Cardiovascular Effects of Marihuana in Man

1974 ◽  
Vol 52 (3) ◽  
pp. 706-719 ◽  
Author(s):  
S. C. Clark ◽  
C. Greene ◽  
G. W. Karr ◽  
K. L. MacCannell ◽  
S. L. Milstein

Twenty-eight subjects, matched by sex and Cannabis experience, received by controlled inhalation under single- and double-blind conditions 600 mg marihuana placebo and marihuana. Forearm, venous and arterial pressures, forearm blood flow, and heart rate were recorded while supine. Derived functions such as "dp/dt", regional arterial resistance, and venous compliance were calculated from these variables. (1) Placebo produced no intoxication or consistent physiological responses. (2) Marihuana produced intoxication in all Cannabis-experienced and half the non-experienced subjects. (3) Cardiovascular responses occurred in response to marihuana in the absence of intoxication, indicating that they were not psychogenically mediated. (4) Inhibition of vagal tone may contribute to the tachycardia seen with marihuana. (5) Reflexly mediated sympathetic responses may be muted in the presence of marihuana.

1982 ◽  
Vol 60 (7) ◽  
pp. 968-976 ◽  
Author(s):  
R. I. Ogilvie

Systemic vascular effects of dopamine, dobutamine, and prenalterol were studied in 45 anesthetized open-chest dogs. Blood flow [Formula: see text] and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant [Formula: see text] showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. Dopamine (2.5–10 μg∙kg−1∙min−1) was the most active drug with dose-related increases in heart rate 6–19%, arterial pressure (Pa) 3–36%, and venous compliance 2–25%. Small doses of dopamine (2.5 and 5 μg∙kg−1∙min−1) reduced arterial resistance of the slow time-constant compartment increasing [Formula: see text] distribution to that compartment 21–42%, whereas larger doses increased both arterial resistance and venous compliance in that compartment. Arterial resistance in the fast time-constant compartment increased with all doses of dopamine. Dobutamine (2.5–10 μg∙kg−1∙min−1) modestly increased heart rate 2–11% and Pa 9–12%) without altering [Formula: see text] distribution demonstrating a relatively flat dose response. Dobutamine 2.5–5 μg∙kg−1∙min−1 increased venous compliance 5–10% while 10 μg∙kg−1∙min−1 had no effect or decreased compliance of both compartments. Prenalterol 3 μg∙kg−1∙min−1 increased Pa 9% primarily by increasing arterial resistance in the fast time-constant compartment without altering heart rate or blood flow distribution. Doses of prenalterol 10–100 times greater caused dose-dependent reductions in Pa and vascular compliance. In this animal model of the circulation with a fixed cardiac output, dopamine had the greatest effect on the peripheral vasculature and chronotropy.


2002 ◽  
Vol 102 (3) ◽  
pp. 307-314
Author(s):  
E.J. ABBINK ◽  
P. PICKKERS ◽  
A. Jansen VAN ROSENDAAL ◽  
J.A. LUTTERMAN ◽  
C.J. TACK ◽  
...  

Glibenclamide inhibits the opening of vascular ATP-sensitive potassium (KATP) channels, which represents a protective mechanism during ischaemia. This effect may imply harmful cardiovascular effects of glibenclamide when used under conditions of ischaemia in patients with Type II diabetes. Acarbose is not associated with effects on the cardiovascular system, because the drug is not absorbed from the bowel. Therefore we hypothesized that treatment of Type II diabetes patients with glibenclamide will impair the vasodilator function of KATP opening, unlike treatment with acarbose. A double-blind randomized cross-over study in 12 patients with Type II diabetes was performed to compare the effects of glibenclamide with those of acarbose on the vasodilator responses to KATP channel opening in the forearm vascular bed. The study consisted of two periods: 8 weeks of treatment with orally administered glibenclamide (10mgċday-1) followed by 8 weeks of treatment with acarbose (300mgċday-1), or vice versa. At the end of each treatment period, forearm blood flow (venous occlusion plethysmography) in response to intra-arterially administered diazoxide, acetylcholine and dipyridamole and to forearm ischaemia was measured. The diazoxide-mediated increase in the forearm blood flow ratio (infused/control arm) was significantly less pronounced after glibenclamide than after acarbose (290±58% and 561±101% respectively; P < 0.0005). Forearm blood flow responses to acetylcholine, dipyridamole and forearm ischaemia were similar during glibenclamide and acarbose treatment. Thus, in patients with Type II diabetes mellitus, treatment with glibenclamide is associated with an attenuated response to KATP opening as compared with treatment with acarbose. This implies that glibenclamide may affect defensive mechanisms under conditions of KATP channel activation.


1988 ◽  
Vol 75 (4) ◽  
pp. 389-394 ◽  
Author(s):  
I. W. Fellows ◽  
I. A. MacDonald ◽  
T. Bennett ◽  
D. P. O'Donoghue

1. On two separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline [0.27 nmol (50 ng) min−1 kg−1] or saline (154 mmol/l NaCl), plus ascorbic acid (5.68 mmol/l), over 30 min. 2. On each occasion, the subjects were exposed to distal body subatmospheric pressure (DBSP), 0 to 50 mmHg (0 to 6.65 kPa) in 10 mmHg (1.33 kPa) steps, before infusion, during the final 15 min of the infusion, and at 15 min and 30 min after the cessation of the infusion. 3. Venous adrenaline concentrations of 2.85 ±0.22 nmol/l were achieved during the adrenaline infusion, compared with 0.49 ± 0.07 nmol/l during the saline infusion (P < 0.001). At 15 min and at 30 min after cessation of the adrenaline infusion, venous adrenaline concentrations had fallen to levels similar to those achieved after the cessation of the saline infusion. 4. Heart rate rose significantly from 58 ±4 beats/min to 67 ±4 beats/min during the adrenaline infusion (P < 0.05), but there was no further significant change in response to 50 mmHg (6.65 kPa) DBSP. At 30 min after the cessation of the adrenaline infusion, heart rate rose from 60 ± 4 beats/min to 78 ± 7 beats/min in response to 50 mmHg DBSP. This increase was significantly greater than that observed before the adrenaline infusion [58 ± 4 beats/min to 69 ±7 beats/min during 50 mmHg (6.65 kPa) DBSP; P < 0.01]. 5. During the infusion of adrenaline, systolic arterial blood pressure rose and diastolic arterial blood pressure fell, but the blood pressure responses to DBSP were unaffected. 6. Forearm blood flow increased significantly during adrenaline infusion but there was no significant difference in the fall in forearm blood flow during DBSP compared with the values before infusion. At 15 min after the cessation of the adrenaline infusion, forearm vascular resistance rose proportionately more in response to DBSP than it had before the adrenaline infusion (P < 0.05). 7. These results are consistent with adrenaline-mediated facilitation of sympathetic neuronal release of noradrenaline in the heart and in the forearm vascular bed.


1988 ◽  
Vol 64 (2) ◽  
pp. 585-591 ◽  
Author(s):  
M. L. Smith ◽  
H. M. Graitzer ◽  
D. L. Hudson ◽  
P. B. Raven

The effect of exercise training mode on reflex cardiovascular control was studied in a cross-sectional design. We examined the cardiovascular responses to progressive incremental phenylephrine (PE) infusion to maximal rates of 120 micrograms/min and the delta heart rate/delta blood pressure responses to lower body negative pressure (LBNP) to -50 Torr in 30 men who were either endurance exercise trained (ET), untrained (UT), or weight trained (WT). During PE infusion, measures of blood pressures, forearm blood flow, heart rate and cardiac output, and calculations of forearm vascular resistance, stroke volume, and peripheral vascular resistance were made at each infusion rate when steady-state blood pressure was attained. No significant differences (P less than 0.05) in forearm blood flow or resistance were observed between the groups at any dose of PE, suggesting that the vasoconstrictor response was similar among the groups. Regression analyses of heart rate against mean blood pressure during the PE infusion were performed to evaluate baroreflex function. A linear model was used and correlation coefficients ranging from 0.82 to 0.96 were obtained (P less than 0.05). The slope of the line of best fit for the ET subjects (-0.57) was significantly less (P less than 0.05) than the slopes obtained for either the UT (-0.91) or WT (-0.88) subjects. In addition, the delta heart rate/delta blood pressure measurements obtained during LBNP reflected a similarly significant attenuation of reflex chronotropic control in the ET subjects.(ABSTRACT TRUNCATED AT 250 WORDS)


1996 ◽  
Vol 81 (4) ◽  
pp. 1516-1521 ◽  
Author(s):  
J. K. Shoemaker ◽  
H. L. Naylor ◽  
Z. I. Pozeg ◽  
R. L. Hughson

Shoemaker, J. K., H. L. Naylor, Z. I. Pozeg, and R. L. Hughson. Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans. J. Appl. Physiol. 81(4): 1516–1521, 1996.—The time course and magnitude of increases in brachial artery mean blood velocity (MBV; pulsed Doppler), diameter ( D; echo Doppler), mean perfusion pressure (MPP; Finapres), shear rate (γ˙ = 8 ⋅ MBV/ D), and forearm blood flow (FBF = MBV ⋅ π r 2) were assessed to investigate the effect that prostaglandins (PGs) have on the hyperemic response on going from rest to rhythmic exercise in humans. While supine, eight healthy men performed 5 min of dynamic handgrip exercise by alternately raising and lowering a 4.4-kg weight (∼10% maximal voluntary contraction) with a work-to-rest cycle of 1:1 (s/s). When the exercise was performed with the arm positioned below the heart, the rate of increase in MBV and γ˙ was faster compared with the same exercise performed above the heart. Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) and placebo were administered orally for 2 days before two separate testing sessions in a double-blind manner. Resting heart rate was reduced in Ibu (52 ± 3 beats/min) compared with placebo (57 ± 3 beats/min) ( P < 0.05) without change to MPP. With placebo, D increased in both arm positions from ∼4.3 mm at rest to ∼4.5 mm at 5 min of exercise ( P < 0.05). This response was not altered with Ibu ( P > 0.05). Ibu did not alter the time course of MBV or forearm blood flow ( P > 0.05) in either arm position. The γ˙ was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 s of below the heart exercise ( P < 0.05). Because PG inhibition altered the time course ofγ˙ at the brachial artery, but not FBF, it was concluded that PGs are not essential in regulating the blood flow responses to dynamic exercise in humans.


1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963


2016 ◽  
Vol 29 (3) ◽  
pp. 543-552
Author(s):  
João Douglas Alves ◽  
Jorge Luiz de Brito Gomes ◽  
Caio Victor Coutinho de Oliveira ◽  
José Victor de Miranda Henriques Alves ◽  
Fabiana Ranielle de Siqueira Nogueira ◽  
...  

Abstract Introduction: Tai-Chi-Chuan and Yoga have becoming popular practices. However is unclear the cardiovascular effects, and if they present similar behavior to aerobic and resistance sessions. Objective: To evaluate the cardiovascular responses during the session and post-exercise hypotension (PEH) of Tai Chi Chuan (TS) and Yoga (YS) in comparison to aerobic (AS) and resistance (SR) exercises. Methods: Fourteen young women (22.3 ± 2 years) apparently healthy performed four sessions (AS, RS, TS and YS). The heart rate (HR), systolic (SBP) and diastolic blood pressure (DBP) were recorded at resting, during (every 10 minutes) and until 50 minutes of recovery. Results: AS, RS, TS e YS showed significant increase in HR compared to resting.AS at 10, 30 e 50 minutes in relation to RS, TS e YS. The RS in relation to TS and YS at 10, 30 and 50 minutes. No significant difference between TS and YS. SBP was significantly increased in AS, RS, TS e YS at 10, 30 e 50 minutes during the session, in relation to rest. AS was significantly higher at 30 e 50 minutes than RS and higher than TS and YS at 10, 30 e 50 minutes. No significant difference in DBP. For PEH, AS, RS and TS significantly reduced at 10, 30 and 50 minutes. YS reduced at 50 minutes. No significant diastolic PEH. Conclusion: TS and YS showed as safe alternatives of exercising in the normotensive young adult woman, despite having lower values, they promote similar hemodynamic behavior to AS and RS.


1998 ◽  
Vol 85 (1) ◽  
pp. 154-159 ◽  
Author(s):  
Jason W. Daniels ◽  
Paul A. Molé ◽  
James D. Shaffrath ◽  
Charles L. Stebbins

This study examined the acute effects of caffeine on the cardiovascular system during dynamic leg exercise. Ten trained, caffeine-naive cyclists (7 women and 3 men) were studied at rest and during bicycle ergometry before and after the ingestion of 6 mg/kg caffeine or 6 mg/kg fructose (placebo) with 250 ml of water. After consumption of caffeine or placebo, subjects either rested for 100 min (rest protocol) or rested for 45 min followed by 55 min of cycle ergometry at 65% of maximal oxygen consumption (exercise protocol). Measurement of mean arterial pressure (MAP), forearm blood flow (FBF), heart rate, skin temperature, and rectal temperature and calculation of forearm vascular conductance (FVC) were made at baseline and at 20-min intervals. Plasma ANG II was measured at baseline and at 60 min postingestion in the two exercise protocols. Before exercise, caffeine increased both systolic blood pressure (17%) and MAP (11%) without affecting FBF or FVC. During dynamic exercise, caffeine attenuated the increase in FBF (53%) and FVC (50%) and accentuated exercise-induced increases in ANG II (44%). Systolic blood pressure and MAP were also higher during exercise plus caffeine; however, these increases were secondary to the effects of caffeine on resting blood pressure. No significant differences were observed in heart rate, skin temperature, or rectal temperature. These findings indicate that caffeine can alter the cardiovascular response to dynamic exercise in a manner that may modify regional blood flow and conductance.


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