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PubMed1975

Control of myocardial oxygen tension by sympathetic coronary vasoconstriction in the dog.

The effect of sympathetic alpha-receptor coronary vasoconstriction on myocardial oxygen tension was studied in open- and closed-chest, chloralose-anesthetized dogs. Blood oxygen tension in the coronary sinus and blood flow in the circumflex coronary artery were continuously measured in a three-part experiment. With stimulation of the left stellate ganglion (15 Hz, 3 msec, 4-7 v, 90-second train) under vagotomy control conditions (part 1), heart rate, blood pressure, and coronary blood flow increased, but coronary sinus oxygen tension decreased from 19 mm Hg to 15 mm Hg. In part 2, beta-receptor blockade with propranolol (2.0 mg/kg. iv) in the same dogs blunted the positive inotropic and chronotropic effects of sympathetic stimulation; coronary alpha-receptor vasoconstriction was unmasked, and coronary sinus blood oxygen tension fell from 17 mm Hg to 11 mm Hg. Since increases in oxygen metabolism were blunted, it appeared that the decrease in coronary sinus oxygen tension was caused by alpha-receptor coronary artery vasoconstriction. This hypothesis was tested in part 3 by the addition of alpha-receptor blockade with Dibozane (3.0 mg/kg, iv). Sympathetic stimulation no longer resulted in a change in either coronary vascular resistance or coronary sinus oxygen tension. These results indicate that the fall in oxygen tension during beta-receptor blockade in part 2 was due to alpha-receptor coronary vasoconstriction. Thus, myocardial oxygen tension may be regulated by coronary sympathetic vasomotion as well as by myocardial oxygen metabolism and local vascular control mechanisms.

Adrenergic alpha-Antagonists↗
PubMed1992

Comparison of the vasoconstrictive and anesthetic effects of intranasally applied cocaine vs. xylometazoline/lidocaine solution.

Cocaine solution has traditionally been the agent of choice for vasoconstriction and anesthesia when applied topically to the nasal mucosa during nasal operative procedures. Because of the relative scarcity and resulting expense of cocaine, there has arisen an impetus for an alternative intranasal solution for mucosal anesthesia and vasoconstriction. As a logical alternative, we have used a mixed solution of xylometazoline and lidocaine with reasonable results. No clinical studies comparing the efficacy of the two solutions exist, however, and there is presently no such solution commercially available. A double-blind, randomized, placebo-controlled study was undertaken to assess the relative efficacy of the preparations. Both solutions resulted in a marked and roughly equivalent degree of mucosal vasoconstriction (as evidenced by comparable increases in nasal airway cross-sectional area). Subjective pain ratings of mucosal pin-prick decreased a surprisingly small degree after application of both solutions. It appears that xylometazoline/lidocaine solution is comparable to cocaine solution for purposes of vasoconstriction and anesthesia during intranasal operative procedures.

Administration, Intranasal↗
PubMed1994

Vasoconstrictive effects of cocaine and lidocaine with epinephrine in the hamster cheek pouch model.

Otolaryngologists frequently use cocaine and lidocaine with epinephrine for their anesthetic and vasoconstrictive effects. However, no studies have visually compared the vasoconstrictive effects of cocaine to lidocaine with epinephrine. This study used the everted hamster cheek pouch model to assess the vasoconstrictive effects of cocaine and lidocaine with epinephrine by measuring the diameter changes of arterioles. Our results showed that locally injected 1% lidocaine with 1:100,000 units epinephrine caused the greatest diameter reduction in arterioles to 32% of the initial resting diameter. Topical 1% lidocaine with 1:100,000 units epinephrine caused a gradual reduction in diameter with findings equivalent to those of injected 1% lidocaine with 1:100,000 units epinephrine at 30 minutes. Topical 5% cocaine HCl showed a minimal response, with a reduction to only 85% of the resting arteriolar diameter. Topical NaCl and injected NaCl controls showed no significant arteriolar reduction. Vasoconstrictive differences between the preparations were statistically significant (p < 0.05). Five percent cocaine is a much weaker vasoconstrictor than locally injected 1% lidocaine with 1:100,000 units epinephrine.

Administration, Cutaneous↗
PubMed2004

Bupivacaine inhibits thromboxane A2-induced vasoconstriction in rat thoracic aorta.

Plasma levels of thromboxane A2 (TXA2), an inflammatory mediator inducing platelet aggregation, bronchoconstriction, and vasoconstriction, are increased in the perioperative period. A major role in the pathogenesis of perioperative thromboembolic and ischemic syndromes is attributed to this prostanoid. Local anesthetics (LA) inhibit signaling of TXA2 receptors expressed in cell models. Therefore, we hypothesized that LA may inhibit vasoconstriction induced by the TXA2 analog U46619 in rat thoracic aorta. Rings (3-mm length) of the rat thoracic aorta were mounted in organ baths and isometric contractile force was measured. Rings, with or without endothelium, were incubated for 60 min in bupivacaine (10(-6) or 10(-5) M) or Krebs-Henseleit solution (control group) and subsequently exposed to cumulative concentrations of U46619 (10(-10) to 10(-6) M). The reversibility of the TXA2-induced vasoconstriction by bupivacaine was also studied. Pretreatment of rings with bupivacaine concentration-dependently diminished TXA2-induced contraction in rat aortic rings. We found no significant differences in relaxing effect of bupivacaine between rings with and without endothelium. Contraction in rings established with U46619 could not be reversed by cumulative concentrations of bupivacaine. Bupivacaine inhibited carbachol-induced vascular relaxation. This study provides experimental evidence that bupivacaine is an endothelium-independent inhibitor of TXA2-induced vasoconstriction of rat thoracic aorta.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2001

Vasoconstrictive drugs increase carbonic anhydrase I in vascular smooth muscle while vasodilating drugs reduce the activity of this isozyme by a direct mechanism of action.

Carbonic anhydrase (CA) is a zinc enzyme that catalyses the reversible hydration reaction of CO2 and plays a major role in the acid-base balance. We have previously shown that certain vasoconstrictive therapeutic agents increase CA I activity whereas vasodilating drugs reduce the activity of this isozyme by a direct mechanism of action. In this paper we studied the effect of other vasoconstrictive and vasodilating agents on CA I activity in order to elucidate the involvement of vascular smooth muscle CA I in vasoconstrictive and vasodilating processes. We studied the in vitro effects of noradrenaline, prostaglandin F2 alpha, thromboxane A2, leukotriene B4, angiotensin II, vasopressin, indomethacin, prazosin, hydralazine, clonidine, reserpine, prostaglandin I2, indapamide, furosemide, amlodipine, verapamil and irbesartan on purified human red blood cell CA I and vascular smooth muscle CA I isolated from rabbits. In vivo, we selected six groups of five rabbits each, which were administered the following substances in acute experiments: orciprenaline (group 1), desmopressin (group 2), verapamil (group 3), irbesartan (group 4), acetazolamide (group 5) and placebo (control group). Vascular smooth muscle CA I activity and systolic blood pressure were determined and compared with those of the control group. In vitro results showed that all the vasoconstrictive agents studied increased purified and human erythrocyte CA I activity as well as vascular smooth muscle CA I, while vasodilating substances reduced the activity of isozyme by a direct mechanism of action. The same results obtained in vivo showed that activation of vascular smooth muscle CA I increased blood pressure while its inhibition reduced blood pressure. The results of this study suggest that pHi changes, induced by activating or inhibiting CA I in vascular smooth muscle, might be responsible for changes in vascular tonus.

Animals↗
PubMed1971

Mesenteric vasoconstriction after endotoxin administration in cats pretreated with aspirin.

1. Study of the delayed responses to lethal doses of endotoxin in cats is complicated by acute pulmonary vasoconstriction which results in hypotension, cardiac failure and pulmonary oedema. This acute response is abolished if the animal is pretreated with aspirin (10-100 mg/kg). In these cats, pretreated with aspirin, arterial pressure and right atrial pressure remain unchanged in the first 2 h after administration of endotoxin. Later, arterial pressure falls and the animals die but no haemorrhagic lung lesions are visible.2. These results confirm our previous conclusion that the delayed lethal response to endotoxin is an independent action and not a secondary consequence of the acute response. The mechanism of the action of aspirin is discussed and it is suggested that it prevents the release by endotoxin of vasoactive substances, possibly from platelets.3. In cats pretreated with aspirin, administration of endotoxin results in a marked mesenteric vasoconstriction. Although arterial pressure does not decrease significantly, superior mesenteric arterial flow decreases to 20% of control in the first hour after endotoxin and remains at this low level until the animal dies. Mesenteric ischaemia may contribute to the cat's death.4. The mesenteric vasoconstriction is not reduced by prior administration of phenoxybenzamine and is only slightly reduced after phenoxybenzamine, hypophysectomy and nephrectomy. It is concluded that catecholamines, vasopressin and angiotensin play at most a minor role in the mechanism of this vasoconstriction and that other unknown factors are predominant.

Angiotensin II↗
PubMed1990

Stereoselective inhibition of thromboxane-induced coronary vasoconstriction by 1,4-dihydropyridine calcium channel antagonists.

The biological activity of the (+)-S- and (-)-R-enantiomers of niguldipine, of the (-)-S- and (+)-R-enantiomers of felodipine and nitrendipine, and of rac-nisoldipine and rac-nimodipine was investigated in vitro and in vivo. Inhibition of coronary vasoconstriction due to the thromboxane A2 (TxA2)-mimetic U-46619 in guinea pig Langendorff hearts, displacement of (+)-[3H]isradipine from calcium channel binding sites of guinea pig skeletal muscle T-tubule membranes, and blood pressure reduction in spontaneously hypertensive rats were determined. The enantiomers were obtained by stereoselective synthesis. Cross-contamination was less than 0.5% for both S- and R-enantiomers of niguldipine and nitrendipine and less than 1% for those of felodipine. From the doses necessary for a 50% inhibition of coronary vasoconstriction, stereoselectivity ratios for (+)-(S)-/(-)-(R)-niguldipine, (-)-(S)-/(+)-(R)-felodipine, and (-)-(S)-/(+)-(R)-nitrendipine of 28, 13, and 7, respectively, were calculated. The potency ratio rac-nisoldipine/rac-nimodipine was 3.5. Ratios obtained from binding experiments and antihypertensive activity were (+)-(S)-/(-)-(R)-niguldipine = 45 and 35, (-)-(S)-/(+)-(R)-felodipine = 12 and 13, (-)-(S)-/(+)-(R)-nitrendipine = 8 and 8, and rac-nisoldipine/rac-nimodipine = 8 and 7, respectively. Highly significant correlations were found between the in vitro potency of the substances to prevent U-46619-induced coronary vasoconstriction and their affinity for calcium channel binding sites as well as their antihypertensive activity.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1995

Alpha-adrenergic receptor antagonism prevents intestinal vasoconstriction but not hypoperfusion following resuscitated hemorrhage.

Resuscitation (RES) after hemorrhage (HEM) results in persistent arteriolar constriction and hypoperfusion of the small intestine (SI) despite restoration of mean arterial pressure (MAP) and cardiac output (CO) to normal values. We postulated that increased adrenergic activity contributes to this vasoconstriction and impairment of flow. A loop of SI from decerebrate rats was exteriorized and suffused with Krebs' solution (37 degrees C, pH 7.4). In initial experiments, the effectiveness of alpha-adrenergic receptor antagonism by phentolamine (PHEN) was assessed. Subsequent groups received either topical PHEN (10(-6) M, n = 6) or saline (n = 6) in the suffusion and were then bled to 50% baseline (BL) MAP for 60 min and resuscitated to BL with shed blood/lactated Ringer's. Intravital microscopy and optical Doppler velocimetry were used to measure large (A1) and small, premucosal (A3) arteriolar diameters and RBC velocity; microvascular blood flow was calculated. MAP and transpulmonary CO were measured. During HEM, control animals developed A1 constriction and hypoperfusion with A3 arteriolar dilation. PHEN treatment prevented A1 constriction and enhanced A3 dilation but did not improve flow. Immediately after RES in controls, microvascular diameters and A1 flow returned to BL; however, over the 2-hr post-RES period there was progressive A1 and A3 vasoconstriction and hypoperfusion despite maintenance of BL MAP and CO. After RES in PHEN-treated animals, A1 flow returned to BL, but progressive hypoperfusion was only partially prevented. alpha-Adrenergic-mediated vasoconstriction contributes to intestinal hypoperfusion after HEM, but other mechanisms are also involved in microvascular responses during RES.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1987

Inhibition of vasoconstriction to cirazoline by calcium-entry blockade after phenoxybenzamine in rat perfused hindquarters.

The effects of phenoxybenzamine and benextramine were assessed with respect to the vasoconstriction to cirazoline in rat perfused hindquarters. Experiments were performed with and without restriction of inward calcium flux by addition of nifedipine (10(-9)-10(-6) M) to the standard physiological solution (PS), or by omission of calcium chloride from the PS. Addition of nifedipine or omission of Ca2+ did not affect the maximal response or potency of the selective but partial alpha 1-adrenoceptor agonist, cirazoline in rat perfused hindquarters. Upon pretreatment with phenoxybenzamine (0.03-30 micrograms/kg, i.v. at -1 h) or benextramine (1 mg/kg, i.v. at -2 h) both the slope and the maximal response to cirazoline were depressed. After phenoxybenzamine but not after benextramine the maximal response to cirazoline was depressed further upon addition of nifedipine or omission of Ca2+ from the PS. It is concluded that phenoxybenzamine selectively inhibits that part of the alpha 1-adrenoceptor mediated vasoconstriction that is independent of extracellular calcium, thereby unmasking a calcium-entry sensitive mechanism of vasoconstriction to cirazoline.

Adrenergic alpha-Agonists↗
PubMed1987

Photoelectric measurement of neurogenic vasoconstriction in jejunal branches of the rabbit mesenteric artery reveals the presence of presynaptic opioid delta-receptors.

The perivascular nerves of rabbit mesenteric arteries were stimulated with 15 pulses at 2 Hz, and decreases in external diameter were measured by means of a photoelectric device. Both extra- and intraluminally added [Met5]enkephalin 1 mumol/l depressed vasoconstriction, although with the second mode of application a larger inhibition occurred. Therefore, in the subsequent experiments all opioids were added into the lumen. [Met5]enkephalin 0.1 mumol/l had no effect. [D-Pen2, L-Pen5]enkephalin 3 mumol/l was less potent than [Met5]enkephalin 1 mumol/l. ICI 174864 1 mumol/l was also without effect when given alone, but antagonized the action of [Met5]enkephalin 1 mumol/l. Ethylketocyclazocine, dynorphin A(1-13), normorphine and DAGO, all 1 mumol/l, were ineffective. [Met5]enkephalin 1 mumol/l did not change the vasoconstriction evoked by the application of noradrenaline (0.1-3 mumol/l). It is concluded that in the mesenteric artery action potential-induced transmitter release, and in consequence vasoconstriction can be inhibited by the activation of presynaptic opioid delta-receptors.

Animals↗
PubMed1987

Myosin content and vasoconstrictive ability of the proximal and distal (renin-positive) segments of the preglomerular arteriole.

The PAP-technique and antibodies to myosin were used to demonstrate the prerequisites for vasoconstriction in the juxtaglomerular part of the preglomerular arteriole as compared with its proximal segment in rats and mice. In contrast with the myosin-positive/renin-negative proximal part of the afferent arteriole no myosin-like activity could be demonstrated in its distal, renin-positive part. In accordance, no thick myofilaments were found in fully differentiated juxtaglomerular epithelioid cells replete with mature secretory granules. Stimulation of the renin-angiotensin system was followed by an increase of the renin-positive/myosin-negative portions of the preglomerular arteriole. Marked interspecies and internephron variations in the length of this vessel segment under control and stimulated conditions were observed. The juxtaglomerular part of the preglomerular arteriole close to the macula densa seems therefore to have only limited capabilities for vasoconstriction. This finding may be of importance regarding the tubulo-glomerular feedback, a mechanism allegedly triggered by the so-called 'macula densa-signal'. It is suggested that this non-contractile segment of the afferent arteriole may represent the renal vascular receptor responsible for the increase of renin secretion during pressure reduction. Unlike the afferent arterioles, most of the efferent arterioles showed the highest level of their weak but distinct myosin-like immunoreactivity in the juxtaglomerular region, indicating some efferent juxtaglomerular vasoconstrictive ability.

Animals↗
PubMed1981

Organic and inorganic calcium antagonists reduce vasoconstriction in vivo mediated by postsynaptic alpha 2-adrenoceptors.

The influence of various calcium antagonists and divalent metal cations on the pressor responses induced by the selective alpha 1-adrenoceptor agonist methoxamine and the selective alpha 2-adrenoceptor stimulating agent B-HT 920 (2-amino-6-allyl-5,6,7,8-tetrahydro-4H-thiazolo[4,5-d]-azepine) was studied in pithed rats. 1. The calcium antagonists verapamil, D 600 and nifedipine, when given intraarterially (i.a.) in doses up to 1 mg/kg did not influence the pressor effects of methoxamine. Only higher amounts of these calcium antagonistic drugs (1 - 3 mg/kg i.a.) somewhat reduced this pressor response. 2. The vasoconstriction due to B-HT 920, as reflected by the increase in diastolic pressure, was markedly inhibited by verapamil, D 600 and nifedipine in a dose-dependent manner. In low doses a parallel displacement to the right was observed, whereas in higher amounts the shift was non-parallel. 3. The divalent cations MN2+, Ni2+ and Co2+ (0.05 - 0.15 mmol/kg i.a.) hardly affected the pressor effect of methoxamine, whereas B-HT 920-induced vasoconstriction was highly sensitive to these metal ions. La3+ and Mg2+ were ineffective. 4. The calcium antagonists verapamil, D 600 and nifedipine displayed only minor affinities for [3H]prazosin (alpha 1) as well as [3H]clonidine (alpha 2) binding sites of rat brain membranes. 5. It is concluded that an influx of extracellular Ca2+ is necessary for the vasoconstriction in vivo initiated by stimulation of vascular postsynaptic alpha 2-adrenoceptors. On the other hand, vasopressor responses to alpha 1-adrenoceptor stimulation are not directly dependent on a transmembrane influx of calcium ions.

Adrenergic alpha-Agonists↗
PubMed1987

Influence of calcium entry blockade on alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction in the forearm of hypertensive patients.

The influence of treatment with the calcium entry blockers PY 108-068 (PY) and PN 200-110 (PN) on alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction has been investigated in the forearms of hypertensive patients. Changes in forearm vascular resistance (FVR) in response to the intra-arterial infusion of drugs were determined at the end of a placebo period and after 2-4 weeks of treatment with PY or PN. The drugs used were the selective agonists methoxamine (alpha 1) and B-HT 933 (alpha 2). During placebo, basal FVR was dose-dependently increased by methoxamine and B-HT 933. Basal blood pressure was lowered during PN but not during PY. Treatment with the calcium entry blockers did not influence the effect of methoxamine, but the vasoconstriction induced by B-HT 933 was attenuated by both of the calcium entry blockers. These results confirm the findings in animal studies that calcium entry blockers preferentially inhibit the alpha 2-adrenoceptor mediated vasoconstriction induced by selective agonists.

Adult↗
PubMed1992

Pharmacological properties of alpha 1-adrenoceptor-mediated vasoconstrictions in dog and monkey lingual arteries: evidence for subtypes of alpha 1-adrenoceptors.

We examined whether alpha 1-adrenoceptor-mediated vasoconstrictions were due to extra- or intracellular Ca2+ movements, and whether they were subdivided into alpha 1-adrenoceptor subtypes in dog and monkey lingual arteries. The NE-induced vasoconstriction in dog lingual arteries was mostly dependent on Ca2+ influx from the extracellular space, since it was readily blocked by a Ca2+ entry blocker, diltiazem, and the NE-induced response was attenuated approximately 90% in Ca(2+)-free solution. On the other hand, in monkey lingual arteries, diltiazem failed to depress the NE-induced dose-response curve, and the response was attenuated only about 60% in Ca(2+)-free solution. The vasoconstrictor response to 10mg caffeine in normal KHS was almost the same as that to 1 micrograms NE in Ca(2+)-free solution in both kinds of arteries, suggesting that alpha 1-adrenoceptor-mediating vasoconstrictions require a different number of sources of Ca2+ in different blood vessels. Pretreatment of preparations with CEC (an alpha 1B-antagonist) significantly suppressed and shifted the dose-response curve for NE to the right in monkey lingual arteries, but it had no significant effect in dog lingual arteries. However, WB4101 (an alpha 1A-antagonist) showed almost the same potency in blocking vasoconstrictor responses as bunazosin in both kinds of arteries (the pA2 values were not significantly different). Moreover, responses to ME (an alpha 1A-agonist) were blocked by diltiazem as well as by bunazosin and WB4101, while CEC had no blocking effect on ME-induced responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1994

Reflex cutaneous vasoconstriction during cold pressor test is mediated through alpha-adrenoceptors.

The effects of the cold pressor test on the coronary circulation have been clearly defined but the effects on the peripheral vasculature are less well understood. To measure the peripheral vasomotor response during cold pressor test perfusion in the upper extremity contralateral to the cold immersion was assessed by laser Doppler flowmetry and skin-surface temperature gradients. To identify the mechanism of vasoconstriction, cold pressor test was performed before and after the administration of phentolamine, an alpha-adrenoceptor antagonist. Vasoconstriction during cold pressor test was demonstrated by both skin-surface temperature gradients and by laser Doppler flowmetry. This vasoconstrictor response was significantly attenuated by the administration of phentolamine. The results demonstrate that the cold pressor test induces an alpha-adrenoceptor mediated vasoconstriction in the peripheral vasculature.

Adult↗
PubMed1992

Vasoconstriction and bronchoconstriction induced by 2,5-di-(tert-butyl)1,4-benzohydroquinone, an endoplasmic reticular Ca2+-ATPase inhibitor, in isolated and perfused rat lung.

The microsomal Ca(2+)-ATPase inhibitor 2,5-di-(tert-butyl)-1,4-benzohydroquinone (tBuBHQ) induced bronchoconstriction and vasoconstriction in the isolated perfused and ventilated rat lung. These effects were accompanied by increased levels of thromboxane and prostacyclin in the effluent perfusate. The effect of tBuBHQ was inhibited by L-655,240, a thromboxane receptor antagonist, indicating thromboxane-A2-mediated bronchoconstriction and vasoconstriction. Accordingly, the cyclooxygenase inhibitor indomethacin largely blocked the effects of tBuBHQ. The involvement of a phospholipase in the generation of thromboxane A2(TXA2) was supported by dibucaine protection on tBuBHQ effects. The results from this study indicate that tBuBHQ, probably by inhibiting the microsomal Ca(2+)-ATPase, can trigger the arachidonic acid cascade leading to the formation of TXA2, which in turn causes bronchoconstriction and vasoconstriction in rat lung.

Animals↗
PubMed2000

Effects of prostaglandins and leukotrienes on hypoxic pulmonary vasoconstriction in rats.

To investigate the effects of prostaglandins (PGs) and leukotrienes (LTs) on hypoxic pulmonary vasoconstriction (HPV), in vivo rats experiment and in vitro perfused lung experiment were conducted. The effect of hypoxia on hemodynamics, concentrations of TXB2 and 6-keto-PGF1 alpha in serum and lung tissue during hypoxia and effects of PGs and LTs on HPV were observed. The results showed that pulmonary arterial pressure (Ppa) and pulmonary vascular resistance were increased during hypoxia, but cardiac output and systemic arterial pressure were decreased. There were increases of the concentrations of TXB2 and 6-keto-PGF1 alpha and their ratio in serum and lung tissue during hypoxia. After use of cyclooxygenase inhibitor (indomethacin) in vivo and in vitro, HPV was augmented respectively, but after use of lipoxygenase inhibitor (diethylcorbamazine) or leukotriene receptor blocker (LY-171883), HPV was attenuated. It was suggested that LTs mediated pulmonary vasoconstriction, PGs inhibited pulmonary vasoconstriction and they played a modulating role during hypoxia.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Effects of acute ingestion of ethanol on hemodynamics and hypoxic pulmonary vasoconstriction in dogs--role of leukotrienes.

The effects of acute intragastric administration of ethanol on hemodynamics and hypoxic pulmonary vasoconstriction were studied in spontaneously breathing dogs. The dogs were given 0.5 g/kg of 10% ethanol (v/v) in 5 min. Hemodynamic measurements were obtained before and 30 min after ingestion of ethanol. Mean pulmonary arterial pressure and pulmonary vascular resistance increased markedly after ingestion of ethanol, and hypoxic pulmonary vasoconstriction was augmented significantly by ethanol as well. Diethylcarbamazine citrate (DEC), a lipoxygenase inhibitor, inhibited these effects of ethanol in a dosage of 200 mg/kg. The above findings suggest that ethanol can induce pulmonary vasoconstriction, which may be predominantly mediated by leukotrienes (LTs).

Animals↗