Paediatric chronic suppurative otitis media in the Free State Province: clinical and audiological features.

BACKGROUND: Chronic suppurative otitis media (CSOM) is a chronic infection of the middle ear cleft. In sub-Saharan Africa >50% of cases occur in children <10 years of age. OBJECTIVES: To describe the otological, audiological and bacteriological findings in children with CSOM. METHODS: We conducted a prospective study at the Ear, Nose and Throat (ENT) Clinic at Universitas Academic Hospital between August 2009 and December 2010. We included all children with CSOM over this period. Patients underwent ENT and paediatric examination, and were tested for HIV. Pus swabs were taken after an ear toilet for routine microbiology, fungal and Mycobacterium tuberculosis culture. We performed audiological testing after the otorrhoea had resolved. RESULTS: Eighty-six children (113 ears) were included, with a median age of 4.6 years (range 1 - 12 years). The mean duration of otorrhoea was 161.7 weeks (range 4 - 572 weeks). Nine patients (10.5%) presented with coalescent mastoiditis and/or intracranial complications of CSOM. Of the 153 organisms identified; Gram-negative bacteria were present in 93 (82.3%) ears, with 94.8% of these being sensitive to quinolones. Only 1 case of tuberculous otitis media was identified. HIV infection was present in 54.6% of patients tested. There was a hearing loss in 44 (66.7%) of the tested affected ears. CONCLUSIONS: There was a long delay between the onset of symptoms and accessing ENT services. Most cases of CSOM were due to quinolone-sensitive Gram-negative aerobes. There was a high prevalence of cholesteatoma, hearing loss and other complications in children in this study.

Effect of hypoxia on endothelium-dependent relaxation of porcine coronary arteries and veins.

In isolated transverse strips of porcine coronary artery and rings of coronary vein both mild (pO2 = 70 +/- 2.6 mmHg) and severe (pO2 = 17.4 +/- 0.8 mmHg) hypoxia (30 min duration) produced a transient contraction depending on the severity of hypoxia. Hypoxia did not influence the contraction evoked by prostaglandin F2 alpha in coronary veins but inhibited it significantly in coronary arteries. In the venous preparations there was no change of the endothelium-dependent relaxation to bradykinin and acetylcholine during mild hypoxia but these responses were inhibited during exposure to severe hypoxia. The endothelium-dependent relaxation to bradykinin produced in coronary arteries was not modified by mild hypoxia but was inhibited in the higher concentration range of bradykinin by severe hypoxia. The results suggest a higher sensitivity of porcine coronary arteries to hypoxia compared to coronary veins that could be due to the different morphology (thickness) of the vessel wall. This may play a role in pathophysiology including hypoxic state during coronary vasospasm.

Effects of lysophosphatidylcholine and palmitylcarnitine--lipid metabolites produced in ischemia--on porcine coronary and rabbit femoral arteries.

In organ bath experiments, amphiphilic lipids lysophosphatidylcholine (LPC) and palmitylcarnitine (PLC) produced a small increase in tension of nonprecontracted strips of porcine coronary artery with a subsequent decrease to initial level after high concentrations of the agents, both in intact and endothelium-denuded preparations. Both amphiphiles produced dose-dependent but incomplete relaxation of intact coronary strips precontracted with high potassium. The effect of PLC was more pronounced. LPC, 3.10(-6) mol.l-1, did not influence Ca++-dose-response relationships, while PLC in concentration of 10(-5) mol.l-1 abolished the decline in the second Ca++-dose-response curve. Neither PLC nor LPC in concentrations of 3.10(-6) mol.l-1 influenced endothelium-dependent relaxation produced by bradykinin precontracted with high potassium porcine coronary artery. Both amphiphiles did not change tension of nonprecontracted and precontracted with phenylephrine, 10(-6) mol.l-1, rabbit femoral artery ring segments or Ca++-dose-response relationships with and without endothelium.

Heterogeneity of the response of venous smooth muscle to arterial endothelium-derived relaxing factor (EDRF) in respect of the role of nitric oxide.

In bioassay and organ bath experiments, the responses of different canine venous preparations to arterial and their own EDRF were studied. Vena jugularis, vena femoralis and vena mesenterica relaxed on both EDRFs released by acetylcholine. Vena saphena, venae cordis and vena portae did not show endothelium-dependent dilation, either under bioassay or in organ bath experiments. All the veins tested relaxed completely after sodium nitroprusside administration. The identity of EDRF and nitric oxide is not confirmed by this study.

Vasomotor tone of isolated porcine coronary veins in response to acetylcholine, noradrenaline, and histamine.

The reactivity of isolated porcine coronary venous segments to acetylcholine, noradrenaline, and histamine was tested in organ bath experiments. Acetylcholine dilated precontracted venous preparations endothelium-dependently. This relaxation was inhibited by atropine indicating the muscarinic nature of this response. Noradrenaline contracted the vessels by an alpha-adrenergic mechanism, whereas beta-receptor-induced dilatation could not be seen. Histamine induced contraction of porcine venous preparations via H1-receptors. These results suggest that the coronary venous system is involved in the regulation of the coronary blood flow in addition to metabolic mechanisms and to nervous influences on the arterial side.

[The influence of preload on the reactivity of coronary arteries]. / Reaktionsverhalten isolierter Koronararterien bei verschiedenen Vorspannungen.

Usually, blood vessel preparations used for in vitro investigations are kept under a certain passive preload. This preload influences the blood vessel reactivity against agonists. Using transverse strips of porcine coronary arteries (Ramus circumflexus) the influence of preload on the amplitude of blood vessel responses induced by acetylcholine, potassium ions and prostaglandin F2 alpha was tested. The optimum preload to obtain a maximum contraction was 1.92 +/- 0.14 g. This value did neither depend on the agonist nor its concentration. However, there was a direct relation between the size of the vessel preparation and the value of the optimum preload. Thus, it is worth taking into account the correct preload when blood vessel preparations are tested in vitro.

Is there an abluminal release of endothelium-derived relaxing factor (EDRF)?

In superfusion bioassay systems of rabbit thoracic aorta and femoral artery ring segments as well as canine femoral artery and coronary ring segments the release of endothelium-derived relaxing factor (EDRF) was stimulated by acetylcholine in donor segments with intact endothelium. The transition of EDRF through the vessel wall ("abluminal release") was not revealed in both bioassay systems. Externally applied acetylcholine did not reach the luminal surface of rabbit thoracic aorta but induced EDRF release in canine femoral artery segments.

The action of acetylcholine on isolated coronary arteries of different species.

The action of acetylcholine (ACh) on extramural coronary arteries (CA) of dogs, pigs, and humans was tested in vitro. ACh dilated precontracted canine CA in dependence on the state of endothelium. This dilation was mediated through muscarinic receptors since atropine inhibited it effectively. Preparations without active precontraction were not influenced at all or slightly dilated. Both human and porcine CA were exclusively contracted by ACh independently of the presence or absence of precontraction. The ACh contraction in porcine CA was found to be endothelium-independent, but also inhibited by atropine as well as the ACh contraction in human CA. Adrenoceptor blockers did not influence ACh reactivity. High concentrations of ACh (greater than 10(-5) mol/l) decreased the further responsiveness of the vessels to the mediator (tested in dogs and pigs only). Spontaneous mechanical activity was registered only in human CA. Different ACh reactivity in dogs compared with pigs and humans is interpreted as species-dependent. It must be taken into account when human coronary physiology is modeled in animals.

Orthostatic cardiovascular regulation during hypoxia and hyperoxia in patients with juvenile hypertension.

10 patients with juvenile hypertension were investigated during normoxia, hypoxia and hyperoxia in comparison to 10 healthy volunteers. The results of heart rate, stroke volume, cardiac output and blood pressure in supine position as well as in passive orthostasis are significantly different in both groups. It seems that in the initial phase of hypertension the arterial chemoreceptors might be on an enhanced functional state.

Coronary smooth muscle reactivity to repeated agonist administration in a long-time experiment in vitro.

The reactivity of isolated extramural coronary arteries of the pig to repeated agonist administration (acetylcholine, prostaglandin F2 alpha and K+-contraction) was investigated in a long-time experiment (20 h, more than 60 reactions). The acetylcholine-evoked contractions show an amplitude increase (phasic component) during the first 10 responses followed by approximately 20 constant reactions and a final amplitude decrease with alternative changes in amplitude. The tonic component of the acetylcholine responses decreases uniformly. The amplitude of K+-contraction increases during the first 10 reactions, and remains nearly constant in the further experiment. Prostaglandin F2 alpha produces a maximum contraction already in its first response, but the amplitudes decrease considerably after 6-8 reactions. The time course of the corresponding contraction upstroke velocity is quite similar compared to the amplitude behaviour. Differences in the smooth muscle reactivity between the used agonists are explained by different activatory mechanisms. Some hints concerning an optimum experimental procedure are given.

Absence of role of endothelium in the response of isolated porcine coronary arteries to acetylcholine.

Isolated precontracted arteries of various vascular beds relax in response to acetylcholine only if the endothelium is present. One explanation for this is that this drug stimulates the endothelial cells to release a vasodilator substance that in turn relaxes the underlying smooth muscle. To determine whether this mechanism is concerned also in the acetylcholine contraction of isolated porcine coronary arteries transverse strips of the extramural part of the left circumflex artery were used for recording isometric tension in the muscle bath. Dose-response curves for acetylcholine showed no significant difference before and after removal of endothelium. As a functional check on the removal of endothelium, the responsiveness of each preparation to a known endothelium dependent dilator (substance P) was tested before and after removal. These findings suggest that endothelial cells are not concerned in the acetylcholine induced contraction of porcine coronary arteries. Acetylcholine appears to act directly on smooth muscle of the porcine artery.

[Disorders of venous blood flow during surgery and the postoperative period as a pathomechanism of venous thrombosis of the legs]. / Störungen des venösen Rückstromes in der operativen und postoperativen Phase als Pathomechanismus der Beinvenenthrombose.

An increased risk of thrombosis is given in slowed movement of blood, damaged vascular wall as well as changed blood composition. The frequency of venous thrombi during and after operative interventions speaks in favour of the importance of the reduced venous return to the heart. In the operative phase the reversible negative inotropic effect of numerous anaesthetics causes a blood stasis with an increase of the filling pressure of the heart (preload) and a reduction of the effect of the Frank-Starling mechanism. While the spontaneous respiration promotes the physiological venous return to the heart, this blood flow is partly inhibited by positive pressure breathing and during opening of the thoracic cage. Also changes of the blood volume have an influence on the venous return to the heart. Additional influences are the reduced muscle tone due to anaesthetics and to muscle relaxants as well as as mechanical injury of the skeletal muscles which led to a retarded blood flow. Apart from these factors in the postoperative phase are additionally present chronic stasis appearances in front of the right heart as well as a reduction of the sensitivity of atrial receptors in the insufficient heart. Also the therapeutic use of vasoactive substances as well as the presence of a varicosis influence the flow rate in the veins. An increased risk for thrombosis also exists after bed confinement because of atrophic changes of the skeletal and vascular muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

[Spontaneous rhythms of the cardiovascular system in autonomic diabetic neuropathy]. / Spontanrhythmen des Herz-Kreislauf-Systems bei autonomer diabetischer Neuropathie.

There are distinct differences of the visually and computerized investigated immediate heart rate rhythms, mean arterial pressure and skin temperature rhythms between 30 diabetics suffering from peripheral neuropathy and 10 healthy volunteers. The characterized disturbance patterns within the higher and lower frequencies of these cardiovascular rhythms suggest pronounced, but not only circumscribed lesions of the vagal efferences.

[Studies on the systemic features of autonomic diabetic neuropathy]. / Untersuchungen zum Systemcharakter der autonomen diabetischen Neuropathie.

Thirty diabetics with peripheral neuropathy underwent complex assessment of autonomic nervous disorders of seven different organ systems. Functional analysis was done of the cardiovascular system (respiratory arrhythmia at rest and during regulated breathing, 3rd order waves of cardiac frequency and of arterial mean pressure, active and passive orthostasis), pupillary regulation (infra-red pupillography), peripheral vasomotor regulation (skin temperature) and sudomotorics (psychogalvanic skin reflex). Involvement of the genitourinary system, of stomach and intestine was evaluated by clinical criteria. Twelve diabetics showed signs of autonomic neuropathy in four to six, eight patients in three organ systems. The amplitudes of respiratory arrhythmia during regulated breathing, spectral analytic evaluation of cardiac frequency waves of 3rd order and cardiac frequency immediate reaction during orthostasis were particularly indicative. The demonstrated disturbance of conduction of centrally generated cardiac frequency waves of 3rd order and the diminished amplitudes of the spontaneous rhythms of acral skin temperatures complement the previously known symptomatology of autonomic diabetic neuropathy. The systemic character of autonomic diabetic neuropathy objectivated by the investigations indicates a metabolic pathogenesis.

[Dynamics of the heart rate in active orthostasis of patients with hemodynamically effective mitral valve stenosis]. / Die Dynamik der Herzfrequenz bei der aktiven Orthostase von Patienten mit hämodynamisch wirksamer Mitralklappenstenose.

Heart rate dynamics in response to active orthostasis of 10 min duration were examined in 48 patients with mitral stenosis and compared with the mean and diastolic pulmonary artery pressure. Classification of the characteristics of the heart rate was done according Drischel and co-workers (1963) using amplitude and time values. In contrast to healthy subjects, in patients with mitral stenosis the best regulatory behavior was observed in type B with lower pulmonary artery pressure, the least favorable regulatory dynamics being predominant in type A with higher pulmonary artery pressure. From a functional diagnostic point of view, regulatory efficiency can be graded on the following descending scale: (1) the best regulatory behavior in type B; (2) a decrease in the amplitude values in type B; (3) transition of the dynamics to type A; and (4) prolongation of the time values in type A. The pathophysiological mechanisms are changes in the sensitivity of dilatation receptors in the intrathoracic low-pressure system and of the carotid baroreceptors.