Validity of the new MCAT for predicting GPA and NBME part I examination performance.
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Biomedical subjects
Publications and source records attributed to C M Brooks.
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This paper treats a number of topics relative to functions of the autonomic nervous system: its role in the sympathies and emotional inter-reactions essential to society and common endeavor; the history and evolution of our knowledge of the structure, composition and function of this system; the recent concurrent genesis of concepts of the roles this system plays. Among the most recently developed ideas of autonomic system function is that of its integrating role and that of its molding role in determining the color and intensities of behavioral responses. These latter concepts are supported by recent discoveries of the role played in sensory reception, in several disease states, in control of the neuroendocrine and endocrine systems, in modulation of cardiovascular function, in regulation of energy release and use, and, finally, in conditioned behavior. It appears that there is considerable plasticity and possibility of drastically modifying cell of this system which normally would have functioned in a quite different way. Modern methods of anatomical analysis have shown that the central representation of the autonomic outflow is not as simplistically and independently organized as often visualized. Furthermore the same centers which control somatic responses also affect autonomic system activity. There is only one nervous system and the autonomic complex is an integral part thereof, participating in all behavior. It is, however, specially concerned with the emotional component, reactions to real or anticipated emergencies, control of the viscera and maintenance of homeostasis. In addition to integrating the activity of body parts it has a modulatory effect on all functions.
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The attitudes of second-year medical students were measured to determine if positive attitude changes could be obtained in a human sexuality course that de-emphasized small group activities. Students were given a semantic differential instrument and were asked to rate four concepts related to human sexuality: (a) my sexuality, (b) masturbation, (c) homosexuality, and (d) my role in understanding sexual problems. Significant changes in student attitudes were reported at the 0x05 level for the concept, my sexuality; at the 0x01 level for the concept, my role in understanding sexual problems; and at the 0x001 level for the concepts, homosexuality and masturbation. Females had more positive attitudes (P < 0x001), pre and post, towards homosexuality than did males. No significant differences were found between married and single students.
A study was made of the control of the hypothalamus and neuroendocrine complex by the specialized receptors: the eye, the ear and the olfactory complex. The ancient and modern evidence that light, acting on the optic system, can influence hypothalamic, hypophyseal, endocrine reactions was reviewed and the recently acquired evidence that an optic-hypothalamic-autonomic-pineal-hypothalamic circuit exists which controls liberation of "releasing hormones". Evidence was presented to show that the ear and eye, extero-and interoceptive influences affect lactation and oxytocin secretion by action through the hypothalamus. It was also shown that electrochemical stimulation of the olfactory bulbs can affect both sexual behavior and gonadotropin secretion. Finally, it was shown that the olfactory system exerts some control over water intake, sodium appetite and antidiuretic hormone secretion. Progress in a long term cooperative study of the role of exteroceptor control of neuroendocrine functions was reported.
Recent studies in rats suggest that vasopressin- and oxytocin-secreting neurons in supraoptic nuclei and paraventricular nuclei of the hypothalamus show two different patterns of activity: one a "bursting" or rhythmic pattern and the other, irregular continuous discharges. This possibility was investigated in cats and dogs anesthetized with chloralose or Nembutal by recording electrical activity of single supraoptic and paraventricular neurons. Only some of the "identified" neurosecretory cells showed rhythmic, intermittent discharges ("bursting" cells in rats); the majority showed an irregular continuous firing pattern. Furthermore, the pattern of discharge sometimes changed from one ot the other during long periods of observation. This occurred without apparent stimulus in certain instances; in others, the rhythmic firing was associated with fluctuation in blood pressure and heart rate and was likely to be caused by changes in baroreceptor activity. Possible origins of rhythmic discharges and the physiological importance of such patterns in terms of hormone secretion are discussed.
(1) In chloralose anesthetized dogs, effects of the left and the right atrial stretch were studied in the same animal. Stretch of the sino-atrial region of the right atrium produced acceleration of the heart rate during, and reversal of response at the termination of, the stretch. Stretch of the left pulmonary vein-atrial junctional region evoked an initial decrease followed by an increase in heart rate. The responses were similar in all animals, despite initial heart rates ranging from 120 to 200 beats per minute. (2) Activity in vagal and sympathetic nerve branches innervating the heart was recorded simultaneously. Care was taken to identify the vagal fibers innervating the heart, and record their activity without contamination of sympathetic impulses. The right atrial stretch evoked an augmentation of sympathetic activity which reached its peak at 20 sec after the beginning of stimulus. The stimulus slightly increased the vagal activity; this change occurred slowly and reached its peak in about 40-60 sec after stretch. At the release of stretch, sympathetic activity generally showed a reversal of response, i.e. activity was inhibited for 30 sec. (3) Stretch of the left atrium produced biphasic changes in cardiac sympathetic nerves; their activity was strongly inhibited for the first 15 sec, then augmented throughout the remainder of the stretch. This effect lasted 30 sec after the cessation of stimulus. Effects on vagal cardiac nerve fibers were smaller; mild augmentation in activity was produced. The onset of this effect was faster than that seen in case of the right atrium stretch. (4) Reciprocal action between vagal and sympathetic cardiac nerves was obvious only in the early phase of left atrium stretch. Effects on the heart were determined by balances in activity of these antagonistic nerves. In contrast with what occurred in cardiac reflexes, carotid sinus distension even in the same animal produced a large increase in vagal activity, and near complete inhibition of sympathetic nerve activity. Thus, good reciprocal action between the two sets of nerves was demonstrated. A difference in the two types of reflexes was thus revealed. (5) Stretch of the right atrium evoked during carotid sinus distension caused an increase in heart rate from the new low level which was produced by baroreceptor activation. Vagal activity which was greatly augmented by sinus distension was decreased by atrial stretch, while previously inhibited sympathetic activity due to sinus distension was augmented by stretch of the atrium. The effect of stretch on vagal activity seems to depend to a degree on the prestimulus level. It is of interest that the powerful baroreceptor reflexes do not mask the cardiac reflexes studied. (6) The relative importance of sympathetic and vagal efferents to atrial stretch reflexes was discussed.
A characterization of the factors controlling overdrive suppression of idioventricular pacemakers was investigated in canine hearts with complete atrioventricular block perfused in vitro. The following results were obtained: 1) overdrive suppression increases as a function of driving rate in a sigmoidal fashion; 2) overdrive suppression is maximal after 3 min; 3) the pause is a function of spontaneous rate prior to overdrive; 4) overdrive causes an initial net K loss; 5) overdrive is followed by a transient net K grain; 6) increasing [K]o does not affect K loss; 7) net K loss with drive is less in pre-driven hearts; 8) net K uptake after overdrive is little affected by ventricular activity; 9) acetylcholine does not alter ventricular K balance; and 10) paired stimulation increases overdrive suppression and K loss whether or not each stimulus is followed by a contraction. The following conclusions are drawn. The factors controlling overdrive suppression include the spontaneous rate prior to drive, the rate, duration and pattern of drive, an increase in [K]o during the drive and a decrease in [K]o after drive, but not on acetylcholine-mediated inhibition.
In a study of autonomic reflexes it was found that some produce a generalized, bilaterally uniform response whereas others have an asymmetric or laterality of action. Recordings from vertebral nerve fibers (mainly vasoconstrictors to forelimb muscles), right and left cardiac sympathetics, and renal nerves show that baroreceptors evoke a bilaterally uniform inhibition but chemoreceptors of the carotid sinus and aortic arch initiate a differential discharge. In the chemoreceptor reflex the vagi are activated and bradycardia generally occurs. Vertebral and renal sympathetic fibers increase their activity bilaterally commensurate with the increase in arterial pressure. Sympathetic discharges to the heart, however, are not uniform; they show ipsilateral inhibition and a strong contralateral increase in activity. Stabilization of blood pressure or inactivation of baroreceptors abolishes the ipsilateral inhibition. In isolation, therefore, the chemoreceptor-induced cardiac sympathetic discharge is just quantitatively stronger contralaterally. In the absence of vagi, heart rate changes differ depending on which chemoreceptors are stimulated, because the pacemaker is on the right. Asymmetrical discharges do occur and, in the eventual response to stimulation of chemoreceptors, reflex interactions actually augment the laterality of effects. Peripheral interactions, in the sense that changes effected by one may induce another reflex, are responsible in part for the balances of autonomic activity ultimately seen as the body reacts to stimuli.
In this study of factors affecting and integrating activity of cardiac tissues, isolated strips of rabbit atria containing the sinoatrial node were subject to sinusoidal stretch. Effects on electrical discharge rates and rhythm of this pacemaker were observed. Repetitive stretch of a few millimeters (20-40% increase in length) caused acceleration and produced oscillations in rate which were roughly proportional to frequency of stretching. At fast frequencies of stretching, the sinus rates oscillated faster but not synchronously. When rate of stretching approached the "resting" rate of the sinus, a "lock'in" occurred, in that sinus rate accelerated but oscillations disappeared. During stretching rates approximately twice resting rate, the oscillations again disappeared. At rates of stretching during which oscillations were synchronous, the time of pacemaker firing changed to coincide with the peak phase of the applied sinusoidal stretch, although several seconds were required for this adjustment. Interval histograms also showed that application of sinusoidal stretch imposed a greater regularity on pacemaker action. It was thus demonstrated that oscillatory processes of the cardiac pacemaker and an interaction of oscillators conceivably can occur in the heart. (Preliminary Publication, The Physiologist, 16 "3, 1973.)
In this study of interactions occurring within the heart, isolated superfused strips of rabbit atria, containing the sinoatrial (s.a.) node, were subjected to sinusoidal subthreshold current pulses of varied frequencies and intensities. A.C. current from an R.C. oscillator was applied through a Grass stimulation isolation unit, push-pull connection, and non-polarizing (Ag-AgCl-KCl-Tyrode Agar-Agar) electrodes. A Grass polygraph and tachometer were used to record the applied pulses and nodal firing rates; simultaneous magnetic tape recordings were obtained and used for data analysis. Suction electrode recordings and oscilloscope displays were used to determine how the cyclic impulses affected cellular activity. The s.a. nodal rhythm was modified by subthreshold A.C. current applications; when frequencies were low, firing rates of the node were modulated by the A.C. and mean rates were reduced. As frequencies were progressively increased, slow waxings and wanings in heart rate were produced. These periodic fluctuations were not readily correlated with either the A.C. frequency nor the intrinsic nodal rate, but were representative of the difference between the two. As applied current frequency neared the pacemaker's intrinsic rate, a synchronization occurred and the discharges locked in at a specific phase of the applied current alternation. This synchronization maintained during slight further increases in A.C. frequency but above a critical rate this relationship broke down and the waxing and wanings in frequency of pacemaker rate again developed. It was concluded that pacemaker action of the s.a. node is effected by integration of cellular activity through electron coupling.
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Interaction of neurogenic and myogenic factors that control heart rate was studied. Sympathetic nerve actions and stretch of the sinoatrial node both have an accelerator effect which appears to be competitive, and additive rather than facilitatory. In contrast with this, the accelerator effects of sinoatrial node stretch were proportionately greater when stretch was applied during a slowing produced by vagus nerve stimulation. The hyperpolarizing effect of vagus nerve stimulation or acetylcholine apparently potentiates the accelerator effects consquent to the depolarizing actions of stretch. The myogenic reaction can be considered as playing a role in maintaining cardiac output and preventing excessive slowing or diastolic distension and a deficient circulation.
Stretching the atria in anesthetized dogs produces reflex changes in heart rate, and in cardiac and renal sympathetic nerve activity. Anemic decerebration, cord transection at C4-C5, and severance of vagal or sympathetic cardiac nerves was done to identify the pathways and centers essential for these reflexes. Stretching the right atrium produced an aceleration of the heart and a definite increase in sympathetic nerve activity. Left atrial-stretch caused biphasic responses: an initial sympathetic nerve inhibition and slower heartbeat folowed by sympathetic excitation and heart acceleration. The afferents responsible were carried mainly by the vagi; efferent neural control of the heart was mostly sympathetic. The reflex inhibition observed was integrated chiefly at the medullary level, but supramedullary structures contributed to the augmentation in sympathetic activity and heart rate. When central connections between vagal afferent and sympathetic efferent pathways were separated by cord transection, atrial stretch caused a decrease in heart rate due to reflex action through the vagal loop. After the cord was sectioned, we found that some afferent impulses from the atria traveling in sympathetic nerves produced a slight reflex augmentation of sympathetic efferent activity, though insufficient to affect the heart rate. Somatosympathetic reflexes evoked in cardiac and renal sympathetic nerves by stimulation of various somatic afferent pathways were also affected by atrial stretch indicating central nervous system interactions. Reflex responses to right atrial stretch were superimposed on accelerations of myogenic origin.
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Continuous low dose peripheral vein pitressin has been shown to be effective in controlling variceal bleeding in seven episodes of bleeding in six patients. No significant side-effects were seen. The expense, delay and hazard associated with superior mesenteric artery catheterization for selective arterial pitressin infusion were avoided. If these results can be reproduced, low dose peripheral vein pitressin infusion may prove to be a valuable addition to the treatment of bleeding esophageal varices.
Transient neutropenia developed in a 62-year-old, white male on maintenance hemodialysis being treated with cimetidine for an in tractable duodenal ulcer. The probable mechanism was peripheral destruction of the granulocyte series, unlike the marrow depression reported with metiamide, another histamine H2 receptor antagonist.
(1) Action potentials were recorded from single neurons in suprachiasmatic nuclei of hypothalamus in urethane anesthetized male rat. The rate of firing ranged from less than 1 to over 10/sec but was generally 4-8/sec, and it varied from one cell to another in the same animal. (2) Repetitive stimulation of optic nerve or light acting on the eye augmented the activity of approximately half of the the suprachiasmatic neurons examined (67 out of 159 cells) while 37 neurons (23%) showed clear inhibition by the same stimuli. (3) Stimulation of the suprachiasmatic nuclei strongly inhibited the electrical activity of cervical sympathetic nerves. Light or optic nerve stimulation also inhibited activity of cervical sympathetic nerves. (4) The rate of discharge of suprachiasmatic nuclei showed, at times, some short duration oscillations occurring every 3-5 min, but at other times the same neuron showed a steady low frequency of firing. (5) Projection of optic nerves to the suprachiasmatic nuclei was demonstrated by anterograde migration of horseradish peroxidase placed in the vitreous body. (6) It was suggested that light excites certain groups of neurons in the suprachiasmatic nuclei which exert inhibitory action on cervical sympathetic nerve. This, in turn, caused a reduction in norepinephrine release by nerve fibers innervating the pineal and a reduction in pineal enzyme production. Thus, neurons in these nuclei contribute to the suppression of pineal enzyme production produced by light.