Drug interaction and anesthesia.
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Biomedical subjects
Publications and source records attributed to T E Macnamara.
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In the intact canine heart a gradient of systolic intramyocardial pressure from a minimum at the epicardial region to a maximum at the endocardial region is well established. No information is, however, available regarding the effects of various anaesthetic agents on this gradient. In the present study the effects of halothane on intramyocardial pressure recorded from subendocardial and subepicardial layers of the canine left ventricular free wall were assessed. Experiments were performed on seven anaesthetised mongrel dogs ventilated with 100% oxygen. Intramyocardial pressure was recorded simultaneously from the inner and outer regions of the myocardium using two Mikro-tip pressure transducers. Halothane concentration in the inspired gas varied from 0% to 2%. In the pentobarbital anaesthetised dog halothane does not significantly change the heart rate. With increasing concentrations of halothane in inspired gas systolic intramyocardial pressure at both endocardium and epicardium decreased significantly from control values. As the halothane concentration increased, the normal differential between systolic left ventricular pressure and endocardial intramyocardial pressure was abolished. The intramyocardial pressure gradient from endocardium to epicardium, however, persisted during systole. During diastole the pressure gradient was reversed, becoming maximum in the epicardial region and minimum in the endocardial region in both control and halothane treated animals. Over the range of 0-2% halothane concentration there was no significant effect on the diastolic intramyocardial pressure gradient. These results suggest that halothane affects the myocardial tissue pressure non-uniformly across the left ventricular free wall and therefore influence sth e transmural distribution of coronary blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
Protamine administration may induce arterial hypoxaemia in dogs and humans. However, the responsible mechanism has not been established. Protamine, as it is a pulmonary vasoactive substance, may interfere with normal hypoxic pulmonary vasoconstriction (HPV) and cause arterial hypoxaemia. This possibility was tested in dogs utilizing a one lung hypoxic model. One lung hypoxic ventilation decreased pulmonary blood flow in the hypoxic lung from 1022 +/- 96 ml X min-1 (mean +/- SEM) to 846 +/- 39 ml X min-1 (p less than 0.05) while increasing blood flow from 833 +/- 85 ml X min-1 to 1109 +/- 101 ml X min-1 (p less than 0.05) in the normoxic lung, resulting in 24 per cent effective diversion of blood flow. Protamine infusion, after heparinization, markedly elevated pulmonary vascular resistance in both lungs but preferentially in the normoxic lung (102 +/- 27 per cent increase in normoxic lung, 60 +/- 6.4 per cent increase in hypoxic lung) and significantly reversed the pulmonary blood flow shift induced by one lung hypoxic ventilation (effective diversion of blood flow was reduced to four per cent). Concurrently, arterial PO2 further decreased. Our results demonstrate that protamine interferes with effectiveness of pre-existing HPV and suggest that this mechanism, at least in part, may be responsible for arterial hypoxaemia observed after protamine infusion. The marked generalized pulmonary vasoconstriction with protamine appears to be the direct force that interferes with pre-existing auto-regulatory HPV. In addition to the well known haemodynamic effects of protamine, protamine infusion may also cause arterial hypoxaemia in those patients in whom HPV plays a significant role in maintaining arterial oxygenation.
Phantom sensation and phantom limb pain are two recognized sequelae of limb amputation. In most previous surveys, amputations were done for arteriosclerotic or trauma related conditions. We studied 25 patients who had lower extremity amputation for neoplasia. In studying the features of pain before and after amputation, we found phantom limb pain in cancer patients similar in presentation and description to that in noncancer amputees. There appeared to be no correlation between the severity of each episode of phantom pain and the overall effect of the pain on the patient's life. The quality and location of the phantom pain did not resemble the preamputation pain. We recommend a multidisciplinary approach to treatment.
We evaluated the effect of halothane on the balance of subendocardial oxygen supply and demand in six dogs by estimating the endocardial viability ratio (EVR) based on the pressure generated within the subendocardium (ENDO-IMP). Concurrently, the conventional EVR based on left ventricular pressure (LVP) was estimated and compared with the EVR based on ENDO-IMP. The subendocardial oxygen supply-demand ratio based on ENDO-IMP (IMP-EVR) was significantly less than EVR based on LVP (LVP-EVR) (0.87 +/- 0.03 vs 1.07 +/- 0.06, P less than 0.05) during the control period. With 0.5% halothane administration, IMP-EVR improved significantly (1.04 +/- 0.07, P less than 0.05) while LVP-EVR remained unchanged (1.08 +/- 0.09). No further changes in EVR (either IMP-EVR or LVP-EVR) were observed with increasing halothane concentrations up to 2%. The relationship between the two indices was weak (r2 = 0.44, P less than 0.001) but statistically significant. Because an estimate of EVR based on direct measurement of subendocardial tissue pressure (IMP-EVR) would reflect more accurately the oxygen supply-demand balance of this region than the LVP-EVR, our results suggest that the oxygen balance of the subendocardium improves with halothane administration. The use of LVP-EVR as a hemodynamic index of subendocardial oxygen balance during halothane anesthesia, therefore, is questionable.
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Microcomputer applications in anesthesiology are increasing rapidly. All areas are affected: research, education, administration and clinical care. In research, microcomputers are accomplishing both process control and analysis, as well as storage of large data banks. In education, computer-aided instruction permits the student to progress at his own speed, while freeing instructor time for individual tutoring. Administrative applications produce more useful information and cost-control with reduced clerical effort. clinical applications offer the possibility of truly integrated monitoring systems that will make automated anesthesia records possible; eventually this will lead to computer-controlled anesthesia. This paper examines the "state of the art" in applications of microcomputers in anesthesia.
Anesthesiologists are now active in the diagnosis of unusual neurologic and neuromuscular disorders. Their skill derives both from a firm understanding of basic sciences and a facility with invasive procedures. Five representative cases are presented to illustrate the scope of diagnostic neuroanesthesiology and the endeavors of the neuroanesthesiologist outside the operating theater.
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Beta-endorphin appears to play a definite role in the biologic response to stress and in the endogenous mechanism of pain perception. Opiates exogenously administered during surgery decrease or even suppress the activation of "stress hormones" such as ACTH and cortisol. In the present study, the authors tried to assess the effects of fentanyl administration on plasma beta-endorphin immunoreactivity PBE(ir) during surgical stress. In one group of nine patients, a standard enflurane-based general anesthetic technique without opiates was used for a staging laparotomy. A second group of ten patients undergoing the same type of surgery received fentanyl (10-20 micrograms/kg) as the primary anesthetic drug. In both groups, multiple blood samples were collected prior to, during, and after surgery, following the same time protocol. PBE(ir), plasma cortisol and, in five patients, plasma ACTH were determined by radioimmunoassay. There was no significant change in PBE(ir) in either group after anesthetic induction. Unlike the enflurane group, the fentanyl group did not demonstrate any significant increase from baseline in PBE(ir) during surgery. There was a significant group difference between enflurane and fentanyl in PBE(ir) levels for both "early" and "late" surgery values, but not for the "awake" values (recovery period) where both groups had elevated PBE(ir) levels. Plasma cortisol and plasma ACTH changes followed a trend similar to those of PBE(ir). The suppression of both cortisol and PBE(ir) responses during surgery after administration of fentanyl provides further evidence for the involvement of the endorphin system in the stress response and for its physiologic association with the hypothalamo pituitary axis.
The effects of enflurane anesthesia on brainstem auditory evoked responses (BAERs) was determined in 10 patients with normal hearing undergoing various surgical procedures. Arterial blood pressure, body temperature, and arterial Pco2 were controlled during the 2- to 5-hour recording sessions. End-tidal enflurane concentrations were continuously recorded on a chemetron Medspect II mass spectrometer in three subjects. BAERs were obtained by, and recorded on a Nicolet CA 1000, from C2 with reference to A1 or !2, with a 2000 click-averaging for each measurement. Enflurane administered at clinical concentrations (0.5% to 3%) produced a consistent changes in BAER latencies. The waves significantly affected (p less than 0.01) were waves III, IV, and V and interpeak latency I-V. The magnitude of theses changes was related to the concentration of enflurane and was magnified by temporarily decreasing the Paco2. These findings confirm similar data obtained in animals which have shown the same effects at doses that can produce generalized seizure activity. BAER analysis shows that changes predominate at the pons and midbrain levels and affect the brain stem conduction time, which likely reflects the action of enflurane on the activity of the reticular activating system.
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Noncardiogenic pulmonary edema occurred in an anesthetized patient during an otherwise uneventful laparotomy. Following transfusion of an individual unit of whole blood, routine intraoperative monitoring detected sudden major pulmonary shunting (increased alveolar-arterial oxygen gradient) and an increased physiological alveolar dead space (increased arterial-alveolar carbon dioxide gradient). The noncardiac pulmonary edema probably resulted from the presence of a leukoagglutinin against the patient's granulocytes in the donor's plasma. This antibody had no apparent specificity for known HLA, neutrophil, or blood group antigens. The acute respiratory failure was transient, resolving in 72 hours with respiratory support. The presence of otherwise unexplained noncardiogenic pulmonary edema during or soon after a blood transfusion should suggest the possible diagnosis of a leukoagglutinin reaction.
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