[Main symptom: "pulse-synchronous tinnitus"]. / Hauptsymptom: "Pulssynchrones Ohrgeräusch".

BACKGROUND: In comparison to cochlear or nerval generated ear noises, pulsatile tinnitus is a rare condition. Due to its own etiology, specific diagnostic steps are necessary. PATIENTS: We present 6 patients with pulsating tinnitus as the leading symptom. By means of these cases the various etiologies, rational diagnosis and therapy will be discussed. RESULTS: Pulsatile tinnitus is frequently caused by an increased blood flow in the cranial vessels through various pathologies. Besides those diseases going along with a general increase of blood circulation, regional alterations can be classified as hypervascular/hyperemic, arterial or venous conditioned. CONCLUSIONS: Physical examination and modern imaging can detect the underlying reasons in a quick and reliable way.

Cardiovascular responses to hypoxia in the spontaneously breathing cat: reflexes originating from carotid and aortic bodies.

The heart rate (fH) and systemic arterial pressure (Pa) responses to transient anoxemic and cytotoxic hypoxia were studied in 18 pentobarbitone-anesthetized, spontaneously breathing cats, by applying N2 tests and i.v. injections of NaCN. Hyperventilation was accompanied by short-latency increases in Pa and fH; they persisted after bilateral vagotomy, sparing the aortic nerves. Acute section of carotid or aortic nerves in different sequences reduced both fH and Pa responses, the contribution of both pairs of nerves being similar. The recording of carotid chemosensory discharges showed transient stimulus-dependent increases in their frequency, to which the ensuing fH and Pa rises were correlated. After sectioning the four buffer nerves, hypoxia provoked long-lasting hypotension and bradycardia. Tachycardia was also observed in response to hypoxia in 4 out of 6 chloralose-anesthetized spontaneously breathing cats, the other two presenting bradycardia. The direction of these cyanide-induced changes in fH was not modified by bilateral vagotomy. It is concluded that tachycardia and hypertension in response to hypoxia are not vagally-mediated consequences of hyperventilation.

Inhibition of aortic chemoreceptor responses by metabolic alkalosis in the cat.

The responses of the same aortic chemoreceptor afferents to steady-state isocapnic hypoxia and to hypercapnia on hyperoxia, before and after the induction of metabolic alkalosis, were investigated in 12 anesthetized cats. Metabolic alkalosis was achieved by intravenous administration of sodium bicarbonate in the average dose of 7 mmol . kg-1. On the average, arterial pH (pHa) increased from 7.383 to 7.650 at an arterial CO2 partial pressure (PaCO2) of 30 Torr. The increase in pHa resulted in a decrease in chemoreceptor activity, the effect being greater at a lower arterial O2 partial pressure. Increases in PaCO2 during hyperoxia resulted in an increased activity of the chemoreceptors both before and after NaHCO3 injection. The stimulatory effect of hypercapnia, however, was attenuated by metabolic alkalosis. At a constant PaCO2, decreases in arterial [H+] by the NaHCO3 administration caused an approximately linear decrease in the chemoreceptor activity. At a constant arterial [H+], higher PaCO2 was associated with a slightly greater activity of the chemoreceptors. These results indicate that the major effect of CO2 is mediated by [H+], but there appears to be another mechanism, albeit small, for the effect of CO2.

Responses of aortic chemoreceptors before and after pneumothorax in the cat.

That the response of aortic chemoreceptors to hypercapnia is considerably smaller than that of carotid chemoreceptors is well accepted, but the mechanism for the difference is not known. It has been suggested that surgical exposure of the carotid body may contribute to the difference. Accordingly, the response of aortic body chemoreceptors to CO2 would be expected to resemble quantitatively that of carotid chemoreceptors after exposure of the aortic bodies by pneumothorax. The effect of opening the chest on aortic and carotid chemoreceptor responses to several levels of arterial CO2 and O2 tension and arterial blood pressure were studied in anesthetized cats. The activity of aortic chemoreceptors increased in spite of a decreased stimulus level in the thoracic cavity after pneumothorax. The activity remained higher than the control at all levels of arterial CO2 and O2 tension and arterial blood pressure. However, the slopes of CO2 response curves, which were initially small, did not change after pneumothorax. Thus a change in the normal environment of the aortic bodies by experimental manipulation did not cause the aortic chemoreceptor responses to resemble those of carotid chemoreceptors.

Relative responses of aortic body and carotid body chemoreceptors to hypotension.

Responses to acute arterial blood pressure changes of a single or a few chemoreceptor afferents from the aortic body and carotid body at constant arterial blood gases and pH were measured in 16 adult cats. During normocapnic normoxia and moderate hypoxia (arterial oxygen tension of 60 Torr) an induced hypotension of 80 Torr increased strikingly the discharge rate of all aortic chemoreceptors but not of most carotid chemoreceptors; hypotension down to the level of 50 Torr stimulated most carotid chemoreceptors only slightly. Hyperoxia eliminated the stimulatory effect of this degree of hypotension on carotid chemoreceptors; it did not affect aortic chemoreceptors to the same extent. Hypoxia augmented the effect on aortic chemoreceptors more than the effect on carotid chemoreceptors. Thus the effect of hypotension was dependent on arterial oxygen tension. The greater effect of hypotension on aortic body chemoreceptor activity indicates a greater normal circulatory constraint for the aortic body. Accordingly, aortic chemoreceptors are more suited to monitor circulatory changes in O2 flow, and carotid chemoreceptors are more suited to monitor arterial gas pressure changes due to respiration.

Anemia as a stimulus to aortic and carotid chemoreceptors in the cat.

In cats anesthetized with alpha-chloralose, the activities of aortic and carotid chemoreceptor nerves were measured during a control period and during anemia where the hematocrit was lowered in steps by dextran-for-blood exchange. With anemia there was a sustained nonlinear increase in firing of aortic chemoreceptors. There was a greater firing of aortic chemoreceptors for a given lowering of hematocrit from an initial low blood hematocrit than for a similar decrease in hematocrit from an initial high blood hematocrit. Tonic carotid chemoreceptor firing was independent of blood hematocrit and was only transiently increased at the time of dextran-for-blood exchange. The lack of effect of anemia on carotid chemoreceptor activity appeared to be due to sympathetic nerve activity. Section of the sympathetic nerves to the carotid chemoreceptors resulted in an increase in carotid chemoreceptor afferent activity during anemia in a manner similar to the increase in aortic chemoreceptor activity.

Influence of arterial hypoxia on cardiac and coronary dynamics in the conscious sinoaortic-denervated dog.

Arterial hypoxia was produced in 10 conscious, chronically instrumented, tracheostomized dogs by allowing them to breathe 7.5% O2 in N2 for 10 min. Hypoxia (Pao2 = 28 +/- 0.7 (SE) Torr) caused significant increases in coronary blood flow (+196%), left ventricular dP/dt max (+60%), aortic blood flow (+48%), heart rate (+50%), and left ventricular systolic (+12%) and aortic (+10%) pressures. Left ventricular end-diastolic pressure and stroke volume were unchanged, while systemic (-30%) and coronary diastolic (-66%) vascular resistances declined significantly. When equivalent levels of arterial hypoxia were produced in four of these dogs after chronic sinoaortic denervation, the coronary, cardiac, and systemic hemodynamic responses were not significantly different, with the exception that the small arterial pressure response was abolished. Thus the peripheral chemoreflexes are not essential for the normal coronary vasodilator and cardiac adjustments to occur during hypoxia in the conscious dog. The data support the hypothesis that a large part of the cardiac adjustments to hypoxia is initiated outside the sinoaortic reflexogenic zones, probably within the central nervous system.