Density of plasma-perfused capillaries in the rat heart during carbocromene-induced vasodilation

Schubothe, M.; Vetterlein, F.; Schmidt, Gerhard

doi:10.1007/bf01906665

Cited by 12 publications

(7 citation statements)

References 32 publications

(27 reference statements)

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“…Using a continuous infusion of microbubbles during MCE, we have previously shown that in the absence of a stenosis coronary hyperemia results in an increase in myocardial microbubble velocity which occurs in proportion to increases in coronary blood flow (CBF) (30), without a change in capBV and hence myocardial signal amplitude. That myocardial blood volume does not change during exogenous hyperemia in the absence of stenosis has also been reported using intravital microscopy (27) and other ex vivo methods (6). We have also previously demonstrated that during coronary hyperemia, unlike in the absence of stenosis, myocardial signal on MCE (hence, capBV) decreases distal to a stenosis (23,29,30).…”

supporting

confidence: 68%

Role of capillaries in determining CBF reserve: new insights using myocardial contrast echocardiography

Jayaweera

Wei

Coggins

et al. 1999

American Journal of Physiology-Heart and Circulatory Physiology

138

145

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To define the role of capillaries in the control of coronary blood flow (CBF) reserve, we developed a model of the coronary circulation and evaluated experimental data in its context. Our model comprised three compartments connected in series (arterial, capillary, and venous), each with its own resistance. The resistance in each vascular compartment was derived from the model based on hemodynamic data obtained in nine dogs during baseline and stenosis, both at rest and during hyperemia. The capillary hydrostatic pressure was assumed to be constant in all stages. Although in the absence of stenosis, the contribution of capillaries to total myocardial vascular resistance was only 25 +/- 5% at rest, it increased to 75 +/- 14% during hyperemia, despite the total myocardial vascular resistance decreasing by 51 +/- 13%. In the presence of a noncritical stenosis, total myocardial vascular resistance decreased by 22 +/- 10% at rest, with no change in capillary resistance. During hyperemia, total myocardial vascular resistance increased by 58 +/- 50% in the presence of the noncritical stenosis. In this situation, because arteriolar and venular resistances were already minimal, the increase in myocardial vascular resistance was due to increased capillary resistance, making it the predominant source (84 +/- 8%) of total myocardial vascular resistance. Myocardial video intensity (VI) on myocardial contrast echocardiography (MCE), which reflects capillary blood volume, decreased distal to the stenosis during hyperemia. In the presence of a flow-limiting stenosis at rest, myocardial VI also decreased, indicating that decrease in CBF was associated with an increase in capillary resistance. Our findings also provide an alternative explanation for the critical coronary closing pressure. Thus, contrary to previously held notions, capillaries play a vital role in the regulation of CBF.

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supporting

confidence: 68%

Role of capillaries in determining CBF reserve: new insights using myocardial contrast echocardiography

Jayaweera

Wei

Coggins

et al. 1999

American Journal of Physiology-Heart and Circulatory Physiology

138

145

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“…Pathophysiological conditions (hypoxia) or pharmacological influences (vasodilators) caused no increase in the density of plasmalabeled capillaries in acute experiments (22,28). Similar results were obtained by vital microscopy using a plasma marker for demonstration of perfused capillaries (24).…”

Section: Introductionsupporting

confidence: 83%

Dilatatory capacity of the coronary system in the anesthetized rat

Vetterlein

Schmidt

1985

Basic Res Cardiol

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The minimal coronary vascular resistance was measured in anesthetized rats. For determination of coronary flow a tube system was inserted which directed the blood from the left carotid artery via the right carotid artery into the ostium of the left or the right coronary artery. A drop chamber in the shunt system enabled flow measurement. Maximal vasodilatation was induced by intra-arterial infusion of adenosine. In non-thoracotomized rats vascular resistance decreased to 20.6% and 20.3% of control values in the left and right coronary artery, respectively (23.8 to 4.9 18.2 to 3.7 mmHg X ml-1 X min X g). Thoracotomy led to increased control values (29.3 mmHg X ml-1 X min X g, right coronary artery). Minimal resistance in this latter group was nearly as low as in the closed-chest rats (4.8 mmHg X ml-1 X min X g). It can be assumed that the coronary dilator reserve in the rat lies within the same range as that of larger species e.g. dogs.

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“…This decrease in the perfusion pressure gradient was probably compensated by an active vasodilation. This vasodilation was associated with accelerated capillary flow velocity (35) and a small increase in the coronary capillary volume parameters. On the other hand, in the Goldblatt model, the decrease in capillary volume parameters at 1 and 3 months could be accounted for by vasoconstriction.…”

Section: H Effect Of Cardiac Hypertrophy On the Capillary Bedmentioning

confidence: 98%

Morphometric analysis of collagen network and plasma perfused capillary bed in the myocardium of rats during evolution of cardiac hypertrophy

et al. 1986

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In order to investigate the consequences of different types of cardiac hypertrophy on myocardial capillary and fibrosis density in rats we describe here, in the same hearts, the pattern of capillary bed density visualized by fluorescein isothiocyanate dextran (FITC-dextran) and the pattern of fibrosis density as determined by automated image analysis. Pressure overload was induced by clipping one renal artery in rats (one-clip, two-kidney Goldblatt hypertension, RHV). Volume overload was induced by creation of an arteriovenous shunt between the abdominal aorta and the vena cava (aorto-caval fistula model ACF). Animals were sacrified at 1, 3 and 6 months following surgical procedure. Immediately prior to sacrifice, FITC-dextran (MW 150,000) was injected with the animal under ether anesthesia. Five minutes later, cardiac diastolic arrest was induced by the i.v. injection of potassium chloride. The heart was rapidly excised and placed in a formaldehyde solution. The degree of cardiac hypertrophy was calculated after measurement of cardiac weight. Left ventricular wall thickness and cavity area were measured by microscopic methods. Capillary density and geometry were determined by morphometric methods, under ultraviolet light microscopy, using a graphic tablet connected to a microcomputer. The degree of myocardial fibrosis, visualized with Sirius Red, was estimated by the use of automated image analysis using light microscopy. In renovascular hypertension, cardiac hypertrophy was maximum at one month (36%) and persisted through the six months of the study. This increase in cardiac mass was concentric, due to a significant increase in ventricular wall thickness and was associated with a marked increase in fibrosis and a significant decrease in subendocardial capillary density. These effects existed already one month and did not change with time. In the aorto-caval fistula model, cardiac hypertrophy was also maximum at one month (+56%), but this eccentric increase in cardiac mass was associated with no significant change in left ventricular wall thickness, but rather with a significant increase in the surface area of the left ventricular cavity. This volume overload hypertrophy was associated with a decrease in subendocardial capillary density which was negatively correlated with time. In contrast to concentric hypertrophy there was no increase in the fibrosis density compared to the sham-operated groups. Despite the identical degrees of hypertrophy, pressure and volume cardiac overload differed in a significant manner in both left ventricular wall thickness and cavity surface area.(ABSTRACT TRUNCATED AT 400 WORDS)

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Density of plasma-perfused capillaries in the rat heart during carbocromene-induced vasodilation

Cited by 12 publications

References 32 publications

Role of capillaries in determining CBF reserve: new insights using myocardial contrast echocardiography

Role of capillaries in determining CBF reserve: new insights using myocardial contrast echocardiography

Dilatatory capacity of the coronary system in the anesthetized rat

Morphometric analysis of collagen network and plasma perfused capillary bed in the myocardium of rats during evolution of cardiac hypertrophy

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