Direct observation of epicardial coronary capillary hemodynamics during reactive hyperemia and during adenosine administration by intravital video microscopy

Kiyooka, Takahiko; Hiramatsu, Osamu; Shigeto, Fumiyuki; Nakamoto, Hiroshi; Tachibana, Hideki; Yada, Toyotaka; Ogasawara, Yasuo; Kajiya, Masahito; Morimoto, Taro; Morizane, Yuki; Mohri, Satoshi; Shimizu, Juichiro; Ohe, Tohru; Kajiya, Fumihiko

doi:10.1152/ajpheart.00088.2004

Cited by 43 publications

(47 citation statements)

References 39 publications

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“…The lens-tip pressure was kept to a minimum (Ͻ2 mmHg), and the RV and LV pressures did not change. In dogs, we also confirmed that the pressure due to the lens probe was close to zero near the end of diastole (16). Thus we were confident that we could visualize coronary microvessels in situ in the rat RV with minimal interference from the microscopy system.…”

Section: Discussionsupporting

confidence: 74%

Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats

Kajiya¹,

Hirota²,

Inai³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats. Am J Physiol Heart Circ Physiol 292: H2737-H2744, 2007. First published January 12, 2007; doi:10.1152/ajpheart.00548.2006.-Pulmonary hypertension (PH) causes right ventricular (RV) hypertrophy and, according to the extent of pressure overload, eventual heart failure. We tested the hypothesis that the mechanical stress in PH-RV impairs the vasoreactivity of the RV coronary microvessels of different sizes with increased superoxide levels. Five-week-old male Sprague-Dawley rats were injected with monocrotaline (n ϭ 126) to induce PH or with saline as controls (n ϭ 114). After 3 wk, coronary arterioles (diameter ϭ 30 -100 m) and small arteries (diameter ϭ 100 -200 m) in the RV were visualized using intravital videomicroscopy. We evaluated ACh-induced vasodilation alone, in the presence of N -nitro-Larginine methyl ester (L-NAME), in the presence of tetraethylammonium (TEA) or catalase with or without L-NAME, and in the presence of SOD. The degree of suppression in vasodilation by L-NAME and TEA was used as indexes of the contributions of endothelial nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), respectively. In PH rats, ACh-induced vasodilation was significantly attenuated in both arterioles and small aretries, especially in arterioles. This decreased vasodilation was largely attributable to reduced NOmediated vasoreactivity, whereas the EDHF-mediated vasodilation was relatively robust. The suppressive effect on arteriolar vasodilation by catalase was similar to TEA in both groups. Superoxide, as measured by lucigenin chemiluminescence, was significantly elevated in the RV tissues in PH. SOD significantly ameliorated the impairment of ACh-induced vasodilation in PH. Robust EDHF function will play a protective role in preserving coronary microvascular homeostasis in the event of NO dysfunction with increased superoxide levels. acetylcholine; N -nitro-L-arginine methyl ester; tetraethylanmonium; catalase; superoxide dimutase; endothelium-derived hyperpolarizing factor PULMONARY HYPERTENSION (PH) causes pressure overload and hypertrophy, finally leading to failure, in the right ventricle (RV) of the heart. Although the right coronary perfusion pressure remains relatively unchanged, the high pressure and hypertrophy of the RV affect the coronary hemodynamics (8, 13), and patients with PH and RV hypertrophy might have symptoms indistinguishable from those of angina pectoris (4, 30). In chronic PH, coronary flow regulation is the only mechanism that maintains the oxygen supply to the RV, since no further increase in the absorption of oxygen is possible (31). The endothelium-dependent vasodilation of coronary small arteries (SAs, diameter ϭ 100 -200 m) isolated from the RV has been shown to be lower in rats with chronic PH (33), whereas in acute PH, endogenous nitric oxide (NO) regulates right coronary blood flow (37). However, the contri...

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Section: Discussionsupporting

confidence: 74%

Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats

Kajiya¹,

Hirota²,

Inai³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Several previous studies in dogs have compared peak coronary hyperemia after occlusion vs. hyperemia induced by intravenous or intracoronary administration of pharmacological agents. These studies have reported similar results between the two interventions (4,19), as well as higher values during RH (9) or higher values with vasodilators (1,11,33). Differences in agents, concentrations, and route of administration seem to underlie the reported disparity.…”

Section: Rh Vs Ahmentioning

confidence: 63%

“…The selective increase in porosity of the glycocalyx might be indicative of an increased plasma flow through this layer, thereby explaining the increase in capillary tube hematocrit during adenosine (12). This increase in functionally perfused capillary volume might underlie the mismatch that has been reported between increases in estimated epicardial capillary volumetric flow and coronary arterial flow during AH but not RH (11).…”

Section: Rh Vs Ahmentioning

confidence: 96%

Hyaluronidase treatment of coronary glycocalyx increases reactive hyperemia but not adenosine hyperemia in dog hearts

VanTeeffelen

Dekker

Fokkema

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Hyaluronidase treatment of coronary glycocalyx increases reactive hyperemia but not adenosine hyperemia in dog hearts. Am J Physiol Heart Circ Physiol 289: H2508 -H2513, 2005. First published July 22, 2005; doi:10.1152/ajpheart.00446.2005.-Because adenosine is commonly used for inducing maximal coronary hyperemia in the clinic, it is imperative that adenosine-induced hyperemia (AH) resembles coronary hyperemia that can be attained by endogenous stimuli. In the present study we hypothesized that coronary reactive hyperemia (RH) is limited compared with AH due to the presence of the glycocalyx and that the AH response is therefore unable to detect glycocalyx modifications. In anesthetized open-chest dogs, blood flow and pressure were measured in the left circumflex artery. RH after 15-s occlusion was compared with an intracoronary infusion of adenosine (650 g; AH) during control conditions and after intracoronary treatment of the glycocalyx with hyaluronidase (20.000 U, 2 ϫ 20 min; n ϭ 6) or heat-inactivated hyaluronidase (n ϭ 5). During control, coronary conductance during RH was 1.49 Ϯ 0.15 ml ⅐ mmHg Ϫ1 ⅐ min Ϫ1 and 76 Ϯ 7% of coronary conductance during AH (P Ͻ 0.05). After hyaluronidase, RH conductance increased (P Ͻ 0.01) by 43 Ϯ 13% and became 93 Ϯ 4% of AH conductance (P ϭ NS). Heatinactivated hyaluronidase had no effect on RH and AH conductance. Our results demonstrate that adenosine-induced coronary hyperemia profoundly exceeds RH and that the difference is virtually abolished on selective removal of the glycocalyx. It is concluded that, compared with RH, adenosine-induced coronary hyperemia is not affected by modification of the glycocalyx. This glycocalyx insensitivity should be taken into account when using adenosine-induced coronary hyperemia as a marker for vasodilating capacity to an ischemic stimulus. coronary circulation; hyaluronidase; dogs TO ASSESS the functional severity of coronary stenoses in the clinic, use of adenosine for inducing maximal coronary hyperemia in patients has been well established (8,10,17,34). Clinical decision-making to intervene is based on intracoronary parameters that are derived during hyperemia, and it is therefore critical that the adenosine-induced hyperemia accurately reflects the coronary hyperemia that can be attained by endogenous stimuli (7). Intravital microscopic studies of cremaster tissue have suggested that adenosine affects capillary perfusion by limiting the effect of the glycocalyx on vascular resistance (3,12,21). The glycocalyx is the carbohydrate-rich matrix that lines the luminal surface of blood vessels and forms the true interface between the endothelium and flowing blood (6,24,26,30). Normally, flowing red blood cells and large dextrans are excluded from the glycocalyx in cremaster capillaries (6, 30, 31). However, it was shown that adenosine superfusion impaired glycocalyx exclusion properties (21). Because an intact glycocalyx strongly reduces the volume available for flow of plasma and red blood cells in capillaries (3,22,30), an impaired g...

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“…After clamping of arterial perfusion line, systolic coronary venous outflow still persists for several heart beats [9,29,47], due to residual blood pooled in the intramyocardial capacitance vessels. To visualize transmural microvascular diameter and flow changes during a cardiac cycle, we developed three types of portable needle-probe videomicroscope with a chargedcoupled device (CCD) camera depending on measuring objectives [19,27,33,53,57]. Type 1 (prototype) The objective of the prototype is to visualize the phasic diameter changes of transmural arterioles and venules.…”

Section: Introductionmentioning

confidence: 99%

Coronary microcirculation in the beating heart

Kajiya

Yada

Hiramatsu

et al. 2008

Med Biol Eng Comput

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The phase opposition of velocity waveforms between coronary arteries (predominantly diastolic) and veins (systolic) is the most prominent characteristic of coronary hemodynamics. This unique arterial and venous flow patterns indicate the importance of intramyocardial capacitance vessels and variable resistance vessels during a cardiac cycle. It was shown that during diastole the intramyocardial capacitance vessels have two functional components, unstressed volume and ordinary capacitance. Unstressed volume is defined as the volume of blood in a vessel at zero transmural pressure. In vivo observation of systolic narrowing of arterioles in mid-wall and in subendocardium indicates the increase in resistance by cardiac contraction.

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Direct observation of epicardial coronary capillary hemodynamics during reactive hyperemia and during adenosine administration by intravital video microscopy

Cited by 43 publications

References 39 publications

Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats

Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats

Hyaluronidase treatment of coronary glycocalyx increases reactive hyperemia but not adenosine hyperemia in dog hearts

Coronary microcirculation in the beating heart

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