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PubMed1986

Increased arterial pH, not decreased PaCO2, attenuates hypoxia-induced pulmonary vasoconstriction in newborn lambs.

Mechanically induced hyperventilation is used in the treatment of newborn infants with persistent pulmonary hypertension syndrome to induce respiratory alkalosis, which may attenuate their pulmonary vasoconstriction. Whether this treatment is effective because of the increase in arterial pH or the decrease in Paco2 was investigated in nine sedated, mechanically ventilated newborn lambs with hypoxia-induced pulmonary vasoconstriction. We found that respiratory alkalosis and metabolic alkalosis were equally effective in attenuating hypoxia-induced pulmonary vasoconstriction, but that hypocapnia (low Paco2 with a normal arterial pH) was ineffective. These results indicate that increased arterial pH, not decreased Paco2, attenuates hypoxia-induced pulmonary vasoconstriction in newborn lambs and possibly the pulmonary vasoconstriction in newborn infants with persistent pulmonary hypertension syndrome.

Alkalosis↗

PubMed1989

Vasoconstriction in telencephalic microvessels: a response to one model for intraventricular hemorrhage in beagle pups.

Telencephalic microvessels were morphologically and morphometrically evaluated in beagle pups at 24, 48, and 72 hours of age following an experimental insult consisting of exposure to acute hypovolemic hypotension followed by rapid corrective blood reinfusion. Animals were anesthetized throughout the procedure and maintained for 75 minutes prior to sacrifice. Microvessels from the germinal matrix, where intraventricular hemorrhage (IVH) most commonly occurs, were compared to those of the adjacent cerebral cortex and choroid plexus. Perfusion, fixation and processing of the tissue followed our previously published protocol (Leuschen et al.: Anatomical Record 208:435-443, 1984). Both germinal matrix and cortical microvessels had collapsed lumens and normal endothelial cell morphology; mitochondria contained distinct cristae, junctional complexes were present and a basement lamina completely surrounded most vessels. Morphometric data on matrical and cortical microvessels supported vasoconstriction. Microvessels from choroid plexus were not vasoconstricted; tight junctions were infrequently seen and microvesicular elements were present. An increased cerebral blood flow to the germinal matrix and the adjacent cerebral cortex has been reported during and immediately following hypovolemic hypotensive insult. By 75 minutes following insult, our ultrastructural studies support a rebound phenomena including vasoconstriction of microvessels. The resulting vasoconstriction and associated cerebral ischemia may play an important role in subsequent tissue damage to the matrical area and ultimately to the etiology of IVH.

Animals↗

PubMed1995

An experimental study of altered nitric oxide metabolism as a mechanism of cyclosporin-induced renal vasoconstriction.

Nephrotoxicity caused by cyclosporin A (CSA) is the result of vasoconstriction of the renal microcirculation. The endothelium-derived relaxing factor nitric oxide (NO) regulates microvascular blood flow in various tissues, and mediates the microcirculatory response during hypertension and sepsis. This study investigated the role of NO in CSA-induced renal vasoconstriction. Hydronephrotic kidneys in rats were suspended in an environmentally controlled tissue bath, and interlobular, afferent and efferent arteriolar diameters and blood flow were measured by in vivo videomicroscopy. CSA was administered alone, with the nitric oxide synthase (NOS) inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) or with exogenous NOS substrate L-arginine. CSA significantly constricted the whole of the renal microvasculature whereas L-NAME alone preferentially constricted the preglomerular vessels. L-Arginine reversed the vasoconstriction induced by CSA whereas L-NAME had no further effect. Preglomerular basal vascular tone is dependent on continuous production of NO and alterations in the L-arginine-NO pathway contribute to CSA-induced renal vasoconstriction.

Animals↗

PubMed2000

Local arterial vasoconstriction induced by octreotide in patients with cirrhosis.

Peripheral vasodilation initiates the hyperdynamic circulation in cirrhosis. Somatostatin and its analogues, such as octreotide, have a vasoconstrictive effect in cirrhotic patients and experimental animals with portal hypertension. The exact mechanism of octreotide-induced vasoconstriction remains unknown. To investigate whether octreotide produces vasoconstriction through suppression of vasodilatory peptides, such as glucagon, or through a local effect, we evaluated the effect of an intra-arterial dose on forearm blood flow (FBF), while measuring systemic glucagon levels. FBF was measured in 10 cirrhotic patients by venous occlusion plethysmography. The brachial artery of the nondominant arm was catheterized, and vasoactive drugs were administered: methacholine 4 microg/min; octreotide 20 microg/h, and octreotide 20 microg/h + methacholine 4 microg/min. Each infusion, lasting 5 minutes, was followed by saline for washout. FBF was measured in both arms during the last minute of each infusion and at the end of washout, with the uninfused arm acting as the control. Nitrates and nitrites, octreotide, and glucagon blood levels were determined at baseline and after each infusion. Percent change in flow (%triangle up) was obtained by comparing the flow during drug administration to that during the preceding saline infusion. Saline infusion did not alter FBF, but octreotide infusion resulted in a 34% +/- 7.7 (P <.005) reduction in FBF in the infused arm. FBF in the control arm was unchanged despite a significant decrease in systemic glucagon levels. Methacholine infusion increased FBF around 300%, which was not altered by the concomitant infusion of octreotide. Octreotide has a local vasoconstrictive effect that seems nitric oxide (NO)-independent. Octreotide probably has a facilitating effect over vasoconstrictors increased in chronic liver diseases.

Arm↗

PubMedDate not supplied

Vasodilatory effect of aerosol histamine during pulmonary vasoconstriction in unanesthetized sheep.

The effects of aerosol histamine on pulmonary vascular resistance during pulmonary vasoconstriction were studied in 12 unanesthetized sheep. Sheep were chronically instrumental with Silastic catheters in the pulmonary artery and left atrium, thermodilution Swan-Ganz catheter in the main pulmonary artery for measurement of cardiac output, and tracheostomy for delivery of hypoxic gas and/or aerosol histamine. Seven minutes of isocapnic hypoxia (FIO2 = 0.12) caused pulmonary artery pressure (PPA) to increase from 17.2 +/- 0.4 to 27.0 +/- 1.0 cm H2O (mean +/- SEM, P less than 0.05) and pulmonary vascular resistance (PVR) to increase from 3.94 +/- 0.33 to 4.71 +/- 0.38 cm H2O x L-1 x min (P less than 0.05). When sheep breathed a combination of aerosol histamine (5 mg/ml) and 12% O2, PPA rose only 21.3 +/- 1.11 cm H2O and PVR decreased to 3.51 +/- 0.31 cm H2O x L-1 x min. This was a significantly (P less than 0.05) smaller response compared to hypoxia alone. Aerosol histamine alone had to significant effect on PPA or PVR. Meclofenamate did not restore the histamine-induced loss of hypoxic vasoconstriction. Aerosol histamine significantly blunted the pulmonary vasoconstriction caused by intravenous serotonin (8 micrograms/kg/min) and intravenous prostaglandin H2-analog (0.74 microgram/kg/min). It was concluded that in the awake sheep aerosol histamine acted as a pulmonary vasodilator only in the presence of pulmonary vasoconstriction.

Aerosols↗

PubMed1994

Adrenoceptor mechanisms in epinephrine-induced anterior choroidal vasoconstriction in cats.

These studies were undertaken to determine the role of epinephrine in the anterior choroidal circulation and to define the relative contribution of adrenoceptor subtypes in this response. Intra-arterial administration of l-epinephrine (0.03-1 microgram) produced vasoconstrictor responses in the anterior choroid of anesthetized cats as measured using laser-Doppler flowmetry. Ipsilateral nictitating membrane contractions were simultaneously recorded. Responses of both organs were blocked by intravenous treatment with the non-selective alpha-adrenoceptor antagonist phentolamine; however, only nictitating membrane contractions were significantly antagonized with the selective alpha 1-adrenoceptor antagonist, prazosin. In contrast, alpha 2-adrenoceptor blockade with rauwolscine had no depressant effect on the nictitating membrane but was a potent antagonist for epinephrine-induced ocular vasoconstriction. This differential ocular receptor type activation was confirmed with the use of more selective alpha-adrenoceptor agonists. Both the alpha 1-adrenoceptor agonist, methoxamine, and the selective alpha 2-adrenoceptor stimulant, B-HT 933, produced choroidal vasoconstriction when given intra-arterially. B-HT 933 was as potent as methoxamine in producing choroidal vasoconstriction which suggests a high ratio of alpha 2-adrenoceptors in this vascular bed. B-HT 933 was much less potent than methoxamine in producing contraction of the nictitating membrane. These results demonstrate the usefulness of laser-Doppler flowmetry in studies of the choroidal circulation and suggest that, unlike the nictitating membrane, epinephrine-induced anterior segment vasoconstriction is mediated by both postjunctional alpha 1- and alpha 2-adrenoceptors with alpha 2-adrenoceptors being predominant.

Adrenergic alpha-Agonists↗

PubMed1987

Evidence for a vasoconstriction-mediating receptor for UTP, distinct from the P2 purinoceptor, in rabbit ear artery.

1. The mechanism of uridine 5'-triphosphate-(UTP-)induced vasoconstriction was studied in the rabbit ear artery. The arteries were incubated and perfused at a constant rate of flow. Vasoconstriction was measured as an increase in perfusion pressure. 2. Noradrenaline, adenosine 5'-triphosphate (ATP) and UTP caused concentration-dependent vasoconstriction. ATP and UTP were approximately equipotent. 3. The vasoconstrictor effect of UTP 300 mumol/l was enhanced by a mixture of atropine, diphenhydramine and methysergide (1 mumol/l each) and not affected by indomethacin 10 mumol/l. 4. Prazosin (0.01-1 mumol/l) and phentolamine (1-10 mumol/l) reduced the vasoconstrictor effect of UTP 300 mumol/l by up to 34%. Prazosin 1 mumol/l failed to diminish the vasoconstrictor effect of UTP 300 mumol/l after the sympathetic nerves had been destroyed with 6-hydroxydopamine. 5. alpha, beta-Methylene-ATP (10-50 mumol/l) elicited transient vasoconstriction. Subsequently, vasoconstrictor responses to ATP 100 or 300 mumol/l were reduced by 88%, whereas responses to UTP 100 mumol/l were enhanced, responses to UTP 300 mumol/l decreased by only 32% and responses to UTP 1000 mumol/l reduced by 74%. After in vitro-denervation with 6-hydroxydopamine or in the presence of phentolamine 1 mumol/l throughout, alpha, beta-methylene-ATP (10-50 mumol/l) reduced the vasoconstrictor effect of UTP 300 mumol/l by 44% and 43%, respectively. 6. We suggest that, in the rabbit ear artery, the non-adrenergic and alpha, beta-methylene-ATP-resistant vasoconstrictor response to UTP is mediated by a separate receptor mechanism, distinct from the P2 purinoceptor.

Adenosine Triphosphate↗

PubMed1988

Further evidence for the existence of alpha 2-mediated adrenergic vasoconstriction in human vessels.

To confirm the presence of alpha 2-mediated vasoconstriction in human vasculature, the effect of selective alpha 1- and alpha 2-agonists (methoxamine and B-HT 933) and antagonists (indoramin and Yohimbine) was studied in fourteen patients with mild, uncomplicated, essential hypertension. Drugs were infused, into the brachial artery at systemically ineffective rates, and concomitant changes in forearm blood flow were measured by strain gauge venous plethysmography. During control conditions, cumulative infusions either of methoxamine or B-HT 933 caused dose-related vasoconstriction, while both indoramin and yohimbine doubled forearm blood flow. Subsequently, the alpha 1-adrenoceptor mediated vasoconstriction produced by methoxamine was shown to be completely blocked by indoramin pretreatment, and to be left unchanged by yohimbine. The alpha 2-vascular stimulation by B-HT 933 was antagonized by previous yohimbine but not by indoramin pretreatment, thus fulfilling the pharmacological requirements for identification of distinct alpha-adrenoceptor mediated excitation-contraction pathways. The data provide further evidence of the existence of alpha 2-mediated vasoconstriction in human forearm vessels.

Adult↗

PubMed1978

Vasoconstriction after adenosine and inosine in the rat isolated hindlimb abolished by blockade of tryptaminergic mechanisms.

The isolated right hindlimb of the rat was perfused at a fixed flow rate through the femoral artery with heparinized blood from the carotid artery of a donor. Single injections of adenosine (1--300 microgram) induced a biphasic response, a long-lasting vasoconstriction preceded by a transient vasodilatation. Inosine (1--300 microgram) produced only vasoconstriction. After repeated administration of 300 microgram of these substances, the vasoconstriction became less prominent, and finally reverted to vasodilatation. The vasoconstrictor response to these substances (300 microgram) was also diminished or reverted to vasodilatation after pretreatment with reserpine or methysergide. From these results, it is concluded that vasoconstriction after adenosine or inosine may be mediated by 5-hydroxytryptamine released from the peripheral stores and that the intrinsic direct action of these substances on the femoral vascular bed is vasodilator.

Adenosine↗

PubMed1988

Physiological mechanism of digital vasoconstriction training.

Recent work in our laboratory has shown that vasodilation produced during temperature biofeedback training is mediated through a nonneural, beta-adrenergic mechanism. Here we sought to determine if the effects of feedback training for vasoconstriction are produced through a neural or nonneural pathway and whether other measures of physiological activity are correlated with these changes. Nine normal subjects received temperature feedback vasoconstriction training in which feedback was delivered only during periods of successful performance. In a subsequent session, the nerves to one finger were blocked with a local anesthetic while finger blood flow was recorded from this and other fingers. Vasoconstriction occurred during feedback in the intact fingers but not in the nerve-blocked finger and was accompanied by increased skin conductance and heart rate. These data demonstrate that temperature feedback vasoconstriction training is mediated through an efferent, sympathetic nervous pathway. In contrast, temperature feedback vasodilation training is mediated through a nonneural, beta-adrenergic mechanism.

Adult↗

PubMed1989

[The role of lipoxygenase and cyclooxygenase metabolites in acute hypoxic pulmonary vasoconstriction in piglets].

The role of lipoxygenase and cyclooxygenase metabolites in acute hypoxic pulmonary vasoconstriction (HPV) was studied in piglets. It has been found that acute alveolar hypoxia induced remarkable pulmonary vasoconstriction, associated with an increase in cardiac output. The hypoxic pulmonary vasoconstriction response was insignificantly attenuated after infusion of DEC. Indomethacin potentiated markedly the increase in pulmonary artery pressure and pulmonary vascular resistance and thus augmented HPV. It is inferred that hypoxic pulmonary vasoconstriction in piglet may be mediated by other important mediators in addition to leukotrienes, but modulated by prostaglandins to prevent an excessive rise in pulmonary artery pressure.

Animals↗

PubMed1996

[Hypoxic pulmonary vasoconstriction].

Hypoxic pulmonary vasoconstriction (HPV) was first described by von Euler and Liljestrand in 1946 and is still the only known vascular feedback control mechanism in the lung. This technique results in a redistribution of blood flow away from poorly ventilated areas into better ventilated regions, thus reducing shunt. HPV functions as a local mechanism that acts in response to alveolar hypoxia but in the smallest areas of the lung, making it an important mechanism in all situations where ventilation perfusion mismatch occurs. to be effective, HPV needs normal pulmonary areas into which blood flow can be diverted. This explains why the efficacy of the treatment depends on the area that is vasoconstricted. The effect on PaO2 is maximal when the amount of the hypoxic lung ist 30-70%. If the area in vasoconstriction is small, the influence on PaO2 is negligible. On the other hand, when most of the lung is hypoxic, there is no significant normoxic region to which the hypoxic region can divert flow. In that case it does not matter, in terms of PaO2, whether the hypoxic region has active hypoxic pulmonary vasoconstriction or not. In this situation HPV becomes a rather detrimental mechanism, because it causes an increase in pulmonary arterial pressure. At some stage a turning point, where the gain in PaO2 is lost due to an increase in right ventricular after-load, inducing a decrease in CO. The reaction is diminished by exogenous manipulations, drugs (inhalation anesthetics, direct vasodilators), endotoxin, very low PaO2 values, vasodilating mediators and changes in the acid-base balance. Acidosis and alkalosis inhibit HPV. Factors like spontaneous or mechanical ventilation, PEEP, open or closed chest, and the type of hypoxia (atelectasis or nitrogen) have no influence on HPV. The small arteries, those less than 500 microns in diameter, were identified as the location of the hypoxic constriction. Pulmonary vascular smooth muscle cells in pure culture undergo reversible and repeated hypoxic constriction. Examination of a histological lung section emphasizes that the small arteries are closely surrounded by alveoli gas on the outside and by mixed venous blood on the inside. Thus, the response is believed to be accounted for by each smooth muscle cell in the pulmonary arterial wall responding proportionally to the local oxygen tension in its vicinity and depending on alveolar as well as mixed venous oxygen pressure. The biochemical intracellular mechanism remains unknown.

Critical Care↗

PubMed2000

Differential effects of the mixed ET(A)/ET(B)-receptor antagonist bosentan on endothelin-induced bronchoconstriction, vasoconstriction and prostacyclin release.

Endothelins are a family of potent endogenous mediators that have been implicated in a number of airway and other diseases. Recently, the non-peptide mixed ET(A)/ET(B) endothelin receptor antagonist bosentan has been successfully tested in the treatment of cardiovascular diseases. It was the aim of the present study to characterize the effects of bosentan on the pulmonary actions of endothelin- (ET-1), endothelin-3 (ET-3) and the ET(B)-receptor agonist IRL1620 in the isolated perfused and ventilated rat lung (IPL) and in precision-cut lung slices (PCLS). In the IPL, bosentan completely prevented the IRL1620-induced vasoconstriction (IC50 3 microM). The inhibition by bosentan of ET-1-elicited vasoconstriction showed a biphasic course, reflecting the inhibition of ET(A)-and ET(B)-mediated vasoconstriction (IC50 0.2 microM and 19 microM, respectively). In addition, bosentan prevented the ET-1- (IC50 6 microM) and IRL1620-induced (IC50 3 microM) prostacyclin release. Bosentan also completely prevented the bronchoconstriction induced by IRL1620 in the IPL (IC50 20 microM) and in PCLS (IC50 13 microM). In PCLS, the pD2-values were ET-1 7.20+/-0.23, ET-3 7.51+/-0.27 and IRL1620 7.33+/-0.29. Bosentan at 100 microM caused a rightward shift of the concentration-response curve of ET-1, ET-3 and IRL1620 by a factor of 5, 46 and 64, respectively. In all cases the slope of the Schild regression was lower than unity, disregarding a simple interaction of bosentan with one receptor. With respect to ET-1-induced bronchoconstriction, in the IPL bosentan in concentrations of up to 10 microM aggravated ET-1-induced bronchoconstriction probably due to the blockade of bronchodilatory ET(A)-receptors (IC50 0.3 microM) and even at 100 microM showed only very little protection from ET- -induced bronchoconstriction in the IPL and in the PCLS. The similar IC50-values for ET-1-induced vasoconstriction and bronchodilation suggest that only one type of ET(A)-receptor is involved. The differing IC50-values between IRL1620-induced bronchoconstriction and prostacyclin release, the slope of the Schild regression and the failure of bosentan to prevent the ET-1-induced bronchoconstriction suggest a complex interaction between the known ET-receptors or the existence of unknown ET(B)-receptor subtypes.

Animals↗

PubMed2001

High concentrations of oxytocin cause vasoconstriction by activating vasopressin V1A receptors in the isolated perfused rat kidney.

The aim of this study was to evaluate the renal vascular effects of oxytocin in Sprague-Dawley rats and in Brattleboro heterozygous or homozygous rats, the latter being genetically deficient in vasopressin synthesis. Studies were performed in vitro, in the isolated kidney perfused in an open circuit with a Tyrode's solution. Oxytocin induced a concentration-dependent renal vasoconstriction in Sprague-Dawley rats, at rather high concentrations (EC50=170+/-39 nM, mean +/- SEM, n=6) with a maximum response amounting to 44% of that elicited by vasopressin (increase in renal vascular resistance: 11.5+/-0.9 mmHg min ml(-1) vs. 26.2+/-2.2 mmHg min ml(-1)). Oxytocin-evoked renal vasoconstriction was abolished by SR 49059, a selective vasopressin V1A receptor antagonist (10 nM), but not by d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr-(NH2)9] vasotocin, an oxytocin receptor antagonist (10 nM). In the presence of SR 49059, oxytocin did not induce renal vasorelaxation. Oxytocin induced renal vasoconstriction in Brattleboro homozygotes and heterozygotes (EC50=59+/-12 nM and 262+/-110 nM; Emax=7.8+/-1.1 mmHg min ml(-1) and 6.9+/-0.4 mmHg min ml(-1), n=5 respectively) with characteristics similar as observed in Sprague-Dawley rats concerning partial agonist activity, low potency and antagonism by SR 49059. Responsiveness to vasopressin did not differ in Brattleboro homozygotes and heterozygotes (EC50 approximately 0.25 nM) and was similar as we reported in Sprague-Dawley rats. These findings indicate that high concentrations of oxytocin induce renal vasoconstriction in the rat by activating vasopressin V1A receptors. The low agonist activity makes it unlikely that oxytocin can substitute functionally for vasopressin at the renal vascular V1A receptor in Brattleboro homozygous rats which are deficient in endogenous vasopressin.

Animals↗

PubMed2005

Regional differences in peripheral vasoconstriction of prepubertal boys.

To elucidate the mechanisms that underlie the greater decline of skin temperature on the limbs in prepubertal boys as compared to young men, we compared cutaneous vascular conductance (CVC) of the boys and men in response to a reduced ambient temperature (T (a)). The boys had a greater surface area-to-mass ratio (A (D)/mass) and a lower mean skinfold thickness on the trunk but not on the limbs compared to the men. As T (a) decreased from 30 to 17 degrees C over 60 min, the skin temperature (T (sl)) on the limbs (as represented by forearm, finger and thigh) decreased significantly more in the boys than in the men; while T (sl) on the trunk (chest, back and abdomen) and forehead decreased to the same extent. The CVC decreased at all body sites in all subjects, but regional difference existed in age-related alterations in CVC responses despite the similar rectal and mean body temperatures of the groups. The decline in the finger CVC was greater for the boys than for the men, suggesting that greater vasoconstriction and greater A (D)/mass on the fingers may have contributed to the lower finger T (sl) of the boys. However, thigh CVC in the boys was similar to that in the men over the 60-minute exposure, indicating that the lower thigh T (sl) of the boys may be the result of greater heat loss owing to the greater A (D)/mass on the limbs of the boys (but not to greater vasoconstriction or subcutaneous fat). The CVC on the chest and back was greater in the boys over the cold exposure, suggesting that similar T (sl )on the chest and back of the boys and men may result from greater cooling owing to the larger A (D)/mass being offset by combination of less vasoconstriction and more conductive heat transfer in the presence of less subcutaneous fat. These results suggest that the age-related difference in T (sl) in response to mild cold stress may not directly reflect that in cutaneous vasoconstriction alone owing to the differences in anthropometric characteristics (such as greater A (D)/mass and lower subcutaneous fat on trunk) between boys and men.

Adult↗

PubMed2002

Patchy renal vasoconstriction after exercise in a child without renal hypouricemia.

Here, I present a case of patchy renal vasoconstriction and renal injury in a girl without renal hypouricemia, following exercise and ingestion of an analgesic. For the previous 2 years, she had suffered from re-current abdominal pain following exercise. Postcontrast renal computed tomographic scan showed low-density patchy areas immediately after contrast medium injection, and then patchy wedge-shaped contrast enhancement 22 h later. These symptoms and signs are typical findings of patchy renal vasoconstriction. Although precise mechanisms for the development of patchy renal vasoconstriction after exercise in patients without renal hypouricemia remain obscure, both exercise and ingestion of an analgesic were active in the development of patchy renal vasoconstriction and renal injury in our patient.

Abdomen↗

PubMed1979

Inappropriate coronary vasoconstriction in patients with coronary artery disease: a role for nifedipine?

Coronary arterial vasoconstriction, well recognized in Prinzmetal's variant angina, may participate in the pathogenesis of classic angina as well. Several recent studies in patients with obstructive coronary artery disease suggest that apparently spontaneous reductions in coronary blood flow can result in myocardial ischemia and even infarction. Evidence supporting the alpha adrenergic nervous system as a cause of such coronary vasoconstriction is reviewed, particularly the results of provocative testing with the cold pressor stimulus. Upon exposure of the skin to cold, patients with coronary artery disease demonstrate an inappropriate coronary vasoconstrictor response, often sufficient to produce angina. Normal patients, by contrast, show no change in coronary vascular resistance. In patients with a diseases coronary circulation, inappropriate vasoconstriction further restricts myocardial perfusion and appears to be little affected by beta adrenergic blocking agents or nitrates in the usual dosages. Nifedipine has proved effective in preventing coronary arterial spasm in patients with Prinzmetal's angina. Studies currently in progress suggest that it is also effective in blocking inappropriate coronary vasoconstriction in patients with typical angina. Nifedipine may thus be a useful addition to the treatment of ischemic heart disease.

Angina Pectoris, Variant↗

PubMed1982

Inhibition of hypoxic pulmonary vasoconstriction by nifedipine.

Nifedipine is a potent slow channel calcium antagonist and systemic vasodilator recently reported to attenuate hypoxic pulmonary vasoconstriction in man. Other systemic vasodilators have also been shown to attenuate hypoxic pulmonary vasoconstriction, but their effects in some species may be mediated by reflex beta-adrenergic discharge. We evaluated the effect of nifedipine on the relation between pulmonary arterial pressure and blood flow during hyperoxia (inspired partial pressure of oxygen [PO2] 200 mm Hg) and hypoxia (inspired PO2 50 mm Hg) in denervated ventilated pig lungs perfused in situ with the animal's own blood. Ten lungs were ventilated with alternating 15 minute periods of hyperoxia and hypoxia. Hypoxia shifted the pulmonary artery pressure (x axis)-blood flow (y axis) relationship to the right and decreased its slope, indicating vasoconstriction. Nifedipine, given as a 0.1, 1, or 10 microgram/kg bolus into the pulmonary artery, caused a dose-dependent reduction of hypoxic pulmonary vasoconstriction. It is concluded that nifedipine is a potent pulmonary vasodilator acting locally within the lung and that it might be useful in the therapy of hypoxic pulmonary hypertension from chronic lung disease in man.

Animals↗