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In general, many similarities are seen between cerebral blood flow and cochlear blood flow in response to vasodilating drugs. Cochlear vessels appear to be weakly controlled by the adrenergic nervous system. Cholinergic agents dilate cochlear vessels, although the vasodilation in the cochlea does not necessarily cause an increase in cochlear blood flow because of the associated hypotension. The effect on the systemic circulation is too profound to make these agents clinically useful. Papaverine, dipyridamole, amyl nitrite, and the plasma kinins produce transient increases in cochlear blood flow. Ten per cent carbon dioxide and 90 per cent oxygen product progressive vasodilation as long as the mixture is inhaled. Hydralazine produces too profound an effect on systemic blood pressure. Histamine and betahistine increase cochlear blood flow but only in doses that produce bronchiospasm in the guinea pig. Nicotinic acid and nicotinyl tartrate have no effect on cochlear blood flow. If one considers safety and efficacy as well as patient tolerance, papaverine appears to be the drug of choice for increasing cochlear blood flow clinically. Histamine and betahistine appear to be acceptable alternatives. Betahistine is no longer available for clinical use because of the failure to demonstrate clinical efficacy of therapy.

The following cases are demonstrated:postoperative deafness probably caused by abnormal blood supply to the cochlea, clinical findings of an acoustic neuroma without tumor, atrophy of cochlear and vestibular nerves, bone-like tissue growth in the labyrinthine trauma, hearing improvement after removal of an arachnoid cyst from the internal auditory canal.

Summary--Because of the topography of the perilymphatic vascular network, the cochlear microcirculation is especially sensitive to the effect of vasoactive substances reaching the perilymphatic space. The cochlear microcirculation is mainly controlled humorally, via the activity of the metarterioles and changes in the flow properties of the blood. Intracochlear histamine reduces the cochlear circulation even more markedly than after intracarotid administration. No systematic effects of parenteral administration of vasoactive substances can be expected on the cochlear circulation. Reversible auditory disorders after stapedectomy may be explicable by the intracochlear release of histamine. The internal release of histamine after sunstroke and cold stress may play a part in sudden dusturbances of hearing.

Freeze-fracture replicas of the guinea pig inner ear were analyzed to study the occurrence and structure of zonulae and fasciae occludentes (tight junctions) and nexuses (gap junctions) in the stria vascularis. Zonulae occludents of the marginal cells, which form a barrier towards the potassium-rich endolymph of the cochlear duct, were demonstrated to be of the "intermediate to tight" type (Claude and Goodenough, 1973). Abundant, extensive cell contacts of the basal cells were identified as fasciae occludentes forming a barrier towards the spiral ligament. Nexuses were found connecting marginal, intermediate and basal cells of the stria vascularis as well as between the basal cells and fibrocytes of the spiral ligament. Frequently, nexuses were seen within the areas of the basal cell fasciae occludentes. It is supposed that nexuses mediate the electrotonic coupling between neighbouring stria vascularis cells and that probably they are an essential factor for the development of the endocochlear potential. It is pointed out that the intercellular spaces of the stria vascularis represent a compartment with high oxygen supply and an important metabolic system. A high intramembrane particle density was observed on some nonjunctional areas of the cell membranes, especially on the A-fracture faces of the marginal cell extensions. It appears that these membranes exhibit a high metabolic activity. Finally, the findings are discussed with respect to the production and maintenance of the endocochlear potential.

Retrograde degeneration of the cochlear neurons has been studied in different types and degrees of peripheral cochlear damage such as acoustic trauma, intoxication, heredodegenerative deafness and others. It starts only when the peripheral dendrites to the inner hair cells are irreversibly damaged. About 10% of the neurons are not affected by retrograde degeneration. They correspond to the type II and III neurons, which also survive after transection of the cochlear nerve and are mainly associated with the outer hair cells. Cochlear damage due to vascular impairment usually leads to a complete loss of cochlear neurons. In hereditary abiotrophic deafness, neuronal degeneration is slower and its extent varies considerably according to the various genetic syndromes.

It has been shown that the microcirculatory system of the cohlear portion of the labyrinth is a complex of vessels adapted to the organ function. The analysis of the blood passages in the cochlear channel has shown that in accordance with the organ structure there occurs a spacious subdivision of the micrcirculatory bed into working units (segments) which are functionally integrated into a single microcirculatory system. Quantitative estimation of the microcirculatory system parameters has shown that 1) the blood volume which comes into the microcirculatory system is distributed between the vessels as following: 26%--arterioles: 8%--precapillaries; 29%--capillaries; 8%--postcapillaries and 29%--venules. 2) 639 capillaries fall on 1 mm-2 of the vascular strip and their diffuse surface is 1,3 mm-2.

The activity of adenylate cyclase and the steady state levels of cyclic AMP (cAMP) were determined in stria vascularis (SV) and organ of Corti (OC) of the guinea pig cochlea. The activities are 12 and 19 pmoles/mg dry weight/minute for OC and SV, respectively. The activity was increased two to four-fold by NaF. The base level of cAMP is 4.2 and 4.4 nmoles/g dry weight in OC and SV, respectively. In contrast to brain, neither ischemia nor barbiturates produced major changes of the steady state levels of cAMP. No in vitro effect of cAMP upon the state of activation of glycogen phosphorylase was noticeable in either tissue. cAMP did not exert a significant in vitro inhibition of strial Na+K+-ATPase. Perilymphatic perfusion of cAMP (10-3 M) and of theophylline (5 times 10-3 M) did not produce changes in the endolymphatic potential (EP), but dibutyryl cAMP (10-3 M) led to a significant increase of EP. The alpha adrenergic blocking agent, phentolamine, produced very complex changes of the cochlear potentials. A possible role of catecholamines and cAMP in the secretory phenomena of the SV and in the transduction and/or transmission processes of the auditory sense organ are discussed.

The vasculature of the chinchilla cochlea was demonstrated with injected Prussian blue contrast. By and large, the vascular pattern is similar to other mammals. The vasculature appears to be richly developed, but separate types of vessels appear to be of small caliber. Particular findings for the chinchilla cochlea were the veins of the scala tympani, formed by a merging of collecting venules, running parallel to the spiral modiolar vein. Furthermore, no vessel of the basilar membrane under the tunnel of Corti was found, and which, when present, is of such great presumed importance for the oxygen supply to the organ of Corti. The scala vestibuli wall appears to be supplied completely arterially, in contrast with that of other mammals. The stria vascularis is broad and well developed, both at the apex and at the basal end.

A new surface preparation method was devised for assessing intracochlear vessels and sensorineurepithelium. The method is a combination of the conventional osmic acid stained surface preparation method and a surface preparation technique with injection of Prussian blue and decalcification of the cochlea. Such a combination preserves most advantages of each and eliminates many of the disadvantages. To preserve the delicate sensory and nervous structures we examined variations of the preparation, paying particular attention to fixation, staining, and decalcification procedures and solutions. Varying the preparation had a less marked effect on external wall structures than on the basilar membrane; the primary changes consisted of variation in staining contrast. The method proved useful for demonstrating the normal anatomy and pathological changes in cochlear vasculature and in sensorineural and supporting structures of the labyrinth in light and phase contrast microscopy at moderate magnifications.