Dynamic changes in the haemodynamic severity of coronary artery stenosis in a canine model

Walinsky, Paul; Santamore, William P.; Wiener, Leslie; Brest, Albert N.

doi:10.1093/cvr/13.2.113

Cited by 70 publications

(12 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This did not occur with angiotensin II which is rapidly metabolized by intrarenal enzymes (Oparil & Bailie, 1973). The resistance to blood flow exerted by a fixed-diameter arterial stenosis is not constant but varies with arterial pressure and distal vascular resistance (Anderson et al 1979a;Gould et al 1974;Mates et al 1978;May et al 1963;Schwartz et al 1979;Walinsky et al 1979;Young et al 1977). In all groups in the present study, the calculated stenosis resistance fell from its initial value over the hour of stenosis.…”

Section: Discussionmentioning

confidence: 44%

The importance of renal vascular tone in determining the severity of renal artery stenosis in dogs.

Anderson¹,

Korner²

1980

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. The effects of the state of renal vascular tone during induction of renal artery stenosis on the subsequent systemic blood pressure and renin responses have been studied in chronically instrumented, conscious dogs.2. In one group of dogs, renal vascular tone was altered by brief (2-3 min) renal artery infusions of ACh, saline, methoxamine or angiotensin II during narrowing of the renal artery to reduce distal pressure to 40 mmHg. The infusions were turned off 1 min later.3. The more vasoconstricted the kidney at the time of stenosis, the slower was the restoration of distal renal artery pressure and the greater the rises in systemic blood pressure, plasma renin activity (PRA) and effective stenosis resistance. At the end of 1 hr of stenosis, the rises in systemic blood pressure were 4-3 + 3.3, 11X3 + 3 3, 28-9 + 3X3 and 26X3 + 2X8 mmHg for the ACh, saline, methoxamine and angiotensin II-infused dogs respectively; rises in PRA were 0-3 + 0-24, 1P18 + 0-42, 5 09 + 1P38 and 4-02 + 0 74 ng/ml. per hr respectively.4. In another group of dogs a given aortic-renal artery pressure gradient was produced on two occasions: (i) with the animal conscious; (ii) under brief sodium pentobarbitone anaesthesia and preparation for surgery. After 24 hr systemic blood pressure had risen by 15-7 + 3-6 mmHg above initial values when stenosis was induced under anaesthesia (P < 0.05) and only by 1-2 + 3-6 mmHg (N.S.) when it was induced with the animal conscious. Corresponding rises in PRA were 1-29 + 0-42 (P < 0.05) and 0-25 + 0.11 (N.S.) ng/ml. per hr. Establishment of a given gradient in the high vascular resistance kidney of the anaesthetized dog thus requires greater narrowing of the renal artery than in the lower resistance renal bed of the conscious animal.5. The tone of the renal vascular bed is a major determinant of the severity of renal artery stenosis.

show abstract

Section: Discussionmentioning

confidence: 44%

The importance of renal vascular tone in determining the severity of renal artery stenosis in dogs.

Anderson¹,

Korner²

1980

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…24 Although the preponderance of evidence favors a deleterious coronary vasoconstrictive effect after such thromboxane A2 release, recent studies have shown a paradoxic decrease in coronary blood flow during vasodilation of the ischemic distal coronary bed.25 27 Hence, vasoconstriction resulting from thromboxane release could conceivably be beneficial: A vasocould potentially prevent both a coronary steal and abrupt increases in stenotic resistance by maintaining appropriate distal coronary pressure. 26 Thromboxane A2, by independently acting on circulating platelets, may lead to mechanical obstruction of this same distal coronary bed, further enhancing the intensity of ischemia. Indirect evidence suggests that the platelet-aggregating effect of thromboxane A2 may play such a role in spontaneously occurring ischemia.…”

Section: Resultsmentioning

confidence: 99%

Thromboxane release during pacing-induced angina pectoris: possible vasoconstrictor influence on the coronary vasculature.

Lewy¹,

Wiener²,

Walinsky³

et al. 1980

Circulation

223

View full text Add to dashboard Cite

SUMMARY We developed a radioimmunoassay for plasma thromboxane B,, the metabolite of the coronary vasoconstrictor thromboxane A,. To see if thromboxane A, is produced during myocardial ischemia, we used atrial pacing to study 14 patients with greater than 75% occlusive coronary artery disease proved by arteriography. Paired samples were taken from the coronary sinus (CS) and an artery (A) for lactate and thromboxane B, analysis before pacing. During and after pacing at 140 beats/min, sampling was repeated. Before, during, immediately after and 10 minutes after pacing, percent myocardial lactate extractions (A-CS/A X 100) were 29.3 ± 3.7%, -21.1 ± 12.8%, -74.3 ± 20.3% and 25.1 + 3.5%, respectively (all changes p < 0.01). Before pacing, five patients had detectable coronary sinus or arterial thromboxane levels. During pacing, 18% and 40% increases occurred in coronary sinus and arterial blood, respectively (0.8 ± 0.1 to 0.9 ± 0.2 pmol/ml, and 0.5 0.2 to 0.7 ± 0.2 pmol/ml). Immediately after pacing, increases of 204% and 132% occurred in the coronary sinus and arterial blood (p < 0.05), respectively (2.3 ± 0.9 pmol/ml and 1.2 ± 0.4 pmol/ml). Ten minutes after pacing, thromboxane B, returned to prepacing levels. These data indicate that thromboxane A, is produced during pacing-induced myocardial ischemia and could alter regional coronary blood flow.ATRIAL PACING coupled with coronary sinus blood sampling has been used extensively to study angina pectoris.' During controlled tachycardia, induced myocardial ischemia is accompanied by increased concentrations of lactic acid,6 carbon dioxide,7 hydrogen ion,7 potassium6 and bradykinin.8 Fox et al.9 observed the release of adenosine from human hearts during angina induced by rapid atrial pacing. Subsequently, Berger et al.,10 in a similar experimental setting, reported the release of prostaglandin F from the coronary sinus during anginal provocation.Hamberg, Svensson and Samuelssonll described another prostaglandin, thromboxane A2, which has been found to have potent coronary vasoconstricting and platelet-aggregating ability.'2-14 Our development15 of a radioimmunoassay to measure thromboxane B,, the stable but inactive metabolite of thromboxane A2, led us to design an investigative protocol using rapid atrial pacing to determine if thromboxane release is involved in the cardiovascular response to ischemia. This study documents increases in both coronary sinus and arterial thromboxane B, concentrations during and after ischemia in patients with arteriographically proved, fixed coronary artery disease.Materials December of 1978 were studied by atrial pacing using a method previously reported,'6 followed by coronary arteriography and ventriculography. Descriptions of these patients are shown in table 1. All were judged to have unstable or accelerating angina pectoris and were candidates for emergency myocardial revascularization. After informed consent was obtained, catheterization of the coronary sinus was performed by means of a #7 Gorlin pacing catheter. An 18-gauge Te...

show abstract

“…The final complication of applying quantitative arteriography results from dynamically changing stenosis, first described by co-workers (1978a, 1980;, experimentally developed further by Walinsky et al (1979), Schwartz et al (1979), and Santamore and Walinsky (1980), and observed by Brown et al (1981aBrown et al ( , 1981bBrown et al ( , 1982Brown et al ( , 1984 in humans. In a significant proportion of human coronary stenoses, some part of the arterial wall is sufficiently intact and flexible that vasomon'on of the stenotic segment (Logan, 1975), or of the artery on either side of the stenosis, may occur.…”

Section: Relation Between Anatomic and Functional Characteristics Of mentioning

confidence: 99%

Quantification of coronary artery stenosis in vivo.

Gould¹

1985

Circulation Research

156

View full text Add to dashboard Cite

Dynamic changes in the haemodynamic severity of coronary artery stenosis in a canine model

Cited by 70 publications

References 0 publications

The importance of renal vascular tone in determining the severity of renal artery stenosis in dogs.

The importance of renal vascular tone in determining the severity of renal artery stenosis in dogs.

Thromboxane release during pacing-induced angina pectoris: possible vasoconstrictor influence on the coronary vasculature.

Quantification of coronary artery stenosis in vivo.

Contact Info

Product

Resources

About