Showing papers in "Survey of Anesthesiology in 1962"

Responses in dental nerves of dogs to tooth stimulation and the effects of systemically administered procaine, lidocaine and morphine

Abstract: The nerves of the teeth of dogs were excited by mechanical, thermal and electrical stimuli, and the responses in single and multifiber nerve preparations of the inferior alveolar nerve described. Differentiation of responses evoked by thermal and electrical stimulation of the pulpal nerves from electrical activity in the periodontal mechano-sensitive innervation was accomplished. The pulpal nerves responding to thermal stimuli were not spontaneously active. Impulses were elicited by hot (> 55°C) or cold ( ca. 50° to 60°C) and by the danger of thermal damage with higher temperatures ( ca. 75° to 80°C). Electrical stimuli were applied bipolarly through electrodes placed in drill holes in the tooth. The conduction velocities of the pulpal nerves were less than 40 m/sec with the majority between 15 and 30 m/sec. The response of the pulpal nerves to long duration (> 10 msec) constant voltage electrical stimuli of greater than rheobasic intensity consisted of a rapid repetitive formation of impulses. Increasing the stimulus voltage increased the number of impulses in the responses and also decreased the time interval (a) between the "make" artefact and each impulse and (b) between successive impulses of the repetition. It is concluded that these changes in artefact-impulse time interval were primarily the result of changes in the response time for the generation of the impulses. With the surface of the tooth kept dry, there was no significant spread of electrical current to periodontal tissue and the electrical stimuli were confined to the pulpal nerves. It is postulated that nonpainful or "tapping" sensations occurring in algesimetric testing and clinical dentistry when monopolar electrical stimulation of the tooth is employed arises from stimulation of nerves in the peridental tissue. The administration of lidocaine and procaine (2 to 20 mg/kg) resulted in a decrease in excitability of (a) pulpal nerves both to electrical and thermal stimulation of the tooth; and (b) mechanosensitive neurons of periodontal tissues. It is concluded that the effects of these local anesthetics were primarily the consequence of an elevation of threshold for excitation and not the result of inability of the nerves to generate or propagate impulses. The observed responses were a balance between two opposing factors: the dose of drug administered and the intensity of the stimulus. Morphine sulfate in doses of 2.5 to 5 mg/kg had no consistent effect upon these dental nerves and receptors. Interpretation of the effects of larger doses was confounded by concomitant changes in respiration or the presence of artificial respiration.

Regulation of cerebral circulation

Abstract: We may not be able to make you love reading, but regulation of cerebral circulation will lead you to love reading starting from now. Book is the window to open the new world. The world that you want is in the better stage and level. World will always guide you to even the prestige stage of the life. You know, this is some of how reading will give you the kindness. In this case, more books you read more knowledge you know, but it can mean also the bore is full.

The cerebral vascular response to reduction in arterial carbon dioxide tension

Abstract: Since the work of Kety and Schmidt in 1948 (1), it has been apparent that the carbon dioxide tension of the arterial blood is an important factor in the control of cerebral blood flow in man. These workers showed that hyperventilation, with its consequent hypocapnia and alkalosis, is associated with a decrease in cerebral blood flow and an increase in cerebral vascular resistance. Conversely, hypercapnia, induced by inhalation of carbon dioxide, resulted in an increase in cerebral blood flow and a decrease in cerebral vascular resistance. Only the effects of marked alterations in carbon dioxide tension were reported. Since this work appeared, it has become evident that the cerebral vessels are commonly confronted with, and can respond to, smaller changes in carbon dioxide tension. Previous studies in this laboratory (2) have defined the threshold and pattern of response of the cerebral vessels to induced hypercapnia. Observations on the cerebral vascular response to reduction in arterial carbon dioxide tension over a wide range, with special emphasis upon the early phases of this response, form the basis of the present report.

Tracheostomy in the management of respiratory problems

Abstract: THIS discussion is concerned with the uses of tracheostomy and mechanical respiratory devices in managing the problems encountered in a large hospital. The material presented here was obtained by a review of the records of all patients on whom tracheostomies were performed at the Massachusetts General Hospital and the Massachusetts Eye and Ear Infirmary during seven of the past thirteen years. Permanent end tracheostomies that were performed in conjunction with laryngectomies are not included. The history of tracheostomy is interesting; descriptions and discussions of the procedure have been recorded since the pre-Christian era. Most of the early discussion was condemnatory. . . .

Acid-base derangements and myocardial contractility: effects as a complication of shock

Abstract: Introduction Shock provokes marked sympathetic activity through hypotensive reflexes and subsequent hypoxia.1-3Both hypoxia and elevated levels of endogenously released sympathetic hormones lead to a severe acidosis characterized by an increase in lactic acid production.4-7In previous animal experiments from this laboratory acidosis has been produced by lactic acid infusion, by hypercapnea, by limiting venous return to that supplied by the azygos and coronary veins, or by rapid intravenous infusions of epinephrine or levarterenol.7,8In all cases acidosis was accompanied by a decrease in ventricular contractile force (VCF) and arterial blood pressure (BP). There was a decrease in the response of the myocardium to injections of test doses of levarterenol. Cardiac output has been observed by others to be significantly decreased during such an addition acidosis.9Conditions which impose a decrease in circulating blood volume have been reported to increase endogenous releases of catechol amines.1,2,5,7

Alterations in response to somatic pain associated with anaesthesia iv. the effect of sub-anaesthetic concentrations of inhalation agents

Abstract: IN the original publication on chlorpromazine, Courvoisier and her associates (1953) reported that this phenothiazine potentiated the intensity and duration of action of analgesic drugs in animals. They did not, however, show that chlorpromazine itself possessed any analgesic action. Schneider (1954) also found that it increased the duration of morphine analgesia in mice. Kopera and Armitage (1954), on the other hand, were unable to demonstrate any potentiation of morphine analgesia by either chlorpromazine or promethazine. All these workers used the same species of animals in their studies, employed the same technique for the measurement of analgesia and injected the same dosage of chlorpromazine (10 mg/kg). More recently, Tripod and Gross (1957), using a similar experimental technique, found that chlorpromazine increased the duration of morphine-induced analgesia, and demonstrated that promazine had a similar action.

Isoproterenol vasomotor reversal by sympathomimetic amines

Abstract: The infusion of large doses of many sympathomimetic amines produced vasomotor reversal of isoproterenol blood pressure effects. The inhibitory blocking agent, DCI, neither reversed isoproterenol vasodilator effects nor reduced the effective doses of active sympathomimetic amines. Hence, it is concluded that, besides possible blockade of inhibitory receptors by the large amounts of the sympathomimetic amines employed, a "sensitization" of the excitatory effector site must take place. Isoproterenol vasomotor reversal was observed in both cats and dogs, anesthetized with either alpha -chloralose or pentobarbital.