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1.  The interaction between pindolol and epinephrine contained in local anesthetic solution to the left ventricular diastolic filling velocity in normal subjects. 
Anesthesia Progress  1996;43(3):78-84.
To evaluate the interaction between the nonselective beta-blocker, pindolol, and epinephrine contained in a local anesthetic solution, the left ventricular diastolic filling velocity was examined with pulsed Doppler echocardiography. Arterial blood pressure (BP), the R-R interval on the electrocardiogram (RR), and Doppler echo-cardiographic measurements were recorded in seven healthy volunteers after 45 micrograms of epinephrine contained in lidocaine (L-E) was injected in the maxilla after pretreatment with 5 mg of pindolol. The administration of L-E caused the elevation of BP and an increase in RR interval. Peak early (E) and peak atrial (A) filling velocities decreased, whereas isovolumic relaxation time (IVRT) and diastolic filling period (DFP) were prolonged. Although the ratio of E to A (E/A) remained unchanged, E/A/DFP was reduced. In contrast, when L-E was given without pindolol pretreatment, RR interval was shortened and BP was unchanged. The increase of both E and A velocities and the shortening of both IVRT and DFP were observed. E/A remained unchanged but E/A/DFP was increased. These results suggested that L-E caused opposite effects on the left ventricular filling velocity in the presence or absence of pindolol. We conclude that epinephrine activates the left ventricular relaxation rate but impairs it in the presence of pindolol.
PMCID: PMC2148763  PMID: 10323111
2.  The effects of the hypothalamus on hemodynamic changes elicited by vagal nerve stimulation. 
Anesthesia Progress  1996;43(2):41-51.
To investigate the means by which neurogenic shock or syncope occur in dentistry, we determined the hemodynamic response to the activation of vagal tone in cats while they were under emotional stress. The hypothalamus and the vagal nerve were electrically stimulated to produce emotional stress and to activate vagal tone, respectively. Hemodynamic changes were recorded during vagal stimulation (Va group) and during vagal stimulation preceded by hypothalamic stimulation (AH + Va group). Although blood pressure decreased in both groups, the degree of hypotensive response in the AH + Va group was greater than the response in the Va group. Total peripheral resistance (TPR) was reduced in the AH + Va group but was increased in the Va group. The blood flow to the skeletal muscles in the AH + Va group was greater than that of the Va group. Reduced TPR, which could be due to vasodilation in the skeletal muscles, was the cause of intensified hypotension in the AH + Va group. Clearly, the hypotension produced by vagal stimulation was worsened when it was preceded by hypothalamic stimulation; this occurrence could be related to the tendency of blood to flow to the skeletal muscles.
PMCID: PMC2148778  PMID: 10323125
3.  Anesthetic considerations of two sisters with Beckwith-Wiedemann syndrome. 
Anesthesia Progress  1996;43(1):24-28.
Anesthetic considerations of 21-mo-old and 4-yr-old sisters with Beckwith-Wiedemann syndrome during surgical repair of cleft palate and reduction of macroglossia are presented and discussed. This syndrome is characterized by exomphalos, macroglossia, gigantism, hypoglycemia in infancy, and many other clinical features. This syndrome is also known as exomphalos, macroglossia, and gigantism (EMG) syndrome. Principal problems associated with anesthetic management in this syndrome are hypoglycemia and macroglossia. Careful intraoperative plasma glucose monitoring is particularly important to prevent the neurologic sequelae of unrecognized hypoglycemia. It is expected that airway management would be complicated by the macroglossia, which might cause difficult bag/mask ventilation and endotracheal intubation following the induction of anesthesia and muscle paralysis, so preparations for airway difficulty (e.g., awake vocal cord inspection) should be considered before induction. A nasopharyngeal airway is useful in relieving postoperative airway obstruction.
PMCID: PMC2153451  PMID: 10323122
5.  An echocardiographic study of interactions between pindolol and epinephrine contained in a local anesthetic solution. 
Anesthesia Progress  1995;42(2):29-35.
An increasing number of dental patients are taking beta-adrenergic blockers for the treatment of hypertension or angina pectoris. If epinephrine-containing local anesthetics are administered to such patients, interactions between epinephrine and the beta-blocking agent may induce cardiovascular complications. We assessed in volunteers the effects of intraoral injection with 2% lidocaine containing 1:80,000 epinephrine (L-E) on cardiac function after pretreatment with the beta-blocking agent pindolol. M-Mode echocardiography was used for the assessment. The injection of L-E after administration of pindolol did not alter cardiac preload, whereas it reduced the stroke volume, due to an increase in afterload and a decrease in myocardial contractility. Reductions in stroke volume and heart rate led to a decrease in cardiac output. Because total peripheral vascular resistance increased markedly, blood pressure was elevated despite the reduced cardiac output. These results suggest that cardiac function of dental patients on beta-blocker therapy can be adversely affected by epinephrine-containing local anesthetics. Therefore, when such an anesthetic solution has to be used in patients on beta-blocker therapy, careful systemic monitoring is needed.
PMCID: PMC2148851  PMID: 8934951
6.  Cerebral arterial blood flow velocity during induction of general anesthesia: rapid intravenous induction versus awake intubation. 
Anesthesia Progress  1993;40(4):122-126.
Changes in middle cerebral arterial flow velocity (MCAV) during rapid intravenous induction and awake intubation using transcranial Doppler sonography were investigated. The study involved 20 patients without disorders of the central nervous or cardiovascular systems who were scheduled for maxillofacial surgery. In the intravenous induction group, anesthesia was induced with sodium thiopental, and orotracheal or nasotracheal intubation was facilitated with succinylcholine chloride or alcuronium chloride. In the awake intubation group, orotracheal or nasotracheal intubation was performed under intravenous sedation with diazepam and topical anesthesia with 4% lidocaine. Arterial blood pressures, heart rate, and MCAV were monitored at specific intervals. During intravenous induction, blood pressures decreased after the administration of thiopental and muscle relaxants and increased during endotracheal intubation. MCAV was remarkably slowed after the administration of thiopental and during mask ventilation. During awake intubation, blood pressures were increased by endotracheal intubation. MCAV was decreased from the administration of diazepam to the transtracheal injection of lidocaine, but returned to the control value from endotracheal spray to endotracheal intubation. These results suggest that smooth awake intubation may be the safest method of induction for patients with cerebrovascular disorders.
PMCID: PMC2148587  PMID: 7943921
7.  Modern history of dental anesthesia in Japan. 
Anesthesia Progress  1993;40(4):109-113.
PMCID: PMC2148583  PMID: 7943918
8.  Giant negative T waves after maxillofacial surgery. 
Anesthesia Progress  1992;39(1-2):28-35.
A patient developed strongly negative T waves following anesthesia for maxillofacial surgery. The electrocardiogram was normal preoperatively, except for a single premature ventricular depolarization, and no abnormalities were noted during the operation. Postoperatively, the T wave gradually inverted in almost all leads and approached the criterion of -10 mm for giant negative T waves in V3 2 days postoperatively. The T wave returned to normal approximately 4 months later. Although the T-wave inversion in this patient may have been caused by surgical trauma to the sympathetic nerve supply to the heart or by myocardial infarction, the exact cause remains undetermined.
PMCID: PMC2148725  PMID: 8507021
9.  The effects of epinephrine and norepinephrine administered during local anesthesia on left ventricular diastolic function. 
Anesthesia Progress  1991;38(6):221-226.
To evaluate the effects of epinephrine (E) and norepinephrine (NE) administered during local anesthesia on left ventricular diastolic function, we examined transmitral inflow patterns with pulsed Doppler echocardiography. Arterial blood pressure, heart rate, and transmitral inflow patterns were measured in 10 healthy volunteers when 3.6 mL of 2% lidocaine containing 1:80,000 E or 1:25,000 NE was injected supraperiosteally in the maxilla. The dosage of drug administered was 45 micrograms for E and 144 micrograms for NE. After the administration of E, heart rate was increased, but blood pressure was unchanged. Peak early velocity (R), peak atrial velocity (A), the ratio of A to R (A/R), and the deceleration rate (Dc) were increased, whereas the isovolumic relaxation time (IVRT) was shortened. The increase of R and Dc and the shortening of IVRT indicated an activation of left ventricular relaxation. After the administration of NE, blood pressure was increased and heart rate was decreased. A decrease in Dc, shortening of the acceleration half-time (AcT), and prolongation of IVRT were observed. These changes reflect impeded myocardial relaxation. We conclude that E activates left ventricular diastolic function and that NE, in contrast, impairs it.
PMCID: PMC2148695  PMID: 1842160

Results 1-12 (12)