The combined effect of cycling cadence and crank resistance on hamstrings and quadriceps muscle activities during cycling.

The effect of cycling cadence and crank resistance on the activity of hamstrings and quadriceps muscles was investigated during cycling movements of able-bodied subjects on a stationary bike with slow and fast speed against different resistance conditions. The ratio of average EMG amplitudes obtained in the two speed conditions (fast/slow) was computed in each resistance condition. This ratio is higher for both muscles if cycling against higher resistance. This shows that in higher resistance condition muscle activities are not only increased but the change of muscle activities with respect to cadence change varied according to resistance condition. Average EMG amplitudes increased at a higher rate with respect to change of cadence when cycling was performed in higher resistance condition. Besides, when cycling faster, hamstrings activity increased generally at a higher rate than that of quadriceps. The correlation between cadence and EMG amplitudes were also investigated. Considering hamstrings, this correlation was low and decreased as resistance increased. The correlation between the time required to drive one cycle and EMG amplitude is negative but in absolute value it is larger than the correlation of cadence and EMG amplitude.

[Military hospitals in Senta (1944-1945)]. / Vojne bolnice u Senti (1944-1945).

Authors have reviewed data on the history of the Soviet Army Military Hospital in Senta during 1944 and activities of the Military Hospital in Senta in the period 1944-1945. The paper also contains a list of the deceased in the Military Hospital with all available data.

Screening, detection and management of depression in elderly primary care attenders. I: The acceptability and performance of the 15 item Geriatric Depression Scale (GDS15) and the development of short versions.

One-hundred and ninety-eight elderly subjects attending their general practitioners (GPs) were asked to complete the 15 item Geriatric Depression Scale (GDS15). Analysable results were obtained from 194 (98%). Of these, 67 (34%) scored above the GDS15 cut-off (4/5) for significant depressive symptomatology. 87.6% found the questionnaire to be acceptable and only 3.6% found it very difficult or very stressful. The GDS15 had a high level of internal consistency (Cronbach's alpha = 0.80). All the individual items of the GDS15 associated significantly (P < 0.01) with total score and 'caseness'. A single question "do you feel that your life is empty?" identified 84% of 'cases'. In an attempt to devise short scales to screen elderly primary care patients for depression, the data were subjected to logistic regression analysis. Ten (GDS10), four (GDS4) and on (GDS1) item versions were generated. Agreement between these short scales and the GDS15 in the original sample was 95, 91 and 79% respectively. Cronbach's alpha was 0.72 for the GDS10 and 0.55 for the GDS4. The short scales were then validated in an independent sample of 120 patients in whom both GDS data and the results of a detailed psychiatric interview (the Geriatric Mental Status Schedule, GMS) were available. The sensitivity and specificity of the GDS10 against GMS caseness were 87 and 77% (cut-off 3/4); those of the GDS4 were 89 and 65% (cut-off 0/1) and 61 and 81% (cut-off 1/2). Sensitivity and specificity for the GDS1 were 59 and 75%. It is concluded that these short scales may be useful in helping GPs and practice staff to identify elderly patients with significant depressive symptoms.

Screening, detection and management of depression in elderly primary care attenders. II: Detection and fitness for treatment: a case record study.

Case note data were obtained for 186 elderly primary care attenders who also completed the 15 item Geriatric Depression Scale (GDS15). The presence or absence in the case notes of a current or past diagnosis of depression, of current treatment of depression, and of a number of clinical features of depression were noted. Case notes were also rated for the presence or absence of contraindications to the use of tricyclic antidepressants (TCAs) and to serotonin-specific reuptake inhibitors (SSRIs). Whereas 65 (35%) patients were rated as 'cases' of depression on the GDS15, only 28 (15%) had a current case note diagnosis of depression and 37 (20%) had one or more current symptoms of depression recorded in the case notes. Patients rated by their GP as having one or more current symptoms of depression scored higher on the GDS15 (P < 0.05) and were more likely to be categorized as a GDS case (P = 0.05). There was no significant relationship between GDS caseness and a current case note diagnosis of depression. Seventy-three patients (39%) had a past history of depression and 53 (28.5%) patients had previously been treated with antidepressants. The former was significantly associated with GDS caseness (P < 0.05). Twenty-four patients (13%) were currently on antidepressants, 19 of them receiving adequate doses (equivalent to at least 75 mg of amitriptyline). Current antidepressant treatment was not associated with GDS 'caseness'.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiorespiratory responses to glutamatergic antagonists in the caudal ventrolateral medulla of rats.

The role of caudal ventrolateral medullary (CVLM) depressor neurons in influencing arterial pressure and ventilation as well as the baroreflex control of arterial pressure was investigated, and the part played by excitatory N-methyl-D-aspartate (NMDA) and non-NMDA receptors in mediating the responses was determined. In urethane-anesthetized, spontaneously breathing rats unilateral microinjections into the caudal depressor area of the broad-band glutamatergic antagonist kynurenic acid (KYN, 5 nmol or 1.58 nmol), or NMDA antagonist 2-amino-5-phosphonovaleric acid (2-APV, 2.7 nmol), or the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 0.257 nmol) caused a respiratory arrest within 4 min and the animals had to be artificially ventilated. Respiratory frequency increased on injecting KYN and CNQX while it did not change significantly with 2-APV. Apnea resulted from progressive decrease in tidal volume. During the apnea ventilation with 5% CO2 did not revive breathing. Mean arterial pressure (MAP) increased significantly with KYN and 2-APV injections but not with CNQX. The baroreflex decrease of MAP, elicited by left or right aortic depressor nerve stimulation, was significantly reduced or abolished after bilateral microinjections of all 3 antagonists. Ventilation as well as the baroreflex usually recovered after 1-1.5 h. Microinjections of the same doses of antagonists into the facial nucleus, as well as application of KYN (25 nmol) to the ventral medullary surface above the hypoglossal rootlets, had no significant effect. The results support previous findings that the CVLM neurons of the rat inhibit sympathetic neurons providing the vasomotor tone, and that an intact CVLM is obligatory for mediating the baroreflex decrease of arterial pressure. The results also indicate that: (1) the CVLM is essential for sustaining ventilation in the rat; (2) only NMDA receptors are involved in maintaining baseline blood pressure while both NMDA and non-NMDA receptors mediate the baroreceptor depressor reflex; and (3) both NMDA and non-NMDA receptor activation is necessary to sustain ventilation.

Adaptive control is enhanced by background estimation.

The automated control of physiological variables must often contend with an unknown and time-varying background (i.e., the output level corresponding to no input). To allow for simultaneous real-time identification of background as well as the parameters of an autoregressive moving average model with exogenous inputs (ARMAX model) during adaptive control, a "floating identifier" (FI) approach was developed which may be used with most recursive identification algorithms. This method separates input and output data into low- and high-frequency components. The high-frequency components are used to identify the ARMAX model parameters and the low-frequency components to identify background. This approach was evaluated in computer simulations and animal experiments comparing an adaptive controller coupled to the FI with the same controller coupled to two other standard least squares identifiers. In the animal experiments, sodium nitroprusside was used to control mean arterial pressure of anesthetized dogs in the presence of background changes. Results showed that with the FI, the controller performed satisfactorily, while with the other identifiers, it sometimes failed. It is concluded that the FI approach is useful when applying ARMAX-based adaptive controllers to systems in which a change in background is likely.

Cardiovascular and respiratory responses to slow ramp carotid sinus pressures in the dog.

The respiratory and mean arterial pressure (MAP) responses to slow ramp pressure stimulation of carotid baroreceptors were compared in pentobarbital-anesthetized vagotomized dogs breathing 100% O2. Carotid sinus pressure (CSP) was raised from 50 (control) to 220 mmHg and then returned to control as linear ramps (+/- 1 mmHg/s) in isolated sinuses. MAP, heart rate (HR), ventilation (VE), frequency (f), and tidal volume (VT) were expressed as percent of control. The maximum difference between responses to positive and negative ramps at a given CSP (MAX) and the average difference (AVG) served as indicators of the hysteresis for each response. In 27 dogs MAP changed monotonically with varying CSP with insignificant (P = 0.27, MAX) or barely significant (P = 0.03, AVG) hysteresis, monotonic function being one that is continuously nondecreasing or continuously nonincreasing. Similar responses were obtained for HR. VE decreased as CSP increased, but the change was not monotonic. During negative ramp, VE increased back to control with an overshoot. Hysteresis for VE was pronounced (P less than 0.0001, both measures). The VE response was primarily determined by f; VT increased with CSP. To eliminate secondary respiratory effects due to alterations in MAP, in seven dogs similar experiments were performed after ganglionic blockade with hexamethonium. Hysteresis in VE and f persisted. To assess the role of changing arterial PCO2 (PaCO2) on VE, the CSP was held constant (after a ramp rise) at 140, 150, or 180 mmHg before reducing it at -1 mmHg/s to 50 mmHg; however, a significant hysteresis in VE was still observed. Further experiments, to eliminate secondary reflexes due to altered PaCO2, were performed in seven dogs after ganglionic blockade and paralysis with Flaxedil, with phrenic nerve activity as an indicator of ("neural") respiration. The hysteresis in VE and f were no longer significant. In summary, the results indicate that 1) slow ramp carotid baroreceptor stimulation elicits both VE and cardiovascular responses, the VE response showing a dramatically higher hysteresis than the cardiovascular responses; 2) the ventilatory hysteresis is partially explained by the secondary changes in PaCO2 and perhaps by cardiovascular variables; and 3) the central processing of the baroventilatory reflex appears to be rate sensitive at a slower rate of pressure change than that which causes rate sensitivity in the baropressure reflex.

Chemoreceptor stimulation on sympathetic activity: dependence on respiratory phase.

Experiments were performed on chloralose-anesthetized, vagotomized, paralyzed, and artificially ventilated cats breathing 100% O2. Peripheral chemoreceptors were stimulated by rapid injections of CO2-saturated NaHCO3 in different phases of the respiratory cycle. Responses of cardiac and renal sympathetic nerves were computed by digital integration. Spontaneous sympathetic activity was consistently modulated by respiration, the modulation being greater for cardiac than for renal nerves. Cardiac nerve responses to peripheral chemoreceptor stimulation depended on the respiratory phase for at least one experimental condition in four of seven animals: the responses were largest during late inspiration and smallest (or absent) during postinspiration and early expiration. Renal nerve responses depended on respiratory phase in only two of eight animals. An average end-tidal CO2 concentration increase from 4.6 +/- 0.8% (SD) to 6.7 +/- 0.9% enhanced the respiratory modulation of spontaneous activity but reduced the responses to peripheral chemoreceptor stimulation. The results indicate that the respiratory modulation of chemoreceptor-induced sympathetic responses was less prominent than the modulation of spontaneous activity. It is hypothesized that the phase dependence of the responses is caused by the spontaneously occurring expiratory diminution of sympathetic activity rather than by an inherent gating of the chemoreceptor reflex.

Species dependence of baroreceptor effects on ventilation in the cat and the dog.

Reflex respiratory responses to brief carotid baroreceptor stimuli in vagotomized pentobarbital-anesthetized cats were characterized and compared with those reported previously for chloralose-anesthetized dogs. To eliminate effects due to the anesthetic choice, dogs were reexamined under pentobarbital. Stimuli were applied to the isolated carotid sinus (CS) of both animals within a single respiratory phase. The stimuli were either steps triggered after one of four delays (5, 25, 50, and 75% of the control phase duration) and terminated at the end of the phase or pulses lasting 300-500 ms. In cats, 80-mmHg steps during inspiration shortened inspiratory duration by 23.2*, 25.0*, 20.4*, and 4.1% (*P less than 0.01) at the above four delays, respectively; inspired volume decreased by 21.4*, 18.0*, 8.0*, and 2.2%. Steps during expiration lengthened expiration by 38.4*, 37.1*, 21.9*, and 3.4%; expired volume changed less than 4%. Qualitatively, similar responses were obtained with steps 40 mmHg in amplitude. In dogs, 40-mmHg stimuli lengthened both inspiration (by 12.8*, 8.9*, -1.2, and -2.5%) and expiration (by 75.2*, 57.9*, 54.0*, and 61.4*%) but tidal volume did not change. Similar differences were observed when pulses were used. Selective baroreceptor denervation in the cat and occipital arterial occlusion in the dog confirmed that the responses were not chemoreceptor mediated. We conclude that although CS baroreceptor activity inhibits ventilation in both cats and dogs, the pattern of the responses is strongly species dependent.

Tonic and baroreflex effects on arterial pressure and ventilation of pentobarbital and nicotine on the rat ventral medullary surface.

Unilateral aortic depressor nerve stimulation caused depression of arterial pressure (baropressure reflex) and ventilation (baro-ventilatory reflex) in urethane-anesthetized, spontaneously breathing Sprague-Dawley rats. Application of sodium pentobarbital to the ventral medullary surface (VMS) depressed baseline arterial pressure and ventilation, and attenuated the baro-pressure reflex, but not the baro-ventilatory reflex. Application of nicotine on the VMS decreased baseline arterial pressure and increased ventilation, but left both baro-pressure and baro-ventilatory reflexes unaltered. The results suggest that some of the structures that affect vasomotor tone may not be involved in the baroreflex inhibition of arterial pressure. Additionally, neither the neural structures near the VMS which modulate CO2 control of ventilation, nor those that affect tonic control of vasomotor tone are likely to be significantly involved in the baro-ventilatory reflex.

Effects of antihistamines and local anesthetics on excess tachycardia in conscious dogs.

Atropine produces cardioacceleration in conscious dogs partly by reversing the pre-existing parasympathetic cardioinhibition and partly by inducing "excess tachycardia" (ET). Because ET occurs independently of adrenergic mechanisms, the present study sought to determine whether ET is generated by a positive chronotropic action of endogenous histamine on pacemaker cell H1 receptors. ET was antagonized in conscious dogs by the H1-receptor antagonists pyrilamine, diphenhydramine, chlorpheniramine and promethazine (1-5 mg/kg i.v.), but not the H2-receptor antagonist cimetidine (2-10 mg/kg i.v.). Pyrilamine (0.1 mg/kg i.v.), but not cimetidine (4 mg/kg i.v.), also eliminated a histamine tachycardia (31 +/- 4.1 beats/min) produced by injecting histamine (22 +/- 14.2 micrograms) into the sinus node artery after pharmacological autonomic blockade. The 30-fold greater dose of pyrilamine required to antagonize ET than histamine tachycardia suggests a nonantihistaminic, and possibly a local anesthetic mechanism of action on ET. Indeed, lidocaine, procaine, propranolol and pyrilamine antagonized ET in doses corresponding to the known relative local anesthetic potencies of these agents. The same doses of pyrilamine, lidocaine and procaine had significantly less effects on a comparable beta adrenergic tachycardia produced by intravenous isoproterenol infusion (0.1-0.5 micrograms/kg/min i.v.) after hexamethonium (10 mg/kg i.v.). The results indicate that H1-receptor blockers antagonize ET because of their local anesthetic effects and not their antihistaminic properties. The results also suggest that the ionic pacemaker mechanisms generating ET and beta adrenergic tachycardia are different.

Respiratory effects of brief baroreceptor stimuli in the anesthetized dog.

To quantify the immediate isocapnic respiratory response to baroreceptor stimulation, pressure in the isolated externally perfused carotid sinuses (CS) of 24 vagotomized alpha-chloralose-anesthetized dogs was increased selectively during either inspiration or expiration as a step (from time of onset to end of respiratory phase) or a pulse (500 ms). The rise time (150 ms), base-line pressure (80 mmHg), and stimulus magnitude (40 mmHg) were similar for the two stimuli. The time of stimulus onset (delay), expressed as a percent of control time of inspiration (TI) or expiration (TE), was varied. TI, TE, and tidal volume (VT) were expressed as percent changes from control. Stimuli delivered early in inspiration lengthened TI [23.5 +/- 6.4% (SE) for step and 11.7 +/- 6.3% for pulse stimuli at 5% delay] more effectively than late stimuli. VT was essentially unaltered. In contrast, step stimuli delivered during expiration caused a lengthening of TE (32.7 +/- 6.3% at 5% delay) that did not depend on the delay (up to 75%). Very late (85%) pulse stimuli lengthened TE (15.2 +/- 5.7%) more effectively than early stimuli. For both stimuli, the expiratory VT was unaltered. When the responses are compared before and after separation of the blood supply of the carotid bodies from the CS region and when they are compared before and after inhibition of reflex systemic hypotension by ganglionic blockade, the observed responses were shown to be due solely to CS baroreceptor stimulation and not to alterations in carotid body blood flow or reflex changes in systemic cardiovascular variables.

Effectiveness of sodium nitroprusside as a function of total peripheral resistance in the anesthetized dog.

To determine the influence of background vasomotor tone on the effectiveness of sodium nitroprusside in decreasing total peripheral resistance, experiments were performed on 12 open-chest dogs under halothane anesthesia. In the first experiment, the vasomotor condition of six dogs was changed by altering the background infusion rate of phenylephrine (0,40, and 0 microgram/min). Increasing background phenylephrine infusion from 0 to 40 micrograms/min significantly enhanced the effectiveness of nitroprusside in decreasing total peripheral resistance. In contrast, the effectiveness of nitroprusside in decreasing arterial pressure was not altered significantly. In a second experiment on six other dogs, phenylephrine was infused continuously at 40 micrograms/min, and the vasomotor condition was changed by the infusion of phentolamine (0, 60-100, 0 microgram/min). Phentolamine significantly diminished the effectiveness of nitroprusside in decreasing peripheral resistance. In contrast, the effectiveness of nitroprusside in decreasing arterial pressure was not altered significantly. Stepwise linear regression analysis indicated that the background peripheral resistance was the hemodynamic variable that could account partially for the changes in nitroprusside effectiveness. Increasing background total peripheral resistance significantly enhanced the effectiveness of nitroprusside in decreasing total peripheral resistance.

The self-tuning controller: comparison with human performance in the control of arterial pressure.

A self-tuning controller was implemented for the automated infusion of sodium nitroprusside to lower mean arterial pressure in anesthetized dogs. The system incorporated a recursive least-squares parameter identifier and a modified minimum-variance controller. The onset delay was estimated on-line, the performance criterion included the cost of control, and requested step-changes were automatically translated into five successive smaller steps to reduce overshoot. The performance of the system in lowering mean arterial pressure was quantitatively compared with that of a well-trained anesthesiologist. In 10 runs in four animals, the automated system performed as well as the physician who devoted 100% of his attention to the task. Since the stability of the self-tuning controller cannot be guaranteed, such a system should be operated only in the presence of appropriate supervisory algorithms.