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Biomedical subjects

M B Kardon

Publications and source records attributed to M B Kardon.

At least 19 recordsLinked to original sources
PubMed1992

ANF does not increase total body venous compliance in conscious rats with myocardial infarction.

To test the hypothesis that atrial natriuretic factor (ANF) increases total body venous compliance through venodilation and thereby reduces cardiac preload, we compared the systemic hemodynamic effects of ANF (99-126) with the venodilator nitroglycerin in conscious rats with myocardial infarction (mean infarct size 25%) induced by coronary artery ligation 3 wk previously. A 30-min ANF infusion (0.5 microgram.kg-1.min-1) decreased mean arterial pressure, central venous pressure, and blood volume by 11 mmHg, 0.8 mmHg, and 3 ml/kg, respectively (P less than 0.02). Nitroglycerin (10 micrograms.kg-1.min-1) similarly reduced arterial and venous pressures (7 and 0.6 mmHg; P less than 0.02) but increased blood volume by 2 ml/kg (P less than 0.05). Both ANF and nitroglycerin reduced mean circulatory filling pressure (MCFP) by 1 mmHg (P less than 0.05). Compared with vehicle infusion, nitroglycerin increased total body vascular compliance as derived from serial MCFP measurements taken during 10% blood volume changes (2.09 +/- 0.12 vs. 2.76 +/- 0.32 ml.kg-1.mmHg-1; P less than 0.05) and reduced extrapolated unstressed volume (34.96 +/- 1.10 vs. 23.79 +/- 3.80 ml/kg; P less than 0.02). In contrast, ANF had no effect on either measurement. These data suggest that ANF and nitroglycerin reduced cardiac filling pressure through different mechanisms; the lack of effects of ANF on total body venous compliance and unstressed volume does not support its venodilating effect in these rats postmyocardial infarction.

Animals↗
PubMed1991

Spontaneously hypertensive rats demonstrate increased renal vascular alpha 1-adrenergic receptor responsiveness.

To determine alpha 1-adrenergic receptor responsiveness of the renal vasculature in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR), phenylephrine (2.5 or 5.0 micrograms.kg-1.min-1 iv) or saline was infused. Effective renal blood flow (ERBF) and glomerular filtration rate were determined by p-aminohippuric acid and inulin clearances, respectively. Peritubular capillary, proximal tubular, and stop-flow pressures (SFP) were measured by micropuncture. Phenylephrine decreased ERBF (6.27 +/- 0.48 to 4.55 +/- 0.65 ml.min-1.g-1; P less than 0.05) and increased arterial pressure and SFP (31.5 +/- 0.9 to 34.2 +/- 1.0 mmHg) in SHR. It only increased arterial pressure and ERBF in WKY without changing SFP. Afferent arteriolar resistance (RA) and glomerular capillary pressure (PG) remained unchanged, whereas efferent resistance (RE) decreased in WKY; in contrast, RA, RE, and PG increased in SHR (RA 21.2 +/- 2.0 to 38.1 +/- 7.1 mmHg.ml-1.min.g, RE 6.9 +/- 0.6 to 13.9 +/- 3.8 mmHg.ml-1.min.g; and PG 49.6 +/- 0.9 to 53.7 +/- 1.1 mmHg; all P less than 0.05). These data demonstrated increased SHR afferent and efferent arteriolar responsiveness; WKY efferent arteriolar hyperresponsiveness was not observed. The findings support the concept of augmented intrarenal vascular alpha 1-adrenergic responsiveness in hypertension that may predispose to subsequent glomerular hypertension.

Animals↗
PubMed1989

Ventricular performance in spontaneously hypertensive rats (SHR) with reduced cardiac mass.

This study was designed to investigate the effect of 4 weeks of captopril treatment on cardiac mass and performance in spontaneously hypertensive rats (SHR). Left (LV) and right (RV) ventricular mass of SHR and normotensive WKY rats was reduced (p less than 0.01). Mean arterial pressure (MAP) and total peripheral resistance index (TPRI) in the treated SHR and WKY were reduced; cardiac (CI) and stroke (SI) indices remained unaltered in SHR but increased in WKY. Ventricular performance (i.e., cardiac pumping ability), assessed by rapid blood infusion, did not differ between untreated SHR and WKY, and between treated and untreated WKY rats. However, the ventricular performance curves for the treated SHR shifted down and to the right from the untreated SHR (p less than 0.01). Moreover, when MAP of treated SHR (with regressed LV mass) was elevated to their pretreatment levels, cardiac performance curves shifted further rightward and downward. In contrast, the performance curves of treated WKY whose MAP was also elevated to the level of untreated WKY were no different from those of untreated WKY. These data demonstrate that captopril treatment (at doses used in this study) reduced MAP in SHR through decreased TPRI while decreasing biventricular mass. Furthermore, the cardiac-pumping ability of previously hypertrophied SHR hearts was reduced, suggesting that certain antihypertensive agents that diminish cardiac mass could produce impaired cardiac function when called upon to increase performance (e.g., when MAP is suddenly raised).

Animals↗
PubMed1986

Atriopeptin III does not alter cardiac performance in rats.

The effects of atriopeptin III (APIII) on systemic haemodynamics were examined in 12 anaesthetized rats. Five minutes following intravenous injection (i.v.) of 10 micrograms/kg APIII, cardiac output CO, measured by electromagnetic flowmetry, stroke volume and mean arterial pressure (MAP) decreased by 14, 13 and 8% (P less than 0.05), respectively, and total peripheral resistance (TPR) increased by 10% (P less than 0.05). Heart rate (HR) and left ventricular end-diastolic pressure (LVEDP) did not change. In order to examine cardiac performance, whole blood was infused into three groups of 12 rats each receiving either no injection, APIII (10 micrograms/kg i.v.) or APIII (10 micrograms/kg i.v.) plus a continuous infusion of phenylephrine to increase MAP to pre-injection levels. Cardiac performance curves did not differ among the three groups. These data indicate that the immediate decreases in MAP and CO produced in rats by a maximum natriuretic bolus dose of APIII were not mediated by a negative myocardial inotropic effect.

Animals↗
PubMed1986

Acute haemodynamic effects of the atrial natriuretic hormone in rats.

Haemodynamic effects of atriopeptin II (AP II) were determined in conscious and anaesthetized rats chronically instrumented with a Doppler flow probe on the ascending aorta. Intravenous injection of AP II (7 micrograms/kg) produced a decrease in mean arterial pressure within 5 min; however, a biphasic change occurred in total peripheral resistance (TPR). At 1 min in the anaesthetized rats, TPR decreased while cardiac output tended to increase, and similar changes occurred in the conscious rats. By 5-8 min the haemodynamic profile had reversed: cardiac output had decreased in both anaesthetized and conscious rats and TPR had increased in anaesthetized rats. Mean circulatory filling pressure (MCFP) was measured during brief circulatory arrest by inflating an intracardiac balloon. Blood volume was measured with 51Cr-erythrocytes and organ blood volume by whole-animal freezing in liquid nitrogen. There were no changes in MCFP in the conscious and the anaesthetized rats, nor in the blood volume or cardiopulmonary blood volume in the anaesthetized rats, at 5-7 min after AP II. Atriopeptin III (10 micrograms/kg intravenously) had no effects on MCFP and the blood volume in the conscious rats at 5 and 15 min after injection. These results suggest multiple mechanisms of action for the acute haemodynamic effects of atrial peptides.

Animals↗
PubMed1986

Conversion factors of high- to low-molecular-weight forms of atrial natriuretic factor.

The atrial natriuretic factor (ANF) is comprised of a 126-amino-acid precursor (pro-ANF) and its biologically active fragments. Partially purified pro-ANF and its larger fragments (greater than 10,000 daltons) have been referred to as high-molecular-weight (Mr) ANF, the partially purified smaller fragments (less than 10,000 daltons) as low Mr ANF. In vitro, mild proteolysis of high Mr ANF yielded low Mr ANF and enhanced biological activity. In the rat, pro-ANF was the predominant atrial form; however, low Mr ANF was largely released from isolated perfused hearts, which suggests that conversion of pro-ANF to low Mr ANF occurred immediately before or during secretion. High Mr ANF was also found in the perfusate of isolated rat hearts and in the plasma of rats, which suggests that some pro-ANF was secreted with low Mr ANF. Evidence for extraatrial conversion and activation of pro-ANF comes from two studies. 1) Intra-renal-arterial injection of high Mr ANF had little renal vascular action, whereas its i.v. injection caused renal vascular dilation, which suggests that the renal vasodilatory action of high Mr ANF became activated during circulation. 2) When high Mr ANF was incubated with rat blood or rat platelets in vitro, its natriuretic activity was converted to low Mr ANF within minutes; the platelet-induced conversion was associated with enhanced activity in relaxing aortic smooth muscle.

Animals↗
PubMed1986

Hemodynamic effects of atrial natriuretic hormone.

The atrial natriuretic hormone (ANH) alters cardiovascular function independent of changes in body fluid volume. Most investigators agree that ANH decreases mean arterial pressure (MAP). However, although some investigators have observed a decrease in total peripheral resistance in association with the decrease in MAP, a more frequent observation has been decreased cardiac output (CO). The mechanism whereby ANH decreases CO is unknown, but does not appear to be the result of direct myocardial depression, reductions in intravascular or cardiopulmonary volumes, or venodilation. Alterations in skeletal muscle and splanchnic blood flow have been reported by some but not all investigators. Although increases in renal blood flow have been reported, they are transitory and have not been consistently observed by all researchers. The cardiovascular effects of ANH appear to be influenced not only by the dose, but also by the cardiovascular control mechanisms that operate at the time of ANH administration. Non-renin-dependent hypertensive models exhibit a decrease in MAP associated with decreased CO, whereas in renin-dependent animals this hypotension is associated with a decrease in total peripheral resistance.

Animals↗
PubMed1985

Cardiovascular effects and regional blood flow distribution associated with angiotensin converting enzyme inhibition (captopril) in essential hypertension.

Systemic and regional hemodynamics and cardiac structural changes were studied in 12 patients with mild to moderately severe essential hypertension before and then 90 minutes and 12 weeks after administration of captopril. Mean arterial pressure was reduced from 111 mm Hg to 96 mm Hg (p less than 0.001), and this was mediated through a fall in total peripheral resistance from 26 +/- 2 units to 23 +/- 2 units (p less than 0.01). The decreased total peripheral resistance was distributed to all circulations studied: kidney, skeletal muscle, skin and the splanchnic organs. Furthermore, left ventricular (LV) mass index diminished without altering myocardial contractility at rest. Thus, captopril lowered arterial pressure through systemic arteriolar dilatation in patients with mild to moderately severe essential hypertension and also reduced LV mass even in patients without evidence of LV hypertrophy.

Adult↗
PubMed1985

Renal response to acute volume overload in conscious rats with atrial appendectomy.

The presence of volume receptors and a potent natriuretic factor (ANF) in mammalian cardiac atria strongly suggests a central role of the atria in extracellular fluid volume regulation. ANF is stored within granules in atrial appendages, and their removal could alter the response to volume overload. We tested this hypothesis in conscious Wistar rats two weeks after sham operative or atrial appendectomy. The results indicate that removal of the atrial appendages significantly reduced their urinary excretion of water, sodium and potassium during the first hour following acute volume overload. It is concluded that atrial appendectomy alters the ability of rats to handle acute volume overload possibly through a reduction in the ANF available for release.

Animals↗
PubMed1985

Atrial extract: hemodynamics in Wistar-Kyoto and spontaneously hypertensive rats.

Partially purified low (LMW) and high-(HMW) molecular-weight atrial natriuretic extracts were administered intravenously (540 micrograms protein/kg) to conscious Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Both LMW and HMW atrial natriuretic extracts produced an immediate decrease in mean arterial pressure that reached maximum within 5 min and returned to control levels within 30 min. In both strains, cardiac output decreased approximately 14% following administration of LMW. Total peripheral resistance increased only in SHR. Organ blood flow was significantly decreased to skin, brain, heart, kidneys, and splanchnic organs of WKY and to skin, muscle, heart, and splanchnic organs of SHR following administration of LMW. Corresponding increases in organ vascular resistance index were observed in brain, heart, and splanchnic organs of WKY and in skin, heart, and splanchnic organs of SHR. To some extent, the changes in organ blood flow may be a reflection of the decrease in cardiac output induced by LMW. After administration of HMW, no significant changes were observed in cardiac output or total peripheral resistance, although they tended to decrease. Organ vascular resistance was decreased to skin, muscle, brain, and splanchnic organs of SHR. Little difference was observed between WKY and SHR responses to atrial natriuretic extracts. These data indicate that atrial natriuretic extracts have an effect on systemic and regional hemodynamics in conscious rats that differs markedly from those of vasodilators such as nitroglycerin or hydralazine.

Animals↗
PubMed1984

Immediate regional blood flow distribution following angiotensin converting enzyme inhibition in patients with essential hypertension.

The increased total peripheral resistance that characterizes essential hypertension is generally reversed by antihypertensive drugs, but the reduction may not be uniform in all regions of the body. In this study, regional blood flow was investigated immediately after the oral administration of 25 mg of captopril in 11 patients with mild to moderate essential hypertension. Within 90 minutes, the total vascular resistance decreased significantly, and the decrease was significant in the kidney. It decreased but not significantly in the splanchnic organs, the skeletal musculature, and the skin. In no region was the blood flow reduced. As captopril has no direct effect on smooth muscle, these effects are likely to have been due to angiotensin converting enzyme inhibition.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Role of site of microsphere injection and catheter position on systemic and regional hemodynamics in rat.

The influences of the site of microsphere injection (intra-atrial vs. intraventricular) and positioning of the left ventricular catheter (aortoventricular vs. atrioventricular) on systemic, renal, and coronary hemodynamics were evaluated in anesthetized rats. The effect of anesthesia on aortoventricular catheter positioning was also evaluated. In anesthetized and open-chest preparations, the systemic and renal hemodynamics were not affected by catheter position or site of microsphere injection; however, myocardial blood flow was dependent on these variables. Variations in coronary blood flow were significantly greater when the catheter was in the aortoventricular position (34 +/- 3%) than with an atrioventricular catheter (11 +/- 2%, P less than 0.01), irrespective of whether the microspheres were injected into the atrium or ventricle. Comparison of anesthetized and conscious rats with aortoventricular catheter indicated lesser variability in coronary blood flow in the conscious rats (P less than 0.01). Therefore, the greater variability of coronary flow measurements in anesthetized rats was caused by the position of the cardiac catheter in the aortoventricular route. However, the variability caused by the aortoventricular catheter was much less in conscious rats. Therefore, coronary flow hemodynamic measurements (microsphere technique) are less variable when they are made in conscious rats.

Anesthesia, General↗
PubMed1975

Changes in left ventricular internal diameter with increasing pericardial pressure.

Changes in left ventricular internal diameter resulting from increasing intrapericardial pressure induced by increasing the pericardial fluid volume were studied in closed chest, anaesthetized dogs. Left ventricular internal diameters were measured by placing an ultrasonic dimension catheter in the left ventricle at the time of the experiments. With increasing pericardial pressure, significant increases occurred in heart rate and mean left atrial pressure. Left ventricular end-diastolic and end-systolic diameter progressively decreased as the pericardial pressure was elevated. After beta adrenergic blockade with propranolol (1 mg/kg), the decline in end-systolic diameter during pericardial tamponade was significantly reduced. These observations indicate the importance of the systolic reserve and the role of beta adrenergic receptors in the adaptation of the left ventricle to increases in pericardial tamponade.

Animals↗
PubMed1975

Reflex heart rate control via specific aortic nerve afferents in the rabbit.

Reflex bradycardia was elicited in rabbits via repetitive electrical stimulation of the central end of the sectioned left aortic nerve. Supramaximal stimulation produced a 16.9 plus or minus 1.3% (SE) increase in the R-R interval when vagal and sympathetic efferent pathways were intact. Reducing the stimulation voltage allowed selective stimulation of the myelinated (A) fibers, and polarizing electrodes placed central to the stimulus site permitted A fiber blockade and selective stimulation of the unmyelinated (C) fibers. When afferent A fibers were selectively stimulated, 64% of the maximum response was obtained; selective C fiber activation elicited 63% of the maximum observed response. Selective stimulation of A or C fibers after either vagotomy or stellectomy indicated that A fiber afferents elicit heart rate responses via both vagal and sympathetic efferents, whereas C fiber afferent information is mediated predominantly via vagal efferents. This afferent-efferent specificity of the aortic baroreceptor pathways suggests baroreceptor mechanisms normally used to modulate heart rate. Small increments in blood pressure would activate low-threshold A fibers and result in reciprocal changes in vagal and sympathetic efferent activity. More substantial increases in blood pressure would activate afferent C fibers and produce additional heart rate effects via vagal efferents.

Animals↗