scholarly journals Effect of Ultrasonic Bone Stimulation of the Mastoid on Renal and Coronary Blood Flow in Humans

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Chester Ray ◽  
Susie Park ◽  
Charity Sauder
1987 ◽  
Author(s):  
T Saldeen ◽  
J Mehta ◽  
W Nichols ◽  
D Lew

Intracoronary thrombus resulting in acute myocardial ischemia can be lysed by thrombolytic agents, such as, streptokinase or t-PA. We examined the potential of a recombitant tissue-plasminogen activator (rt-PA)and a fibrin (ogen)-degradation productpentapeptide 6A, Ala-Arg-Pro-Ala-Lys, corresponding to aminoacids 43-47 in the BB-chain of fibrinogen, which causes marked increase in coronary blood flow and stimulates prostacyclin release, in restoring coronary blood flow in dqgs with experimentally-induced thrombus. An occlusive thrombus was created in the circumflex (Cx) coronary artery in 8 dcgs by electricalstimulation of the endothelial surface. The electrically-induced Cx thrombus consisted primarily of platelets and fibrin. After the occlusive thrcmbus was stable without electrical currant, rt-PA (10ug/kg/minute for 30 minutes intravenously)or peptide 6A (5 unoles/minute for 20 minutes intracorcnary) were randomly administered. Infusion of t-PA restored coronar blood flow (peak 22 ±12 ml/minute, mean ±SD) in five of seven animlas. The time to flow restoration was 12.3 ± 9.1 minutes and the reflow persistedfor20.0 ± 10.9 minutes. Peptide 6A administration also restored coronary blood flow (peak 20 ± 4 ml/ minute) in seven of eight animals with occlusive coronary thrombus. Mean time to blood flow restoration (4.3 ±2.9 minutes) wasshorter(P>0.05) than with rt-PA, but thereflow persisted only for the duration of tine infusion (16.3 ± 10.2 minutes).Peptide 6A adninistration was associatedwith a significant (P±0.05) increase in plasma 6-keto-PGF1α indicating stimulation of prostacyclin release. In addition, plasma t-PA concentrations also increased (F>0.01) at the peak effect of peptide 6A indicating releaseof endogenous t-PA as another potentialmechanism of the thrombolytic effects of peptide 6A. This study demonstrates that peptide 6A exerts coronary thrombolytic effectsccmpa rable to those of t-PA in a canine model of coronary thrombosis.


1984 ◽  
Vol 62 (11) ◽  
pp. 1374-1381 ◽  
Author(s):  
R. D. Janes ◽  
D. E. Johnstone ◽  
J. A. Armour

Electrical stimulation of the major sympathetic cardiac nerves and ganglia in chloralose-anesthetized, open-chest dogs elicited specific changes in heart rate, coronary blood flow, regional intramyocardial pressure, or intraventricular pressure. The effects produced by stimulation of a cardiac nerve were similar to, but never greater than those produced by stimulation of the ipsilateral stellate ganglion. Coronary blood flow was increased when neural stimulation increased intramyocardial pressure. In contrast, coronary blood flow was not altered significantly when neural stimulation induced tachycardia without increasing intramyocardial pressure. It is concluded that in the intact heart, electrical stimulation of the sympathetic cardiac nerves or ganglia increases coronary blood flow by augmenting intramyocardial pressure, not chronotropism.


2017 ◽  
Vol 2017 ◽  
pp. 1-3
Author(s):  
Thirunavukarasu Kumanan ◽  
Mahesan Guruparan ◽  
Ratnasamy Vithiya ◽  
Indika Gawarammana

It is known that a number of toxic substances produce myocardial injury by several mechanisms involving interruption of coronary blood flow due to stimulation of clotting mechanism and coronary vasospasm. Number of toxic substances may cause direct myocardial toxicity independent of coronary blood flow. Acute myocardial injury due to stings and bites is a rare entity and not well understood. Here we illustrate a case of myocardial injury due to Russell’s viper envenomation.


1964 ◽  
Vol 5 (4) ◽  
pp. 323-336 ◽  
Author(s):  
Hideo UEDA ◽  
Katsuro SHIMOMURA ◽  
Hitoshi GOTO ◽  
Hisakazu YASUDA ◽  
Kiyoshi ITO ◽  
...  

1989 ◽  
Vol 256 (3) ◽  
pp. H735-H744 ◽  
Author(s):  
S. E. Martin ◽  
D. M. Pilkington ◽  
J. C. Longhurst

Topical application of bradykinin or capsaicin to abdominal visceral organs produces adrenergically mediated, reflex increases in mean arterial pressure and cardiac work. To determine the effects on coronary blood flow, the left main coronary artery of anesthetized cats was perfused at constant pressure with a servo-controlled pump. Cardiovascular parameters were measured during reflex stimulation before and after beta-adrenoceptor blockade with propranolol. Before propranolol, reflex activation led to increases in the double product and myocardial oxygen consumption, usually accompanied by increases in coronary blood flow. However, in 32% of the observations, decreases in flow were observed. During beta-adrenoceptor blockade, reflex stimulation produced increases in cardiac work, whereas the increases in coronary blood flow were attenuated. Marked decreases in average coronary blood flow were observed more frequently (42%). In the presence of propranolol, contrary to the unblocked state, increases in oxygen consumption were achieved by increased oxygen extraction. Subsequent alpha-adrenoceptor blockade with phentolamine abolished all reflex changes. These data indicate that during stimulation of abdominal visceral chemoreceptors, the major coronary response is vasodilation, but in a sizable fraction of cases, abdominal visceral reflexes can produce sympathetically mediated coronary vasoconstriction.


Sign in / Sign up

Export Citation Format

Share Document