinically relevant concentrations.