Comparison of oil recovered from tea tree leaf by ethanol extraction and steam distillation.

Two methods for the determination of oil and oil major components from tea tree (Melaleuca alternifolia) leaf are quantitatively compared. A microwave assisted ethanol extraction and a 2-h hydrodistillation technique were used on both dry and fresh leaf from a low and a high oil concentration tree. There was no significant difference between dry and fresh leaf. The distillation technique recovered 88% and 82% of the extractable oil for the low and high concentration material, respectively. For both samples this distilled oil was composed of lower absolute amounts of sesquiterpenoids and marginally lower amounts of monoterpenoids. Extending the distillation to 6 h increased the sesquiterpenoid recovery but this resulted in a reduction in both the absolute and relative amounts of the oxygenated monoterpenoids, terpinen-4-ol and 1,8-cineole.

Georg Bartisch: Ophthalmodouleia, der Augendienst, 1583. A treatise on service of the eyes and a review of the chapter on strabismus.

In 1583, Georg Bartisch, oculist and cutter for bladder stones at the court of Duke August I of Saxony, published at his own expense a 273 page textbook of ophthalmology. It contained 91 wood cuts and, in the present volume, they are presented in brilliant colour as they were in the original books prepared for presentation. The book was one of the first medical treatises to be published in the German vernacular instead of traditional Latin. It has been translated into English and published in gothic type to simulate the original. Treatment of diseases of the eye by medicines or surgery are reported in great detail. It gives an account of ophthalmology at the time of the early Renaissance when enlightenment was beginning to overtake the darkness of the Middle Ages.

John Wilkins MRCS, FRCS (Edin.), 1826-1905: his house at 121 Collins Street East, Melbourne.

The three-storeyed house at 70 Collins Street (formerly 121 Collins Street East), Melbourne, was built in 1857 as a home and surgery for Dr John Wilkins. It was associated for 100 years with surgical practice, especially general surgery and eye and ENT diseases, then with obstetrics and gynaecology, but in time had to yield to commercial pressures. However, the exterior remains intact, its special architecture reminiscent of its early elegance.

John Wilkins, surgeon, 1826-1905: experiences in Williamstown (Melbourne) and New Zealand.

John Wilkins was a prominent colonial surgeon for 15 years in Williamstown, Victoria. During the early gold rushes he prospered from investments in property. In Melbourne he aimed to become a recognized authority in diseases of the eye and throat, but he did not achieve his aims, and caused bitterness in the medical community by advertising. After 10 years he moved to Dunedin where he produced the first publication on anaesthesia in New Zealand. He moved to Christchurch, but found contentment in Auckland where he practised general medicine with special consultations in general surgery and diseases of the eye, ear, nose and throat, and where he lived for the remainder of his life.

The bust of Aubrey Bowen, oculist.

A fine marble bust of Aubrey Bowen may be seen at The Royal Victorian Eye and Ear Hospital. Aubrey Bowen had a distinguished and interesting career which has been previously described in the Australian Journal of Ophthalmology. The bust also has an interesting history.

A history of primary angle closure glaucoma.

The satisfactory control and cure of attacks of primary angle closure glaucoma spans one hundred years following von Graefe's iridectomy in 1856. Gonioscopy was required to validate the theories of shallow anterior chamber and pupillary obstruction, but the gonioscopists looked for the causes of angle closure in their own territory at the angle in the periphery of the anterior chamber and disregarded the center. General agreement of the importance of pupil block was thereby delayed for over ten years. Advances in pharmacology and the invention of laser surgery gave opthalmologists a comfortable control of a formerly distressing, blinding disease.

Acute glaucoma--1941.

PURPOSE: To describe the treatment of acute glaucoma before the technological and pharmacological advances that followed World War 2. METHOD: A narrative of personal experience is presented. CONCLUSIONS: In 1941, acute congestive glaucoma received heroic treatment - strong miotics, blood-letting by leeches, purging with mercury. If satisfactory response did not occur within four hours, a broad iridectomy was performed on the hard, congested eye. Affected eyes commonly remained blind or with severely reduced vision.

Curran, barkan, and chandler: a history of pupillary obstruction and narrow angle glaucoma.

SUMMARY: Edward J. Curran was the first to show that glaucoma could be caused by an impedance to the flow of aqueous through the pupil and that iridectomy removed the obstruction. He observed that full iridectomy was not necessary because the iris lay so heavily on the lens that forward flow could only occur at the periphery; so only a small peripheral hole was required. By gonioscopy, Barkan divided glaucoma into two types according to the site of mechanical block: (a) within the trabecular spaces (wide-angle) or (b) narrow angle blocked by iris against the trabecular spaces (narrow-angle or iris block glaucoma). Progress was slow, and not until 1951 in articles by Haas and Scheie, and by Chandler, were the full mechanisms of pupillary obstruction (narrow angle closure) peripheral iridectomy explained. Only later, with laser iridotomy, were all of Curran's goals achieved when no instruments had to enter the anterior chamber to relieve the pupil block and either prevent angle closure or allow angles to reopen.

Edward J Curran and pupillary obstruction.

PURPOSE: To present the importance of the concepts of Edward J Curran in relation to primary angle-closure glaucoma, and include a biographical sketch. METHOD: An historical method is adopted. RESULTS: Curran's propositions of pupillary obstruction and its relief by peripheral iridotomy were conceded only after 30 years, and had to await laser surgery for fulfillment. CONCLUSIONS: Edward J Curran's name should be enshrined in the history of ophthalmology.

Preservation of left ventricular function and coronary flow by angiotensin I-converting enzyme inhibition in the hypertensive-diabetic Dahl rat.

The effect of the angiotensin I-converting enzyme (ACE) inhibitor benazepril (55 mg/kg orally) on the preservation of cardiac performance in diabetic-hypertensive Dahl S rats was investigated. Diabetes mellitus was produced by streptozotocin. Fasting (4-h) blood glucose levels were 279 +/- 50 mg/dL in diabetic Dahl salt-sensitive v 79 +/- 5 mg/dL in nondiabetic Dahl salt-sensitive rats. Cardiac performance was determined at the end of 8 weeks in an isolated perfused working heart apparatus. Peak left ventricular pressure (LVPmax), left ventricular peak negative dP/dt, and coronary flow were depressed in diabetic Dahl S rats (P < or = .05 v control). These deficits in cardiac function were not observed in diabetic Dahl S rats chronically treated with benazepril. The beneficial effects of benazepril apparently were independent of systolic blood pressure reduction. Although plasma ACE activity was increased in diabetic Dahl S rats, plasma renin activity was reduced. This suggests that the beneficial effects of ACE inhibition may be due to an effect upon the kinin system rather than the renin-angiotensin system. The benazepril-associated preservation of cardiac function in this study suggests that ACE inhibitors may be beneficial in the treatment of diabetic heart disease.

Acute hypotension alters hemodynamic response to methionine-enkephalin in conscious dogs.

In the conscious dog, intravenous administration of methionine-enkephalin produces simultaneous increases in both heart rate (HR) and mean arterial blood pressure (MAP). This report describes both depressor and cardioaccelerator responses to methionine-enkephalin (10 micrograms/kg IV) in conscious dogs following acute hypotension induced by either bolus injection of isoproterenol (0.1-5.0 micrograms/kg IV) or infusion of sodium nitroprusside (SNP, 3-8 micrograms/kg/min). Cardiovascular responses to methionine-enkephalin were blocked by naloxone. Pretreatment of the dogs with the beta-adrenergic receptor antagonist propranolol failed to prevent the hypotensive response to methionine-enkephalin following SNP infusion. The results indicate that the hemodynamic responses to methionine-enkephalin can be altered by acute manipulation of blood pressure. These results may have implications relative to the role of endogenous opiates in regulation of blood pressure, especially in acute hypotensive states.

Failure of interleukin-2 to alter systolic blood pressure in Dahl salt-sensitive rats.

The effect of interleukin-2 (IL-2) on systolic blood pressure in Dahl salt-sensitive rats was investigated. The treatment group received human IL-2 injections (5000 units/kg). Control animals received subcutaneous saline injections. Both groups of animals were placed on a diet containing 1.5% sodium the day of the first injection and maintained on that diet for the duration of the study. Systolic blood pressure increased in both the IL-2 treated and the control groups (P = .0001) over 7 weeks. The increase in SBP was the same for both groups (P = .8823 for between group differences). At the end of 7 weeks, when SBP in both groups was elevated to a similar degree, the IL-2 group and the control group were each administered 5000 units/kg of IL-2. SBP in both groups remained elevated, showing no decrease over the next two weeks. These results indicate that perhaps unlike in SHR, IL-2 does not alter systolic blood pressure in Dahl salt-sensitive rats.

Endothelin produces systemic vasodilation independent of the state of consciousness.

The effects of endothelin, ET-1, on pulmonary and systemic hemodynamics were studied in the open chest dog and changes in systemic arterial pressure in dogs under conscious and anesthetized states were compared. Rapid intravenous (IV) bolus injections of ET-1, 100-1,000 nanograms/kg, significantly decreased systemic arterial pressure, and significantly decreased systemic vascular resistance whereas left atrial pressure and pulmonary vascular resistance were not altered. Reductions in systemic arterial pressure in response to bolus injection of ET-1, 100 and 300 nanograms/kg IV, during conscious state and during anesthesia were similar, respectively. The present data suggest that ET-1 dilates the systemic vascular bed independent of the animal's state of consciousness. The present data also suggest that when compared to the systemic vascular bed, the pulmonary vascular bed is less responsive to bolus administration of ET-1.

Interactions between circulating peptides and the central nervous system in hemodynamic regulation.

Enkephalins and endothelins are endogenous peptides, which, at least at pharmacologic doses, produce complex hemodynamic responses after intravenous administration. The enkephalins, when injected into conscious animal models and humans, increase blood pressure, heart rate and minute ventilation. This response occurs by activation of specific opiate receptors located outside the bloodbrain barrier; the actual mechanism involves an increase in adrenergic autonomic nervous system tone and a decrease in cholinergic tone. These opiate receptors may activate afferent fibers, perhaps nicotinic cholinoceptors; in many ways their properties are suggestive of chemoreceptors. Furthermore, enkephalin responses appear to be modulated by gamma-aminobutyric acid complexes, in that the reversal of the excitatory hemodynamic responses seen in the conscious state to vasodepressor responses after barbiturate anesthesia may result from alteration of the state of activation of the gamma-aminobutyric acid complex. The enkephalin receptors are localized to the vertebral artery vascular distribution; the specific site may be the area postrema, a blood-brain barrier-deficient circum-ventricular organ demonstrated to modulate heart rate and blood pressure and to represent a target site for circulating angiotensin II. Endothelin increases heart rate and blood pressure when infused slowly into conscious or anesthetized dogs, although barbiturates do blunt the increase in heart rate. The mechanism appears to involve modification of autonomic tone, but also some element of direct vasoconstrictor activity. Interestingly, rapid bolus doses of endothelin produce only vasodepressor responses, suggesting that the rate and concentration at which circulating endothelin reaches afferent receptors or vasoconstrictor sites on vascular smooth muscle may determine the net hemodynamic response observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic actions of endothelin in conscious and anesthetized dogs.

The newly described endogenous peptide, endothelin, was administered to five chronically instrumented conditioned dogs. Endothelin produced significant and simultaneous increases in both heart rate (HR) and mean arterial pressure (MAP) in conscious dogs. Endothelin also produced significant increases in MAP in anesthetized animals. Ganglionic suppression induced by hexamethonium (10 mg/kg) and atropine (0.1 mg/kg) blocked HR responses and markedly inhibited the pressor responses to endothelin in conscious animals. These results suggest that endothelin in part acts to elevate blood pressure and heart rate through modification of autonomic nervous system tone. When endothelin and angiotensin II were administered in mole equivalent doses, angiotensin II produced a pressor response of greater magnitude than did endothelin in conscious animals.

N-allylnormetazocine: hemodynamic actions and inhibition of leucine-enkephalin hemodynamic activity in conscious dogs.

The hemodynamic actions of dl-, d-, and l-N-allylnormetazocine (NANM) were examined. dl-NANM significantly increased heart rate and systemic arterial pressure in a dose-dependent manner. Naloxone (1 mg/kg) inhibited the hemodynamic actions of 0.5 mg/kg dl-NANM. At a dose of 0.25 mg/kg, l-NANM, but not d-NANM, significantly increased heart rate and mean arterial pressure. The effects of l-NANM were blocked by naloxone but not by naloxone-methylbromide, indicating that the opiate effects are mediated by receptors located in the central nervous system. At a higher dose (0.5 mg/kg), d-NANM consistently produced small increases in heart rate and blood pressure which were statistically significant. The hemodynamic actions of Leu-enkephalin were inhibited by pretreatment with dl-NANM and l-NANM but not d-NANM. These results indicate that NANM has opiate hemodynamic activity which resides with the levorotary isomer. Dextrorotary isomer activity is nonopiate or possibly nonspecific. Furthermore, there appears to be a inhibitory interaction between NANM-opiate and enkephalin hemodynamic actions. This suggests that NANM-opiate receptors may be involved in modulation of the hemodynamic response to circulating enkephalins.

Clinical types of primary angle closure glaucoma.

There is no internationally adopted terminology for the clinical types of primary angle-closure glaucoma. Descriptions of three clinical types: 1. intermittent angle closure; 2. acute and subacute angle closure; and 3. creeping angle closure are presented with reasons for the division into and naming of these types. Chronic angle closure is not a distinct form but a late derivation from various types of angle closure.

The effect of area postrema lesions on hemodynamic responses to systemic methionine-enkephalin in conscious dogs.

In the intact conscious dog, intravenous methionine-enkephalin (ME) increases heart rate and mean arterial blood pressure (MAP). These hemodynamic responses are produced at lower dosages when ME is injected into the vertebral artery, but not the carotid artery, suggesting that ME receptors are localized in the vertebrobasilar artery circulation. The area postrema (AP), a circumventricular organ devoid of a functional blood-brain barrier, represents a likely site for these receptors. We have tested the effects of chronic AP ablation upon hemodynamic responses to ME in conscious dogs. In three dogs with subtotal AP destruction, ME responses were preserved. However, in another dog with complete ablation of both the AP and the area subpostrema, ME responses were eliminated. These results indicate that total destruction of the AP, and perhaps of deeper structures as well, is necessary to abolish hemodynamic responses to ME.