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Biomedical subjects

D D Gutterman

Publications and source records attributed to D D Gutterman.

At least 37 records · Page 2Linked to original sources
PubMed1997

Effects of glycosylated hemoglobin on vascular responses in vitro.

UNLABELLED: Vascular responses to endothelium-dependent vasodilators are greatly impaired in vivo, while isolated blood vessels from animals with diabetes mellitus demonstrate less consistent degrees of impairment. Glycation of proteins, such as hemoglobin, has been implicated in the vascular abnormalities associated with diabetes. OBJECTIVE: The purpose of this study was to test the hypothesis that glycosylated hemoglobin is capable of reducing endothelium-dependent vasodilator responses, possibly explaining impaired dilation observed in vivo. METHODS: To test this hypothesis, the effect of glycosylated hemoglobin (GH) on vascular responses was studied in several vascular beds, including ventricular microvessels and coronary, mesenteric, femoral, and renal arteries. Coronary arterioles were isolated and mounted between two glass pipettes in a pressurized (30 cmH2O) organ chamber. Isolated artery segments were studied using a standard isometric ring technique. RESULTS: In ventricular microvessels, 10 nM nGH (non-GH) and GH both attenuated the relaxation to Ach. A lower concentration, 1 nM nGH or GH, did not alter dilation to Ach. In coronary, femoral, mesenteric and renal artery segments, endothelium-dependent responses were not altered by the presence of 10 or 100 nM nGH or GH. CONCLUSION: In coronary microvessels, and coronary, femoral, mesenteric and renal arteries, GH is not responsible for the impaired endothelial function associated with diabetes mellitus.

Acetylcholine↗
PubMed1997

Role of adenosine receptor subtypes in neural stunning of sympathetic coronary innervation.

Adenosine plays an important role in postischemic dysfunction of cardiac sympathetic nerves because exogenously infused adenosine produces and adenosine deaminase prevents "neural stunning." We examined whether adenosine acts via a specific receptor mechanism to produce neural stunning. Anesthetized dogs were treated with propranolol to attenuate increases in coronary flow due to adrenergic stimulation of myocardial metabolism. A 15-min occlusion of the left anterior descending coronary artery (LAD) attenuated subsequent LAD coronary vasoconstriction to bilateral sympathetic stimulation during reperfusion by 75% (P < 0.05). Coronary infusion of the adenosine-receptor antagonist 8-p-sulfophenyltheophylline (nonspecific), 8-cyclopentyl-1,3-dipropylxanthine (A1 specific), or 3,7-dimethyl-1-propagylxanthine (A2 specific) during LAD occlusion prevented the attenuation of sympathetic coronary constriction. In separate experiments, either the specific adenosine agonist N6-cyclopentyl-adenosine (A1 specific) or CGS-21680 (A2 specific) or a combination of both agonists was infused into the LAD for 15 min. Neither agonist alone attenuated subsequent sympathetic coronary constriction. In contrast, 15 min after the combined administration of both agonists, sympathetic vasoconstriction was reduced. We conclude that adenosine is capable of attenuating neurogenic coronary constriction through a receptor-mediated mechanism. Activation of more than one receptor subtype is necessary to produce neural stunning.

Adenosine↗
PubMed1997

Myogenic constriction of human coronary arterioles.

Myogenic constriction is an important mechanism of blood flow regulation; however, it has never been demonstrated in the human coronary circulation. We examined responses of human coronary resistance vessels in vitro to changes in intraluminal pressure and evaluated the role of protein kinase C (PKC). Microvessels (passive diameter 44-227 microns) were dissected from atrial appendages obtained during cardiac surgery and studied under conditions of zero flow. In response to stepped increases in pressure, there was a graded response such that at 100 mmHg, vessels constricted to 55 +/- 4% of their passive diameter. There was an inverse relationship between vessel diameter and myogenic responsiveness. Basal tone was attenuated by inhibition of voltage-dependent calcium channels (VDCC) with diltiazem and by inhibition of PKC with calphostin C. Activation of PKC with phorbol 12-myristate 13-acetate (PMA) enhanced basal tone. Active myogenic constriction was also impaired by calphostin C and augmented by PMA. Arterioles from patients with hypertension demonstrated enhanced myogenic constriction compared with vessels from normotensive patients (0.55 +/- 0.04 vs. 0.74 +/- 0.03; P < 0.01). These results demonstrate myogenic constriction in the human coronary microcirculation. Regulation of extracellular calcium by VDCC and intracellular calcium by PKC are important in mediating the magnitude of basal tone and myogenic responsiveness of these vessels.

Adolescent↗
PubMed1997

Oxygen-derived free radicals contribute to neural stunning in the canine heart.

Oxygen-derived free radicals (ODFR) contribute to delayed recovery of myocardial function after brief ischemia. We examined the effect of ODFR scavengers on ischemia-induced dysfunction of cardiac sympathetic nerves. Mongrel dogs were anesthetized and instrumented for recording heart rate, arterial pressure, systolic wall thickening, and left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX) flow velocities. Bilateral stellate stimulation was performed, measuring changes in an index of coronary vascular resistance (% delta CVR) before and after 15 min of LAD occlusion. Superoxide dismutase (SOD) and catalase (CAT) were infused intravenously for 30 min beginning 10 min before occlusion. With vehicle (n = 13), % delta CVR was significantly attenuated in LAD after ischemia and 30-min reperfusion [39 +/- 3 to 13 +/- 2%, P < 0.05; for LCX, 42 +/- 4 to 45 +/- 7%, P = not significant (NS)]; however, no attenuation was seen in dogs in which SOD and CAT were infused (n = 10; for LAD, 39 +/- 5 to 41 +/- 5%; for LCX, 46 +/- 7 to 47 +/- 6%; P = NS). Baseline and stimulated changes in hemodynamics were similar between groups. The % delta CVR in the LCX (control) bed was not affected by SOD and CAT. Recovery of myocardial function (percent of baseline) was greater in SOD and CAT after reperfusion (26 +/- 16% vs. -30 +/- 11% at 90 min of reperfusion, P < 0.05). We conclude that ODFR contribute not only to myocardial stunning but also to neural stunning of sympathetic cardiac innervation after brief ischemia.

Animals↗
PubMed1996

Role of parabrachial nucleus in baroreflex-mediated coronary vasoconstriction.

Coronary vasoconstriction is a component of the baroreflex response to bilateral carotid occlusion. The central pathways responsible for this reflex constriction are incompletely understood, but previous studies show that activation of parabrachial nucleus (PBN) elicits coronary vasoconstriction and that PBN shares prominent anatomic connections with other central baroreflex centers, including the nucleus of the tractus solitarius. Therefore, we examined whether PBN plays a role in baroreflex mediated coronary constriction and whether cell bodies rather than fibers passing through this region are involved. Anesthetized cats were instrumented for continuous measurements of heart rate, arterial pressure, and coronary flow velocity. Bilateral carotid occlusion following propranolol and vagotomy increased arterial pressure (63 +/- 10%) and an index of coronary vascular resistance (34 +/- 6%). Bilateral microinjections of lidocaine (1%, 400 nl) into PBN reversibly attenuated the coronary constriction (19 +/- 5%) with little effect on the change in arterial pressure. It was further demonstrated that autoregulatory responses to the increase in pressure could not fully account for the observed changes in coronary constriction. In a separate group of animals, kainic acid (50 mM, 300 nl) abolished the baroreflex increase in coronary resistance (43 +/- 1 vs. -9 +/- 9% after) without affecting the increase in arterial pressure (54 +/- 12% increase before vs. 55 +/- 20% increase after kainic acid). We conclude that PBN is a necessary component of the baroreflex pathway mediating coronary vasoconstriction. Furthermore, cell bodies in PBN, rather than simply fibers passing through that region, participate in the reflex coronary vasoconstriction.

Animals↗
PubMed1995

Role of adenosine in postischemic dysfunction of coronary innervation.

We sought to determine the role of adenosine in the sustained but reversible decrease in cardiac neurotransmission that occurs after brief ischemia. Adult mongrel dogs were anesthetized and instrumented for measurements of heart rate, arterial pressure, and left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX) flow velocities. Changes in coronary vascular resistance were measured during bilateral stimulation of the stellate ganglia. After beta-adrenergic blockade and bilateral vagotomy, stellate stimulation increased coronary vascular resistance in the LAD and LCX beds 28 +/- 2% and 30 +/- 3%, respectively. After a 15-minute infusion of adenosine into the LAD, the peak increase in LAD resistance was significantly reduced (18 +/- 2%) compared with LCX (34 +/- 5%) and control (P < .05, n = 6) resistance. The LAD response after infusion of the vasodilator papaverine was unchanged (n = 6). Intracoronary infusion of adenosine deaminase (n = 10) but not vehicle (n = 5) into the LAD during a 15-minute LAD occlusion prevented the attenuation in constriction to stellate stimulation. We conclude that adenosine, exogenously infused or endogenously produced, is capable of reducing cardiac neurotransmission.

Adenosine↗
PubMed1995

Use of an indwelling catheter for examining cardiovascular responses to pericardial administration of bradykinin in rat.

OBJECTIVE AND METHODS: Epicardial application of pharmacologic agonists has been used to study nociceptive and reflex responses to agents such as bradykinin. We utilized a model where intrapericardial bradykinin was administered in a closed-chest rat. The procedure allows for reproducible administration of microliter doses of pharmacologic agonists in both conscious and anesthetized animals. RESULTS: Bradykinin (BK) has been shown to produce sympathoexcitatory reflexes when applied to the heart. BK typically produced a dose-dependent (0.001-10 micrograms) decrease in arterial blood pressure and tachycardia in pentobarbital-anesthetized rats. In contrast, in alpha-chloralose-anesthetized or awake rats, pericardial administration of BK produced a dose-dependent (0.001-10 micrograms) increase in arterial blood pressure and tachycardia. Maximal cardiovascular changes were produced by 1 microgram BK. The maximum change in arterial pressure was +33.6 +/- 9% in awake, +38.9 +/- 6% in chloralose-anesthetized, and -20 +/- 7% in pentobarbital-anesthetized rats. In alpha-chloralose-anesthetized rats, tachyphylaxis to pericardial administration of 1 microgram BK occurred at 5 and 15, but not at 30 min dosing intervals. Administration of the receptor selective B2-antagonist D-Arg,[Hyp3,Thi5,8 D-Phe7]-BK (200 micrograms) or the mixed B2/B1 antagonist [Thi5,8,D-Phe7]-BK (200 micrograms), produced similar attenuation of the pressor and tachycardia responses to BK. Bilateral transection of the cervical vagus nerve, bilateral removal of the stellate ganglion or ganglion blockade (hexamethonium), but not administration of indomethacin, reduced the magnitude of the tachycardia to BK. Only ganglionic blockade significantly reduced the pressor response to BK. CONCLUSIONS: These results demonstrate that pericardial administration of BK produces a tachycardia and pressor effect in awake and alpha-chloralose-anesthetized rats and a tachycardia and depressor effect in pentobarbital-anesthetized rats. These responses appear to be mediated through activation of BK (presumably B2) receptors on cardiac vagal and sympathetic afferents, and may include a direct action of BK on the heart. This model of pericardial administration of pharmacologic agonists may be useful in studies of cardiac pain and reflex responses.

Animals↗
PubMed1994

Inhibition of nitric oxide synthesis augments centrally induced sympathetic coronary vasoconstriction in cats.

The principal effect of sympathetic activation on the coronary circulation is an alpha-adrenergic coronary vasoconstriction in the presence of beta-receptor blockade. Secondary effects include vasodilation due to beta-adrenoceptor stimulation and alpha 2-mediated release of endothelium-derived relaxing factor (EDRF) from the coronary vascular endothelium. We hypothesized that blockade of nitric oxide synthesis (nitro-L-arginine methyl ester, L-NAME) would augment coronary vasoconstriction to sympathetic stimulation as a result of a decrease in alpha 2-mediated EDRF release. In chloralose-anesthetized cats, hypothalamic stimulation produced increases in coronary vascular resistance [maximum 26 +/- 9% (SE)] and arterial pressure (41 +/- 7%) and a decrease in coronary blood flow velocity (15 +/- 6%). L-NAME (3 mg/kg iv) increased baseline arterial pressure from 69 +/- to 92 +/- 7 mmHg (P < 0.05). After L-NAME, a greater increase in coronary vascular resistance (55 +/- 20%, P < 0.05), a decrease in coronary blood flow velocity (24 +/- 7%, P < 0.05), and a similar pressor response (34 +/- 7%) were observed in response to hypothalamic stimulation. L-Arginine reversed the effect of L-NAME on coronary vasoconstriction to hypothalamic stimulation. Similar increases in arterial pressure (from 73 +/- 3 to 91 +/- 5 mmHg, P < 0.05) with vasopressin (0.01-0.05 U/min) failed to enhance coronary vasoconstriction to activation in anterior hypothalamus. We conclude that inhibition of EDRF synthesis augments centrally induced sympathetic coronary vasoconstriction in the cat.

Animals↗
PubMed1994

Detection of cardioembolic sources with echocardiography.

Cerebral ischemic events remain a common cause of morbidity and mortality in the United States. Although the majority of patients with strokes have cerebrovascular disease, up to 20% of stroke patients have a cardioembolic source, especially younger patients or those with associated cardiac disease. TTE offers limited potential for identifying a cardioembolic source. In contrast, TEE is superior in detecting most cardioembolic sources and should be considered in stroke patients in whom there is a high clinical suspicion for a cardiac source of embolus and whose TTE is technically difficult or negative (Table 3).

Echocardiography↗
PubMed1993

Use of echocardiography in detecting cardiac sources of embolus.

Up to 20% of all ischemic strokes are felt to be the result of emboli from the heart. High resolution transthoracic (TTE) and transesophageal (TEE) echocardiography have been the principal diagnostic tools for detecting associated cardiac abnormalities and for guiding medical and surgical approaches to these patients. In addition to identifying the precise location and morphological characteristics of intracardiac masses, echocardiography has improved our ability to predict embolic potential of these masses. Specific cardiac lesions that are predisposed to stroke and are readily identifiable by echocardiography include: cardiac thrombi, valvular vegetations, cardiac tumors, aortic atheroma, atrial septal aneurysm, and regional left ventricular wall abnormalities. Careful interrogation of patients with cerebrovascular accidents has identified a potential cardiac source of embolus in approximately 30%. This is largely due to the advent of TEE, which has provided much better assessment of posterior cardiac chambers including left atrium and left atrial appendage. Use of TEE in identifying a cardiac source of embolus is indicated in patients with stroke who are young, have no apparent cerebrovascular disease, or have recurrent embolic events. Echocardiography is an essential diagnostic tool in evaluating patients with a suspected cardiac source of embolus. TTE and TEE provide invaluable information regarding the majority of cardiac sources of embolus.

Brain Ischemia↗
PubMed1993

Coronary vasoconstrictor pathway from anterior hypothalamus includes neurons in RVLM.

We have previously identified discrete brain sites [anterior (AHA) and lateral hypothalamus, periaqueductal gray, pontine parabrachial nucleus, lateral reticular formation, and rostral ventrolateral medulla (RVLM)] in the cat, in which electrical or chemical activation produces coronary vasoconstriction. This study examines whether the most rostral (AHA) and caudal (RVLM) of these sites are connected as part of a common pathway mediating coronary vasoconstriction. In chloralose-anesthetized cats, electrical stimulation in the AHA produced maximum increases in arterial pressure (41 +/- 10%) and coronary vascular resistance (28 +/- 9%). Microinjection of lidocaine into the RVLM attenuated the increases in arterial pressure (10 +/- 3%) and coronary vascular resistance (5 +/- 1%) in response to electrical stimulation in the AHA (P < 0.05 vs. before lidocaine). Lidocaine nonspecifically inhibits neural elements in the region. gamma-Aminobutyric acid in the RVLM, which selectively inhibits cell bodies and not fibers passing through the RVLM, attenuated the increase in coronary vascular resistance (38 +/- 8 to 14 +/- 3%; P < 0.05) but not the increase in arterial pressure (87 +/- 12 to 92 +/- 16%) in response to electrical stimulation in the AHA. These data indicate that coronary vasoconstriction in response to electrical stimulation in the AHA requires cell bodies in the RVLM; however, the associated pressor response is mediated by fibers passing through the RVLM. We conclude that a polysynaptic descending pathway that mediates sympathetic coronary vasoconstriction descends from the AHA through a synaptic connection in the RVLM.

Animals↗
PubMed1993

Coronary vascular response to the cerebral ischemia reflex.

Most centrally mediated sympathoexcitatory reflexes produce increases in arterial pressure, heart rate, and peripheral vascular resistance, including coronary vasoconstriction. Cerebral ischemia also causes large increases in arterial pressure and peripheral vasoconstriction but with modest or variable changes in heart rate. To examine the effect of cerebral ischemia on coronary vascular resistance, we produced cerebral ischemia in 14 cats by occluding the right brachiocephalic and left subclavian arteries for 30 seconds. After vagotomy and beta-blockade, a marked increase in arterial pressure (89 +/- 14%) and coronary vascular resistance (52 +/- 7%) was seen. After inhibition of the carotid baroreceptor reflex by surgical denervation and application of topical lidocaine, the increase in arterial pressure to cerebral ischemia was not affected, but the increase in coronary vascular resistance was attenuated (33 +/- 6%; p < 0.05 versus before denervation) to a level expected with autoregulation. To evaluate the possible contribution of the chemoreflex on coronary blood flow during cerebral ischemia, we conducted separate experiments in which nicotine was injected into both carotid arteries. Coronary constriction was not observed. Adrenalectomy and upper extremity ischemia likewise did not alter coronary vascular resistance. We conclude that cerebral ischemia elicits neurally mediated coronary vasoconstriction as a result of baroreceptor hypotension rather than directly. The relative absence of neurogenic coronary constriction and changes in heart rate suggest that sympathoexcitation during cerebral ischemia is directed more toward the peripheral vasculature than the heart.

Adrenalectomy↗
PubMed1992

Prediction of immediate ventricular arrhythmias after coronary artery ligation.

OBJECTIVES: Our aim was to test the hypothesis that increased beat to beat morphologic variations in the body surface electrocardiogram (ECG) are associated with fragmented diastolic electrical activity that appears after coronary artery ligation and to correlate the appearance of spontaneous ventricular fibrillation after coronary ligation with the magnitude of the ECG beat to beat variability. BACKGROUND: Unstable and variably delayed electrical activation precedes the development of ventricular fibrillation in dogs with acute ischemia. Detection of these highly variable low amplitude signals from the body surface is currently impossible. We have developed a system designed to measure the degree of beat to beat variability of the ECG. METHODS: With high fidelity electrocardiography, subtle beat to beat ECG morphologic variations were detected in epicardial and body surface electrograms and quantified as the variance of the ECG voltage at specific points of the cardiac cycle. The ratio of the variance at the QRS offset to that of the QRS onset (beat to beat variability index) was then calculated. RESULTS: Ventricular fibrillation developed in 12 of 27 dogs after left anterior descending coronary artery ligation. In 7 of the 12 dogs it occurred immediately (< 15 min) after ligation; in the other 5 it developed late (> 15 min) after ligation. Dogs with subsequently immediate ventricular fibrillation had a significantly higher beat to beat variability index than that of dogs with late or no ventricular fibrillation both before coronary ligation (4.7 +/- 1.4 vs. 1.1 +/- 0.2 and 0.8 +/- 0.1, respectively, p < 0.001) and after ligation (6.4 +/- 2.6, 1.0 +/- 0.6 and 1.2 +/- 0.6, respectively, p < 0.001). In dogs that developed ventricular fibrillation immediately after coronary ligation, the arrhythmia was preceded by fragmented diastolic electrical activity on the epicardial electrogram and a simultaneous increase in the beat to beat morphologic variability of the terminal portion of the body surface ECG QRS complex. CONCLUSIONS: Beat to beat QRS offset morphologic variations appear to be increased before and further increased after coronary artery ligation in dogs that develop ventricular fibrillation immediately after ligation. Increased beat to beat variability index may be associated with the presence of electrophysiologic instability and can predict early ventricular fibrillation.

Analysis of Variance↗
PubMed1992

Patterns of hemodynamic responses associated with central activation of coronary vasoconstriction.

Previous studies in our laboratory have identified several central sites from which coronary vasoconstriction can be elicited by electrical stimulation. The present study was conducted to determine if specific patterns of hemodynamic responses are associated with activation of the coronary vasoconstrictor pathway in the hypothalamus, pons, and medulla. Cats anesthetized with chloralose were instrumented for recording arterial pressure, heart rate, and coronary, femoral, renal, and mesenteric blood flow velocities. After vagotomy and atenolol (1 mg/kg iv), anterior hypothalamus (AHA), parabrachial nucleus (PBN), a site very close to the ventral surface of the pons lateral to the pyramidal tract, and rostral ventrolateral medulla (RVLM) were stimulated electrically. Stimulation produced a decrease in coronary blood flow that was associated with all of the cardiovascular components of the defense reaction, an integrated response that included a decrease in hindquarter vascular resistance (blocked by methyl atropine), increases in renal and mesenteric vascular resistances, and a pressor response, except no change in renal vascular resistance from RVLM. Different patterns of hemodynamic responses were obtained from sites outside the coronary vasoconstrictor areas. From these results we conclude that coronary vasoconstriction is a frequent component of the defense reaction.

Animals↗
PubMed1992

Effect of brief myocardial ischemia on sympathetic coronary vasoconstriction.

The purpose of the present study was to determine whether sympathetic coronary vasoconstrictor responses are altered after brief ischemia and reperfusion. Adult mongrel dogs were anesthetized and instrumented for measurements of heart rate, arterial pressure, left ventricular pressure, left ventricular dP/dt, anterior myocardial wall thickening, and left circumflex coronary artery (LCX) and left anterior descending coronary artery (LAD) blood flow velocities. Changes in coronary vascular resistance were recorded during intravenous bolus doses of norepinephrine and bilateral electrical stimulation of the stellate ganglia. After beta-adrenergic blockade and bilateral vagotomy, electrical stimulation of the stellate ganglia increased coronary vascular resistance in the LAD and LCX beds by 38 +/- 5% and 39 +/- 5%, respectively. After a 15-minute LAD occlusion, repeat electrical stimulation produced increases in coronary resistance of 16 +/- 3% and 45 +/- 8%, respectively (p less than 0.05 for the LAD before versus after the occlusion). The peak increase in coronary vascular resistance to two doses of norepinephrine was unchanged. After a shorter period of myocardial ischemia (7 minutes), similar increase in coronary resistance to stellate stimulation were observed before (27 +/- 4%) and after (26 +/- 6%) myocardial ischemia. The mechanism of this impaired sympathetic coronary vasoconstriction was further tested by examining the responses to bretylium and tyramine. Brief ischemia did not alter the coronary constrictor responses to either bretylium or tyramine, suggesting that mechanisms governing prejunctional release of norepinephrine are intact in the postischemic coronary arterial bed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Role of medullary lateral reticular formation in baroreflex coronary vasoconstriction.

We have recently identified a polysynaptic pathway traversing discrete regions of the hypothalamus, midbrain, and medulla, along which site-specific electrical and chemical activation produces coronary vasoconstriction as part of a sympathoexcitatory response. We tested for the potential functional significance of this pathway by examining the hypothesis that a medullary component is involved in carotid baroreflex induced coronary vasoconstriction. Coronary flow velocity was measured with a Doppler probe in anesthetized cats. Following vagotomy and propranolol, bilateral carotid occlusion produced an increase in mean arterial pressure (56 +/- 14%, means +/- S.E.M.) and in coronary vascular resistance (51 +/- 13%) which was greater than that (29 +/- 6%) expected from the concurrent rise in arterial pressure during aortic constriction. Bilateral microinjections of lidocaine into the medullary lateral reticular formation attenuated the reflex increase in pressure (11 +/- 2%) and virtually abolished the rise (8 +/- 2%) in coronary resistance. After one hour recovery, carotid occlusion again increased aortic pressure (56 +/- 13%) and coronary vascular resistance (47 +/- 15%). Microinjections of lidocaine outside this medullary region did not impair the coronary vasoconstrictor response to carotid occlusion. We conclude that the medullary lateral reticular formation contains neural elements which participate in baroreflex-induced changes in arterial pressure and coronary vascular resistance. Components of the previously described central coronary vasoconstrictor pathway may play a role in pathophysiological conditions associated with increased coronary vasomotor tone.

Animals↗
PubMed1991

Activation in the region of parabrachial nucleus elicits neurogenically mediated coronary vasoconstriction.

A role for parabrachial nucleus in cardiovascular regulation is suggested by evidence that electrical stimulation in this region elicits increase in heart rate and arterial pressure. We hypothesized that parabrachial nucleus may also be involved in control of coronary vasomotor tone. After beta-adrenergic receptor blockade in anesthetized cats, electrical stimulation in the region of parabrachial nucleus produced no change in heart rate, an increase in arterial pressure (34 +/- 6 mmHg), and a transient reduction in coronary blood flow velocity (-21 +/- 2%). Coronary resistance (72 +/- 9%) and femoral resistance (189 +/- 31%) increased markedly. The decrease in coronary blood flow velocity was abolished by stellate ganglionectomy or alpha 1-adrenergic blockade without altering pressor or femoral responses. Injection of the neurotransmitter L-glutamate or kainic acid into parabrachial nucleus also elicited coronary vasoconstriction. We conclude that electrical or chemical activation in the region of parabrachial nucleus elicits coronary vasoconstriction as part of a generalized sympathetic activation. The fact that the coronary response is elicited by chemical activation suggests that cell bodies in the region of medial parabrachial nucleus and subceruleus, as opposed to fibers of passage, are involved in this central neural coronary vasoconstriction.

Animals↗