Coronary resistence

It is a coronary dilator and claimed to dilate coronary resistance vessels. It probably... 

Prostacyclin lowers peripheral, pulmonary, and coronary resistance. It has been used to treat both primary pulmonary hypertension and secondary pulmonary hypertension, which sometimes occurs after mitral valve surgery. A commercial preparation of prostacyclin (epoprostenol) is approved for treatment of primary pulmonary hypertension, in which it appears to improve symptoms and prolong survival. However, because of its extremely short plasma half-life, the drug must be administered as a continuous intravenous infusion through a central line. Several prostacyclin analogs with longer half-lives have been developed and treprostinil was recently approved for use in pulmonary hypertension (Horn, 2002). This drug is administered by continuous subcutaneous infusion. 

Coronary vasoconstriction has been demonstrated for major epicardial coronary arteries (7) and for the small intramural coronary resistance vessels (8) and may occur because of local vasoconstrictors derived from platelets present in the thrombus, such as serotonin, thromboxane A2, and thrombin. 

Dipyridamole (Persantine) evolved from a synthetic study of pyrimido (5,4-d) pyrimidines as a coronary vasodilator over three decades ago. Some early studies indicated that the increased coronary flow alleviated ischemic 02 demand and was therefore useful prophy-lactically in angina. With the advent of well-controlled as well as long-term studies in more recent years, it became apparent that the drug cannot be convincingly shown to have the efficacy it was believed by some to have—this in spite of the fact that it does dilate coronary resistance vessels, but not the conductance vessels the nitrates dilate. 

The large coronary arteries normally contribute little to coronary resistance. However, in variant angina, coronary vasoconstriction results in reduced blood flow and ischemic pain. Ca channel blockers, but not nitrates, have been shown to influence mortality and the incidence of MI favorably in variant angina and should be included in therapy. 

Zhao, D.D., Namba, T., Araki, J. et al., Nipradilol depresses cardiac contractility and 02 consumption without decreasing coronary resistance in dogs, Acta. Med. Okayama., 47, 29-33, 1993. 

Tiefenbacher, C.P., Bleeke, T., Vahl, C., Amann, K., Vogt, A., and Kubler, W. (2000) Endothelial Dysfunction of Coronary Resistance Arteries Is Improved by Tetrahydrobiopterin in Atherosclerosis, Circulation 102, 2172-2179. 

Another observation that militates against a direct effect of PO2 on vascular smooth muscle is that within 1-2 s, after the onset of reactive hyperemia, the coronary venous blood becomes bright red (high POj). If POj directly affected coronary resistance one would expect a prompt return of CBF to control levels after release of a brief (10-60s) eoronary occlusion. Hence, it is evident that the decrease in coronary vascular resistance observed with hypoxemia is probably secondary to the release of a vasodilator substance triggered by an inadequate oxygen supply to the myocardium. 

CBF, coronary blood flow, MVO2, myocardial oxygen consumption PCI ADO, pericardial infu-sate adenosien concentration (see text for details) CVR, coronary resistance O2 EXT, oxygen extraction by the heart CSO2, coronary sinus blood oxygen levels. Values are means SEM. 

BEYAR Regarding the locus of control. Is there any idea where exactly the control of the coronary resistance takes place Is this the direct effect on the smooth muscle or maybe a secondary effect from other sources of metabolic substances ... 

The direct coronary vasoconstrictor effect of sympathetic activation can be unmasked by beta receptor blockade with propranolol that blunts the increase in myocardial metabolism due to sympathetic activation (Feigl, 1975a). After pretreatment with propranolol electrical stimulation of the sympathetic fibers to the heart results in an increase in coronary resistance and a fall in coronary sinus venpus oxygen tension. Both the coronary vasoconstriction and the fall in coronary sinus oxygen tension during sympathetic stimulation were prevented by subsequent alpha receptor blockade. 

Berne RM, DeGeest H, Levy MN (1965) Influence of the cardiac nerves on coronary resistance. Am J Physiol 208 763-769... 

The calculation procedure is based on seeking, for each layer, a value of (y) which corresponds to PVOj (y) = 20 mmHg. This represents a control mechanism which affects the coronary resistance by changing the microvascular tonus according to the local PO2 value. No hypoxia is assumed to occur (i.e. (y) = MVOj... 

Archie JP (1978a) Minimum left ventricular coronary resistance in dogs. J of Surg Res 25 21-25 Bailer D, Bretschneider HJ, Hellige G (1979) Validity of myocardial oxygen consumption parameters. Clin Cardiol 2 317-327... 

The coronary resistance at each point y is assumed to vary between (y) (maximum vasodilatation) and (y) (maximum vasoconstriction). A regulatory function. T f (y), ranging between 0 and 1 represents the tonus of the wall and related to the coronary resistance by ... 

The total coronary resistance is assumed to be a function of the transmural pressure, i.e. ... 

Since endothelial and vascular smooth muscle cells can rapidly synthesize and metabolize histamine, a possible homeostatic role for histamine in cardiovascular physiology has been suggested (Gross et al., 1984). Catecholamine-stimulated histamine release from vascular tissue (Schayer, 1960 Rand et al., 1982) may function to attenuate the effect of catecholamines on heart rate, contractility, and coronary resistance (Gross et ai, 1984 Giacomini and Reis, 1986). Histamine may exert its effects on catecholamine activity by forcing an uncoupling of the P-receptor from the transductional protein, Gs (Levi et ai, 1991). 

Femoral arterial pressure and peripheral and coronary resistance in dogs were reduced by XI, while coronary flow, cardiac output and contractile force Increased. The proper-... 

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