[Current trends in medical therapy of chronic peripheral obliterating arteriopathies].
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Biomedical subjects
Publications and source records attributed to M Sangiorgi.
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Cardiorespiratory reflex responses during the initial phase of dynamic and static contraction of hindlimb muscles were studied in anesthetized dogs. Muscle contractions were elicited by stimulating the femoral and gastrocnemius nerves at 3 and 100 Hz with the intensity of 2.0-2.5 times the motor threshold for a 20-s period. Rhythmic contractions caused a decrease in arterial pressure (Pa) and heart rate (HR) and increased pulmonary ventilation (VE) by increasing frequency (f) without significantly changing VT. Tetanic contractions provoked an increase in Pa and HR and a hyperpnea resulting from a rise in both f and VT. Similar responses were also obtained in anesthetized dogs with carotid sinuses denervated and cervical vagi cut. The abrupt increase in VE at the start of both types of exercise was not associated with immediate significant decreases in end-tidal CO2 values. These two patterns of cardiocirculatory and respiratory responses were closely similar to those reported in anesthetized rabbits in previous studies. Both patterns of responses were reflexes initiated by activation of muscle receptors verified by interrupting the afferents from the contracting muscles. It is concluded that, during dynamic and static work, two distinct muscular reflex mechanisms might exert their drives, related to the muscular metabolic rate, on the circulatory and respiratory function.
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In anesthetized rabbits, rhythmic contractions of the gastrocnemius muscle elicited by stimulating the gastrocnemius nerves (40 trains/min of 0.5-ms rectangular pulses at 2.0-2.5 mult of motor threshold), increased pulmonary ventilation by increasing frequency (f). Expiratory duration (TE) was greatly reduced, while inspiratory time (TI) was much less changed. Mean expiratory flow (VT/TE) was increased consistently more than mean inspiratory flow (VT/TI). Arterial pressure (Pa) and heart rate (HR) were decreased. During tetanic contractions (100 Hz, 2.0-2.5 X T) tidal volume (VT) increased considerably more and f considerably less than during rhythmic exercise, TE was shortened, and TI was only slightly affected. Pa and HR, after a transitory reduction, increased over the resting levels. Similar responses were also obtained in deafferented rabbits with carotid sinus, aortic, and cervical vagus nerves cut. These two patterns of cardiorespiratory changes were initiated by activation of muscle receptors verified by interrupting the afferents from the contracting muscles. It is concluded that, in the anesthetized rabbit, two different muscular reflex mechanisms are involved in controlling the pattern of breathing and ventilation during muscular exercise. One mechanism, predominantly activated during dynamic exercise, decreases TE and increases f, the other mechanism, mainly activated during static exercise, increases the inspiratory drive, thus increasing the depth of breathing.
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In 15 anesthetized rabbits the reflex changes in arterial pressure, heart rate and respiratory rate in response to injections of bradykinin inorganic phosphate and prostaglandins into femoral artery have been studied. Intraarterial injection of bradykinin produced a reflex fall in arterial pressure, bradycardia and tachypnea. The latency of response ranged from 6 to 7 sec. The threshold dose was about 50 ng. This effect was accompanied by a consistent increase in the afferent discharge in the saphenus nerve. Isotonic mixtures of Na2HPO4 and NaH2PO4 at pH 7, PGE1, PGE2, and PGA, when injected into femoral artery even in high doses, failed to produce any significant cardiocirculatory or respiratory reflex responses. Infusion of PGE1 (1 ug/min) into femoral artery, although inactive by itself, enhanced the reflex effect of bradykinin.
In anesthetized and deafferented rabbits, rhythmic and static contractions of the hindlimb muscles were elicited by stimulating the femoral nerve at 3 and 100 Hz with the intensity of 2.0-2.5 times threshold for the motor fibers. Rhythmic contractions caused a decrease in systemic blood pressure, heart rate, and vascular resistance of the resting hindlimb with hyperpnea. Tetanic contractions caused a rise in arterial pressure, in vascular resistance of the nonexercising hindlimb, and in pulmonary ventilation with small increases in heart rate. These responses were not obtained after sectioning the somatic nerves of the exercised limb or when the cut central end of the femoral nerve or the intact nerve in curarized animals was stimulated with the same intensity of 2.0-2.5 times the motor threshold. Both depressor and pressor responses were, therefore, reflexes initiated in the contracting limbs. Removal of the skin from the exercising limb did not change the typical patterns of response. The most likely source of the observed reflexes is that from receptors activated by metabolites released in the exercising muscles.
Eight normotensive patients with electrocardiographic criteria for left ventricular hypertrophy with giant negative T waves were studied with Thallium-201 imaging and M-mode echocardiography. In all the patients Thallium scanning demonstrated increased thickness of the left ventricular walls. In five of the above cases areas of increased uptake were noted in the apical region which had increased thickness as compared to the rest of the left ventricular wall. Echocardiography showed in one subject obstructive hypertrophic myocardiopathy and in another two asymmetric septal hypertrophy. In the remaining patients there was always present septal and posterior wall hypertrophy. Reliable echocardiograms of the apex were done in five subjects and in these hypertrophy was noted. The results of the two techniques were compared and correlated clinically and with the literature. The authors conclude in agreement with other studies that the picture of electrocardiographic left ventricular hypertrophy with giant negative T waves is indicative of hypertrophic myocardiopathies. Specifically, for us, the apical hypertrophy may be the only feature of the myocardiopathy or be part of a generalized left ventricular hypertrophy which is usually asymmetric septal hypertrophy.
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