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Biomedical subjects

P Wicker

Publications and source records attributed to P Wicker.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1987

Effects of chronic exercise on the coronary circulation in conscious rats with renovascular hypertension.

Since various studies suggest that chronic physical conditioning promotes myocardial vascularity, we investigated whether it could prevent the coronary reserve abnormalities of hypertensive cardiac hypertrophy. One week after operation, female Sprague-Dawley rats with two-kidney, one clip Goldblatt hypertension were either subjected to a moderate exercise program by swimming (n = 21) or kept sedentary (n = 16) for 9 weeks. Sedentary (n = 16) and exercised (n = 15) sham-operated rats served as controls. Maximal coronary blood flow and minimal coronary resistance, either per unit mass or for the entire left ventricle, an index of the functional cross-sectional area of the coronary resistance vessels, were determined in conscious, unrestrained rats by left atrial microsphere injection following maximal vasodilation with carbochrome (12 mg/kg). Following exercise, left ventricular mass was moderately (+5-10%) but significantly increased in normotensive rats, whereas left ventricular hypertrophy was significantly accentuated in the hypertensive rats. Minimal coronary resistance for the entire left ventricle was significantly decreased (-24%) in normotensive rats but did not change significantly in hypertensive rats. Minimal coronary resistance per unit mass (the coronary vasodilator reserve) tended to decrease in normotensive rats (-17%), whereas it tended to be further augmented in hypertensive rats (+13%). However, these differences were marginally significant and were not associated with any changes in maximal coronary blood flow per unit mass (the coronary flow reserve). Thus, in normal rats, exercise promoted myocardial arterial vascularity in parallel with the development of cardiac hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Failure of swimming exercise to improve capillarization in cardiac hypertrophy of renal hypertensive rats.

Female Sprague-Dawley rats were made hypertensive by the two kidney/one clip Goldblatt procedure, while control animals were sham-operated. One week later, half of the animals were subjected to a moderate swimming exercise and the other half remained sedentary. Thus, four experimental groups, each consisting of 14 rats, were formed: control animals that were exercised or kept sedentary and corresponding renal hypertensive animals either exercised or sedentary. In hypertensive rats, a significantly increased left ventricular weight and reduced coronary reserve were found. Cardiac hypertrophy in hypertensive rats was characterized by a lower number of capillaries on a tissue cross-section, larger heterogeneity of the capillary net, and a less uniform orientation of capillaries in space. Total length of capillaries in the hypertrophic hearts increased significantly, but less than the increase in cardiac weight, resulting in reduced capillary length density. Chronic swimming for 2 hr/day for a period of 6 weeks, subsequent to a 4-week acclimation period, did not significantly influence any of the investigated indexes of capillaries from hypertrophic hearts. In the normotensive rats, chronic swimming resulted only in a moderate increase in total capillary length associated with a small increase in the left ventricular weight of similar degree. Thus, chronic exercise in normotensive rats induced a moderate increase in total capillary length per left ventricle, while it did not alleviate impaired capillarization of hypertrophic hearts from hypertensive rats.

Animals↗
PubMed1986

Short- and long-term treatment of mild to moderate hypertension with verapamil.

Forty-three patients with mild to moderate hypertension (supine diastolic blood pressure 95 to 115 mm Hg) were entered into a short-term (3 months) study. All received verapamil, 120 mg 3 times a day. After 1 month of treatment on verapamil alone, supine diastolic blood pressure was normalized (less than 95 mm Hg) in 29 patients (67%). These patients continued with verapamil at the same dosage. In 14 nonresponders (supine diastolic blood pressure greater than 95 mm Hg) a combination of althiazide (15 mg/day) and spironolactone (25 mg/day) was added. This resulted in diastolic blood pressure normalization in 9 additional patients. Verapamil induced a slight but moderate decrease in heart rate after 1 month, but no further decrease was observed thereafter. During the trial, 21% of patients reported adverse effects, mostly transient and mild. No patient had to discontinue treatment because of them. Twenty-six patients on verapamil alone were followed for 1 year. Systolic and diastolic blood pressure was adequately controlled in all patients except 1. In 13 the dosage was decreased to 120 mg 2 times a day. There were no significant differences in blood pressure between this group and patients given 120 mg 3 times a day. It is concluded that verapamil is an effective and safe antihypertensive agent in mildly to moderately hypertensive patients. Because a dosage of 120 mg 2 times a day was as effective as 120 mg 3 times a day, the former should be recommended, as it may improve patient compliance.

Blood Pressure↗
PubMed1986

Comparison of the effects of muzolimine and a fixed combination of diuretics in essential hypertension.

The efficacy and tolerance of the loop diuretic muzolimine were compared with those of a fixed combination of hydrochlorothiazide and amiloride in patients with mild to moderate hypertension. After a placebo lead-in period, patients whose supine diastolic blood pressure was between 90 and 115 mm Hg were randomly allocated either to muzolimine, 20 mg/day, or to hydrochlorothiazide, 50 mg/day, and amiloride, 5 mg/day. The mean duration of follow-up was 4.7 months in both groups. Both muzolimine and the combination significantly decreased the mean blood pressure. The two treatments were similar in efficacy. The incidence of side effects during the trial was similar with both treatments, and no serious adverse reactions occurred. Eleven subjects in the muzolimine group were entered into an open long-term study. In all these subjects the blood pressure remained adequately controlled throughout the 4 to 6 months of additional follow-up and no side effects were reported. Muzolimine appears to be an effective and safe antihypertensive agent.

Administration, Oral↗