Delays in uptake of surgery for childhood cataract at a child eye health tertiary facility in sub-Saharan Africa.

BACKGROUND: Timely uptake of surgery is vital in the control of childhood blindness due to cataract. The aim of this study is to determine the uptake of surgery as well as the frequency and reasons for rescheduling of surgery for childhood cataract in a tertiary hospital in southwest Nigeria. METHODS: A retrospective study of children with childhood cataract seen at the Paediatric Ophthalmology unit of the University College Hospital, Ibadan between 2011 and 2015. Demographic and clinical information was retrieved from case records. Caregivers of children who did not have surgery were contacted by telephone to elicit reasons why surgery was not done. RESULTS: A total of 164 children were included in the study; 90 (54.9%) were male. The median age at presentation was 4 years with a range of 2-180 months. A total of 64 (39.0%) children had unilateral cataract. All patients were scheduled for surgery, but 123 (75%) underwent surgery. Surgery was rescheduled in 42 (34.1%) of those who had surgery. Reasons for rescheduling included financial constraints, illness, delay in paediatrician evaluation to ascertain fitness for anaesthesia and strike actions by health workers in the hospital. CONCLUSION: Three quarters of the children had surgery, though it had been rescheduled, at least once, in about one-third of them. Delayed uptake of surgery was mainly due to inability to afford treatment and strike actions. The need for improved coverage of health insurance especially for the paediatric age group in developing countries cannot be overemphasized. This is because good vision is an integral part of child development.

A GIS - based method for assessment and mapping of noise pollution in Ota metropolis, Nigeria.

A detailed method used for assessing and mapping noise pollution levels in Ota metropolis, Nigeria using ArcGIS 10.5 Software is presented in this paper. Noise readings were measured at a time interval of 30 min for each site considered using a precision grade sound level meter. The noise map developed was based on the computed values of average equivalent noise (LAeq) for the selected locations. Results of this study show that the A weighted sound level (LAeq), the background noise level (L10) and the peak noise level (L90) vary with location and period of the day due to traffic characteristics especially traffic volume, vehicle horns, vehicle mounted speakers, and unmuffled vehicles at road Junctions, major roads, motor parks and commercial centres. Based on the U.S. Department of Housing and Urban Development (HUD) recommendations and standards, only one (1) out of the 41 locations considered is under normally acceptable situation, while 12 locations are under normally unacceptable and the noise levels of the rest locations are clearly unacceptable. Results of this study are useful as reference and guideline for future planning and regulations on noise limit to be implemented for urban areas like Ota Metropolis. •Instrumentation used in this study for the environmental noise measurements consisted of a precision-grade sound-level meter - Model 8922 RS232.•The Geographical Positioning System (GPS) device (model: Magellan eXplorist 310) was used to obtain the exact coordinates of each location where noise level readings were recorded.•ArcGIS 10.5 software was used in this study to develop noise map for Ota Metropolis.

Dataset on noise level measurement in Ota metropolis, Nigeria.

Datasets contained in this article are noise level measurement carried out at 41 different locations in Ota metropolis, Nigeria. The noise readings were measured at a time interval of 30 min for each site considered using a precision grade sound level meter. The analysis was based on the noise descriptors LAeq, L10, L90, LD, TNI and NEI. Results from the study reflects that the highest and lowest equivalent noise levels (LAeq) were recorded at commercial areas (96 dB (A)) and residential areas (52 dB (A)), respectively, the background noise level (L90) has the highest and lowest values at commercial areas (77 dB (A)) and residential areas (44 dB (A)), respectively and the peak value (L10) has the highest value and lowest value at the commercial areas (96 dB (A)) and residential areas (56 dB (A)). Based on the WHO recommendations and standards, only 2 out of the 41 locations considered are under normally acceptable situation while the noise levels of other areas are not acceptable. Noise map developed in this study provides enough information for technical controls and interim legislation against environmental noise pollution in the metropolis. Moreover, considering the noise emission standards, planning and promoting the citizens awareness about the high noise risk could help to mitigate the effect of noise in Ota, Metropolis. The noise data in this study are useful as reference and guideline for future regulations on noise limit to be implemented for urban areas in Nigeria and developing countries at large.

Electrophysiological and biochemical changes in rabbit hearts stored at 4 degrees C for 6 or 24 h.

This study examines the electrophysiological and metabolic changes that occur in rabbit hearts during hypothermic storage in vitro. Hearts were microperfused at 4 degrees C for 6 or 24 h with either normal Krebs-Henseleit buffer (KHB) or KHB containing 2,3-butanedione monoxime (BDM). After hypothermic storage, hearts were rewarmed to 37 degrees C with KHB. Cardiac function was then assessed in Langendorff perfusion mode. Electrophysiological changes were also assessed from the ventricular paced-evoked responses. After storage, mitochondria were isolated from the hearts and their respiratory control ratio, rate of ATP synthesis and outer membrane intactness were assessed. Compared with values from fresh non-stored hearts, hearts stored hypothermically for 24 h showed significant decreases in both left ventricular developed pressure and coronary flow when reperfused in Langendorff mode. On the other hand, the decrease in left ventricular developed pressure in hearts that were stored for only 6 h (with or without BDM) was not significant. Compared with values obtained from fresh non-stored hearts, hypothermic storage significantly decreased the R-wave amplitude, and both the R-E and ST-E intervals of paced-evoked responses. This was true for hearts microperfused for 6 h (with or without BDM) and for hearts microperfused with buffer containing BDM for 24 h. The ST-R intervals in hearts microperfused hypothermically for 6 h were prolonged, but this change was not statistically significant compared with those obtained from unstored hearts. In hearts microperfused with KHB containing BDM for 24 h, the ST-R interval was significantly prolonged. Hypothermic microperfusion for 24 h significantly decreased both the mitochondrial coupling ratio and the rate of ATP synthesis. In hearts microperfused with BDM for 6 h, mitochondrial coupling ratios and the rate of ATP synthesis were not significantly different from those in fresh hearts. In conclusion, the present study has shown that long-term hypothermic storage significantly impaired both paced-evoked responses and mitochondrial function. Inclusion of BDM in the perfusion buffer during storage significantly ameliorated some of these changes.

Effect of sodium nitroprusside and L-arginine methyl ester on rat hearts stored at 4 degrees C for 24 h.

1. This study examined the effects of altering nitric oxide levels with sodium nitroprusside or L-arginine in rat hearts stored hypothermically.2. Hearts were microperfused at 4 degrees C for 24 h with a modified Krebs-Henseleit buffer (KHB) that contained either sodium nitroprusside, L-arginine, L-arginine methyl ester or dexamethasone.3. After hypothermic storage, hearts were rewarmed to 37 degrees C with KHB alone or KHB containing sodium nitroprusside or L-arginine. Cardiac function was then assessed in either Langendorff mode or working heart mode.4. Compared with values from fresh unstored hearts, hypothermic stored hearts showed a significant decrease in coronary flow and left ventricular developed pressure when the stored hearts were perfused in Langendorff mode. These hearts also produced less aortic flow and cardiac output when perfused in the working mode.5. Hearts hypothermically microperfused with buffer containing either L-arginine or sodium nitroprusside and then reperfused in the Langendorff mode with untreated KHB buffer had the highest left ventricular developed pressure and coronary flow values. Aortic flow and cardiac output were also higher in these hearts.6. In all groups of stored hearts, the concentrations of both ATP and creatine phosphate were significantly low, when compared with values from freshly isolated hearts. Addition of dexamethasone to the buffer either during storage or during reperfusion had no beneficial effect on high-energy phosphate loss or cardiac performance of stored hearts.7. This study showed that the addition of nitric oxide donors to storage buffer significantly improves cardiac function on normothermic reperfusion. The improved functional recovery is unrelated to the high-energy phosphate content of these hearts.

Effect of protein kinase C inhibitors and 2,3-butanedione monoxime on the long-term hypothermic preservation of isolated rat hearts.

1. This study examines the protective effect of staurosporine, chelerythrine, Ro 31-8220 and 2,3-butanedione monoxime in rat hearts during hypothermic storage. 2. Hearts were microperfused at 4 degrees C for 24 or 48 h with a storage buffer that in some cases contained one of these protein kinase C inhibitors either alone or in combination with 2,3-butanedione monoxime. After hypothermic storage, hearts were rewarmed to 37 degrees C with Krebs-Henseleit buffer. Cardiac function was then assessed in either Langendorff mode or working heart mode. 3. Compared with values from fresh non-stored hearts, hypothermic stored hearts showed a significant decrease in both coronary flow and left ventricular developed pressure when the stored hearts were reperfused in Langendorff mode. The decrease in coronary flow and left ventricular developed pressure was more pronounced in hearts stored for 48 h than in those stored for 24 h. 4. Hearts stored for 24 or 48 h, with or without the protein kinase C inhibitors, and then perfused in working mode generated less aortic flow and less cardiac output than fresh unstored hearts. 5. Hearts preserved in solutions containing staurosporine, chelerythrine, Ro 31-8220 or 2,3-butanedione monoxime had significantly higher left ventricular developed pressure values on reperfusion than hearts stored without any such drug. 6. Addition of 2,3-butanedione monoxime to a storage buffer containing either staurosporine, chelerythrine or Ro 31-8220 further improved left ventricular developed pressure, aortic flow and cardiac output values in these stored hearts. The group of hearts stored in a buffer containing 2,3-butanedione monoxime and chelerythrine gave the highest left ventricular developed pressure value seen during reperfusion. 7. The ATP and creatine phosphate concentrations of hearts stored in buffer alone were significantly lower than those of fresh unstored hearts, irrespective of the duration of storage. ATP concentrations were better preserved in hearts stored in a buffer containing 2,3-butanedione monoxime or/and one of the protein kinase C antagonists than those stored without such antagonists. A positive correlation was found between peak cardiac output values and the concentrations of combined high-energy phosphates in various groups of stored and reperfused hearts. 8. The present study showed that inhibition of protein kinase C during long-term hypothermic storage significantly increased high-energy phosphate concentrations and also improved contractile function during reperfusion.

Long-term preservation of the rat isolated heart with staurosporine and 2,3-butanedione monoxime.

The present study was designed to investigate the effectiveness of staurosporine and 2,3-butanedione monoxime (BDM) in preserving cardiac function of long-term hypothermic-stored hearts. Rat isolated hearts were perfused very slowly at 4 degrees C for 16 hr with a storage buffer solution containing staurosporine and BDM. Heart functions were then examined during 2 hr of normothermic reperfusion. Isovolumetric left ventricular-developed pressure (LVDP), its differential, heart rate, and coronary flow were measured in 5 groups of hearts: controls (fresh unstored hearts), stored drug-free hearts, stored staurosporine-treated hearts, stored BDM-treated hearts, and stored BDM + staurosporine-treated hearts. Hearts that had been perfused with staurosporine or BDM during hypothermic storage attained LVDP values that were 37% or 70%, respectively, of that shown by the control group. Hearts perfused without any drug in the storage buffer attained an LVDP value that was 20% of the control value. Heart rates of stored and then normothermically reperfused hearts were lower than, but not significantly different from, values in the control group. Coronary flow values in all stored hearts were significantly lower than the control values. Thus, BDM, and to a lesser extent staurosporine, applied during prolonged hypothermic storage improved cardiac function during normothermic reperfusion.

Coronary vessels contain enzymes that liberate kinin-like vasodilator substances.

The presence of an acid optimum (pH 6) enzyme capable of generating a spasmogenic, vasodilator polypeptide from human plasma kininogen has been demonstrated in dog coronary arteries, veins and in the wall of the left ventricle. This enzyme also cleaved the tripeptide kallikrein substrate Val-Leu-Arg-pNA. Highest amounts were present in the coronary arteries. Gel filtration (Sephacryl S-300) of coronary artery extracts gave a peak for this acid optimum enzyme of 38, 300 +/- 800 Daltons. Its activity was inhibited by pepstatin but not by aprotinin or soya bean trypsin inhibitor. This enzyme, which is similar to a cathepsin, may play a role in the processing of peptide hormones in the heart and coronary vessels.

Effect of dopexamine hydrochloride in the early stages of experimental myocardial infarction and comparison with dopamine and dobutamine.

The effect of dopexamine hydrochloride on myocardial performance, and on the susceptibility of the myocardium to generation of arrhythmias during the development of myocardial infarction has been compared with dopamine and dobutamine in 2 experimental models of myocardial ischemia. All 3 agents improved cardiac function in the presence of a developing infarct. Dopamine and dobutamine increased myocardial contractility (left ventricular dP/dt and left ventricular dP/dt/P), which would be expected to increase oxygen consumption and thus further compromise the ischemic myocardium. Dopexamine hydrochloride, however, improved cardiac function mainly by reducing afterload. The infusion of dopamine and dobutamine resulted in a high (100%) incidence of ventricular arrhythmias compared with only 63% with dopexamine hydrochloride. The effects of these agents on early ischemic arrhythmias after coronary artery ligation in anesthetized rats were also studied. Dopexamine hydrochloride reduced the incidence and severity of arrhythmias in the early stages of ischemia: At a dose of 0.25 micrograms/kg/min, the total number of ectopic beats was reduced to 375 +/- 175, from 1,250 +/- 330 in control rats (p less than 0.05). Dopexamine hydrochloride also significantly reduced mortality from ventricular fibrillation and there was a slight reduction in the incidence and duration of ventricular tachycardia and fibrillation.

The response of captive rodents to the migration of Ancylostoma caninum larvae.

The distribution of the larvae of Ancylostoma caninum in tissues of captive wild rodents (Rattus rattus) and the leucocytic and behavioural responses of these rodents were studied after experimental oral infection. There was a wide distribution of larvae in tissues with a preponderance of the larvae in the skeletal muscles of the anterior part of the body in older infection. The rats responded by an elevation of total leucocytes and eosinophils in blood, alternation of locomotory activity and behavioural dominance that may have a correlation with predation and epidemiology of A. caninum in a sylvatic setting.

The effects of the combined administration of beta-adrenoceptor antagonists and non-steroidal anti-inflammatory drugs on ligation-induced arrhythmias in rats.

Pretreatment of anaesthetized rats with intravenously administered beta-adrenoceptor antagonists or non-steroidal anti-inflammatory drugs (NSAIDs) reduced the incidence and severity of ventricular arrhythmia which resulted from acute coronary artery ligation. The beta-adrenoceptor antagonists preferentially suppressed the immediate (Phase 1A) arrhythmia while the NSAIDs suppressed the delayed (Phase 1B) arrhythmias. Combined administration of beta-adrenoceptor antagonists and the NSAIDs produced a more pronounced antiarrhythmic effect than either of the drugs alone.

The effects of verapamil, prenylamine, flunarizine and cinnarizine on coronary artery occlusion-induced arrhythmias in anaesthetized rats.

In male rats, anaesthetized with pentobarbitone, ligation of the main left coronary artery causes an early phase of ventricular arrhythmias which last about 30 min. In approximately 60% of control animals, ventricular fibrillation occurs but since spontaneous reversion to sinus rhythm may occur, mortality is of the order of 30%. When administered intravenously 15 min prior to ligation, verapamil (0.01 and 0.05 mg kg-1), prenylamine (0.5 mg kg-1), flunarizine (0.1, 0.25, 0.5 and 1.0 mg kg-1) and cinnarizine (0.25, 0.5 and 1.0 mg kg-1) protected against these arrhythmias. Higher doses of verapamil (0.1 and 0.5 mg kg-1), prenylamine (5 mg kg-1) and flunarizine (2.5 mg kg-1) did not afford a similar protection and mortality was increased to or above control values. Death was due in prenylamine-treated rats to atrioventricular block leading to asystole whereas in those administered verapamil or flunarizine it was a consequence of persistent ventricular fibrillation. Prior to ligation, a sustained fall in mean arterial blood pressure was observed only following the administration of the highest doses of prenylamine, flunarizine and cinnarizine. Heart rate was reduced by administration of only the highest dose of prenylamine. These studies show that although the four calcium antagonists studied, i.e. verapamil, prenylamine, flunarizine and cinnarizine do suppress ischaemia-induced arrhythmias, this protective effect may be limited to a narrow concentration range.

Antiarrhythmic actions of meptazinol, a partial agonist at opiate receptors, in acute myocardial ischaemia.

1 The intravenous administration, to anaesthetized rats, of meptazinol (1 and 2 mg kg-1), a partial agonist at opiate receptors, greatly reduced the incidence of ventricular extrasystoles that resulted from acute coronary artery occlusion. The incidence of ventricular fibrillation (VF) was reduced from 50% (in the controls) to 10% and the mortality from 30% to zero. 2 In similar doses, pretreatment with meptazinol also reduced ventricular arrhythmias, including fibrillation, in conscious rats subjected to coronary artery occlusion. In this model, survival at 16 h was increased from 27% in the controls to 50% and 83% respectively in rats pretreated with 1 and 2 mg kg-1 of the drug. 3 In antiarrhythmic doses, meptazinol had little effect on either heart rate or systemic arterial blood pressure. 4 Intracellular action potential recordings from papillary muscle removed from rats given meptazinol (2 mg kg-1) 15 min previously showed an increase in APD50 and APD90 of more than 40%. There was no effect on dV/dtmax. When superfused with meptazinol in vitro normal rat papillary muscle stimulated at 1 or 3 Hz showed an increase in APD90 and a decrease in dV/dtmax. 5 The antiarrhythmic effect of meptazinol in these models can probably be explained by direct actions on the cardiac muscle action potential (increase in APD) although effects on opiate receptors cannot be ruled out. It is suggested that meptazinol might be useful in relieving pain, and in reducing the severity of arrhythmias in the early stages of acute myocardial infarction.

Naloxone inhibits early arrhythmias resulting from acute coronary ligation.

The intravenous administration of naloxone 15 min before acute coronary artery ligation in both anesthetized and conscious male rats markedly reduced the incidence and severity of the ventricular arrhythmias that occur within 30 min of the onset of myocardial ischaemia. The incidence of ventricular fibrillation was especially reduced and, in conscious rats, the survival 16 h after ligation was increased from 27% (in the controls) to 58 and 73% after 2 and 4 mg/kg naloxone respectively. One possible explanation of these results implies a detrimental effect of released endorphin in the early stages of myocardial ischaemia.

Lidoflazine in the early stages of acute myocardial ischaemia.

1 Pretreatment of anaesthetized rats with intravenously administered lidoflazine (an antianginal agent) reduced the incidence and severity of ventricular arrhythmias which resulted from acute coronary artery ligation. Ventricular fibrillation was completely prevented by doses of 50 micrograms/kg and 2 mg/kg and no animal so treated died ( contrast 50% incidence of fibrillation in the controls and 30% mortality). 2 In anaesthetized greyhound dogs, lidoflazine (2 mg/kg) administration resulted in transient reductions in systemic arterial pressure, LV dP/dt max and cardiac output. Coronary sinus Po2 was markedly increased, indicating pronounced coronary vasodilatation. 3 Lidoflazine pretreatment inhibited the increase in epicardial ST-segment elevation which resulted, in dogs, from short (3 min) occlusions of the left anterior descending coronary artery. This effect was especially marked at sites where, in control occlusions, ST-segment elevation was most pronounced. 4 Lidoflazine greatly reduced the number of ventricular ectopic beats which usually resulted from more prolonged (30 min) periods of acute coronary artery occlusion. There was no ventricular fibrillation in these dogs (contrast 25% incidence in the controls). 5 Lidoflazine did not modify the ventricular fibrillation which results from reperfusion of a previously ischaemic area of the left ventricular wall.

Creatine phosphate suppresses ventricular arrhythmias resulting from coronary artery ligation.

The effects of various doses of creatine phosphate have been examined in a rat model of acute myocardial ischaemia. When given directly into the lumen of the left ventricle in pentobarbitone-anaesthetised male rats, creatine phosphate (50 and 100 mg/kg) markedly reduced the incidence of ventricular ectopic beats, and especially the incidence and duration of ventricular tachycardia and fibrillation which normally resulted from acute coronary artery ligation in this model. This protection was observed even if 1 of 2 h elapsed between creatine phosphate administration and coronary artery ligation. Electrophysiological studies on papillary muscles removed from rats 1 h after administration showed that creatine phosphate both decreased the maximum rate of depolarisation and prolonged the duration of the action potential. These results confirm our previous work in dogs that creatine phosphate is effective against early postinfarction ventricular arrhythmias, at least if given locally. It is suggested that these effects are due, at least in part, to a prolongation of the cardiac muscle action potential. Whether this is the result of maintaining energy production early in myocardial ischaemia is unclear.

Calcium antagonists prevent early post-infarction ventricular fibrillation.

The intravenous administration of either nifedipine (in doses of 5-50 microgram/kg), or nisoldipine (5-1000 microgram/kg) markedly reduced, or abolished, the serious ventricular arrhythmias (tachycardia and fibrillation) that result from acute coronary artery artery ligation in pentobarbitone-anaesthetized rats. Ventricular ectopic activity, which is pronounced in the first 30 min post-ligation period in this model, was also significantly decreased by nifedipine and niludipine (10 and 50 microgram/kg) and by the highest dose (1 mg/kg) of nisoldipine. These results demonstrate the marked efficacy of these calcium antagonists in this experimental model and raise the possibility that, if given prophylactically, they might reduce the incidence of sudden cardiac death following re-infarction in patients.

Suppression by orally-administered nifedipine, nisoldipine and niludipine of early, life-threatening ventricular arrhythmias resulting from acute myocardial ischaemia.

The oral administration to rats of the calcium antagonists nifedipine, nisoldipine and niludipine (3 mg/kg, 1-1.25 h before acute coronary ligation) greatly reduced the duration of ventricular tachycardia and fibrillation (VF) occurring in the first 30 min post-ligation period. The duration of VF was especially reduced (by 74-92%). None of the animals so treated died compared with a 40% mortality in the controls.