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Biomedical subjects

P Wicker

Publications and source records attributed to P Wicker.

At least 19 recordsLinked to original sources
PubMed1992

Differences in left ventricular structural and functional changes between pheochromocytoma and essential hypertension. Role of elevated circulating catecholamines.

Experimental findings suggest that catecholamines increase protein synthesis and play a role in cardiac hypertrophy. We hypothesize that elevated circulating plasma catecholamines in pheochromocytoma influence cardiac structural and functional remodeling. We compared 15 patients with surgically proven pheochromocytoma and 15 with untreated essential hypertension; we matched the patients for age, sex, body surface area, and blood pressure (BP) levels. Left ventricular hypertrophy (LVH) was identified by M-mode echocardiography in six patients with pheochromocytoma and in four with essential hypertension. Among both groups there were no differences in cardiac structure, no correlation between left ventricular mass and BP, no significant differences in mitral E-F slope, no correlation between either plasma norepinephrine or plasma epinephrine levels, and no differences in the left ventricular structural indices measured. In the pheochromocytoma group, left ventricular end systolic stress and end systolic diameter were significantly lower and left ventricular percent fractional shortening was higher. Plasma norepinephrine levels were higher in the pheochromocytoma group, but did not differ among patients of that group with and without LVH. We conclude that in both pheochromocytoma and essential hypertension, only a subset of patients develop evidence of LVH, and that in pheochromocytoma, the elevation of circulating plasma catecholamines is not necessarily associated with LVH. These results indicate that factors other than catecholamines and BP determine the development of LVH in pheochromocytoma.

Adolescent↗
PubMed1992

Wound dressings.

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Bandages↗
PubMed1991

Theatre nursing in Australia.

A herniorraphy is the same wherever it is carried out, in any part of the world. If that was all our job was about, as some would have us believe, then life would be simple indeed. However, it never ceased to amaze me how many different ways there were to carry out the same job. In Adelaide we 'wet-set' our instruments, in Darwin we had small pre-packed trays which were set on trolleys sideways, and in Perth we had pre-sterilised boxes of instruments which we laid out on trolleys ourselves.

Australia↗
PubMed1991

Buyers and sellers.

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Economic Competition↗
PubMed1990

Morphometry of the small arteries and arterioles in the rat heart: effects of chronic hypertension and exercise.

STUDY OBJECTIVE: The aim of the study was to characterise small coronary arteries and arterioles quantitatively in rat left ventricle and septum under various experimental conditions. DESIGN: Morphometric analysis of resistance vessels was carried out in rats divided into four experimental groups: (1) control animals sedentary; (2) control animals exercised (moderate swimming); (3) renal hypertensive animals sedentary; (4) renal hypertensive rats exercised. Hypertensive animals received the two kidney/one clip Goldblatt procedure; control animals were sham operated. SUBJECTS: Experimental animals were 28 female Sprague-Dawley rats. MEASUREMENTS AND RESULTS: In hypertensive rats, there was a significant increase in left ventricular mass and a reduced coronary reserve. Morphometric analysis of 10,000 resistance vessels in the coronary bed showed that cardiac hypertrophy in hypertensive rats was characterised by increased wall thickness in arterioles and small arteries and an increased lumen to wall ratio, particularly in vessels of 30-100 microns size. The number of capillary profiles per arteriole in cross section was also decreased in the hypertensive rat. Chronic exercise increased the number of capillaries per arteriole in controls but not in hypertensive rats. Swimming did not affect the architecture of the resistance vessels. CONCLUSIONS: Chronic renal hypertension, but not swimming, produces subtle but significant changes in structure of coronary resistance vessels.

Animals↗
PubMed1990

Coronary reserve is depressed in postmyocardial infarction reactive cardiac hypertrophy.

After a myocardial infarction (MI), the remaining myocardium undergoes a compensatory reactive hypertrophy. Although coronary perfusion to the surviving myocardium can be an important determinant of cardiac function in this setting, there are no available data regarding myocardial blood flow in reactive hypertrophy. Accordingly, we measured coronary blood flow and reserve using radioactive microspheres in rats 4 weeks after induction of an MI by ligation of the left coronary artery. Maximal coronary dilation was induced by Carbochrome, a potent coronary vasodilator, infused at a rate of 0.45 mg/kg/min up to a total dose of 12 mg/kg. Sham-operated rats served as controls. All animals in the infarct group had a large MI affecting 30-51% (average, 41%) of the left ventricle. Left ventricular end-diastolic pressure was significantly elevated (30 +/- 6.5 vs. 8.0 +/- 2.5 mm Hg in sham-operated rats, p less than 0.01) and baseline hemodynamic indexes of cardiac performance were significantly (p less than 0.01) reduced in this group. Myocyte cross-sectional area measurements were used as an index to quantify the degree of reactive hypertrophy and indicated that the infarcted animals had, on average, a 30% hypertrophic response of the surviving left ventricular myocardium. In the infarcted animals, both coronary flow and vasodilator reserve in the surviving myocardium were depressed. Maximal coronary blood flow in the remaining myocardium was significantly lower than that measured in the sham-operated animals (839 and 1,479 ml/min/100 g, respectively; p less than 0.001). Similarly, minimal coronary resistance was significantly higher in the MI group as compared with the sham group (0.12 vs. 0.07 mm Hg/ml/min/100 g, respectively; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

A reevaluation of the hemodynamics of pheochromocytoma.

We examined the hemodynamic features of 24 untreated patients with surgically proven pheochromocytoma during steady-state periods and compared them with 24 untreated essential hypertensive patients individually matched for sex, age, body surface area, and arterial blood pressure. We found that, despite having 10-fold higher levels of circulating catecholamines, pheochromocytoma patients have hemodynamic characteristics similar to patients with essential hypertension and that, in individual patients, the ratio of circulating norepinephrine to epinephrine had no relation to the hemodynamic profile. In both groups, increased total peripheral resistance is primarily responsible for maintenance of hypertension. These results suggest that, unlike the acute administration of catecholamines, long-term exposure to high levels of circulating catecholamines does not produce hemodynamic responses characteristic of this group of compounds. This might be due in part to desensitization of the cardiovascular system to catecholamines and might explain the clinical observation that some patients can be completely asymptomatic despite harboring an actively catecholamine-secreting pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1990

Mast cells in the rat heart during normal growth and in cardiac hypertrophy.

Mast cells in rat hearts were studied quantitatively during normal postnatal growth and in two types of cardiac hypertrophy. Normally, cardiac mast cell density in 11-12-day-old animals is very low, but increases markedly in the following 2-3 weeks to its highest values, with a subsequent decline toward adult values. At the peak of mast cell density, the percentage of mast cells in close proximity to capillaries is also highest. In adult animals, mast cell counts are significantly higher in the right ventricle than in the left. This relation is preserved even when the right ventricle is hypertrophic, as in rats born at simulated high altitude. Chronic hypertension and swimming have little effect on the mast cell density in rat hearts. Conspicuous changes in the mast cell density at the time of capillary proliferation seem to indicate a special role played by these cells in the formation of new vessels.

Altitude↗
PubMed1989

Circulatory effects of acute normovolaemic haemodilution in rats with healed myocardial infarction.

This study evaluated the haemodynamic response to different degrees of acute normovolaemic haemodilution with hetastarch at rest and during preload and afterload stress in 123 anaesthetised Sprague-Dawley rats divided according to cardiac status (sham operated, n = 46; no myocardial infarction, n = 47; large myocardial infarction, n = 30). Histological infarct size was 41 (SEM 2)%. Cardiac output was recorded using an electromagnetic flow probe. The preload test was achieved by rapid infusion of blood adjusted for packed cell volume, while the afterload test was achieved by an aortic clamp technique. Prior to haemodilution, rats with large myocardial infarction had lower (p less than 0.05) cardiac index, stroke volume index, left ventricular dp/dt, and oxygen delivery, and higher left ventricular end diastolic pressure compared with sham operated rats and rats with no myocardial infarction. Haemodilution to a haematocrit of 30% in all three groups resulted in a similar significant (p less than 0.05) rise in cardiac index and stroke volume index such that blood pressure was maintained despite the decrease (p less than 0.05) in peripheral resistance. Compared with sham operated rats, rats with large myocardial infarcts haemodiluted to packed cell volume of 20% had a more limited rise in cardiac index of 14 (SEM 6) v 45(12)%, p less than 0.05, and a greater fall in oxygen delivery of 50(5) v 28(9)%, p less than 0.05 which was associated with a higher left ventricular end diastolic pressure of 6.6(1.0) v 3.7(0.4) mm Hg, p less than 0.05. Following preload and afterload stress, rats with large myocardial infarcts had lower (p less than 0.05) left ventricular developed pressure, peak cardiac index and peak stroke volume index compared with sham operated rats and rats with no myocardial infarction, independent of packed cell volume. The data suggest that large myocardial infarctions impaired the ability of the left ventricle to pump blood and generate pressure. This diminished left ventricular performance was most apparent in response to preload and afterload stress and at the lowest level of haemodilution employed (packed cell volume 20%).

Animals↗
PubMed1989

Alterations of coronary blood flow and reserve with aging in Fischer 344 rats.

To determine whether aging affects the coronary circulation, left and right ventricular coronary blood flow and vascular resistance at rest and after maximal vasodilation were measured by left atrial injection of radioactive microspheres in conscious, unrestrained male Fischer 344 rats at 4, 12, and 20 mo of age. As a function of age, maximal coronary blood flow per 100 g of tissue decreased by 43% in the left ventricle at both 12 and 20 mo, whereas a 44 and a 47% reduction was found in the right side of the heart at the same time intervals. Minimal coronary vascular resistance per 100 g of myocardium increased by 56 and 36% in the left ventricle and by 48 and 44% in the right at 12 and 20 mo, respectively. No change was found in total minimal coronary resistance for either ventricle despite an increase in myocardial mass. Maximal coronary blood flow per 100 g to the endocardium was depressed more than epicardial flow, leading to a 24% reduction in the endocardial-to-epicardial flow ratio at 20 mo. Coronary vascular reserve per 100 g, expressed as the increase in coronary blood flow during maximal coronary vasodilation, was greater in the right than in the left ventricle at all ages. It is concluded that the changes in coronary hemodynamics associated with maturation and aging are comparable with those seen in pressure overload hypertrophy with an increased vulnerability potential of the myocardium to ischemic episodes, particularly of the subendocardial region of the left ventricle.

Aging↗
PubMed1989

Cocaine-induced small vessel spasm in isolated rat hearts.

Cocaine abuse has been associated with pathologic cardiovascular events including acute myocardial infarction (AMI) and sudden death. Although coronary vasospasm has been proposed as a possible mechanism, the ability of cocaine to induce coronary spasm has not been conclusively demonstrated. In these studies, isolated rat hearts were perfused with cocaine (100 micrograms to 500 micrograms/ml) for 1 minute, perfusion-fixed with glutaraldehyde, and histologically assessed for evidence of coronary spasm through light and electron microscopy. Light micrographs revealed that cocaine induced spasm in coronary arterioles up to 65 microns in diameter, whereas larger caliber vessels did not constrict. Ultrastructurally, vacuolation was observed in the endothelial and smooth muscle cells of constricted arterioles. Endothelial integrity was maintained and interendothelial junctions remained intact. Morphologic evidence of constriction was supported by data obtained from Langendorff-heart preparations in which cocaine reduced myocardial flow rate under constant pressure conditions and increased aortic perfusion pressure under constant flow conditions. Spasm induced by cocaine was prevented by the calcium entry blocker nitrendipine, but not by phentolamine, an alpha-adrenergic antagonist. The finding of small vessel spasm in this study may explain the significant number of clinical cases of cocaine-associated AMI in which the main coronary arteries appear angiographically normal.

Animals↗