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PubMed1991

Responses to renin inhibition in conscious primates.

A method for the measurement of renal clearances was adapted in a novel manner to the conscious marmoset. Twenty-four hours before an experiment, animals underwent surgery for placement of both femoral arterial and venous catheters. A catheter was also implanted into the urinary bladder through the abdominal wall. The urinary catheter consisted of two tubes. One tube was connected to a pump, which removed the urine, while the other tube remained open to prevent the formation of a vacuum inside the bladder. Using this technique, we kept renal clearances stable for at least 3 h. All catheters were removed the day after the clearance experiment, and the bladder was reconstructed using microsurgical techniques. The bladder operation did not appear to produce lasting anatomical or functional changes, since the animals were able to void spontaneously and, after 3 mo, the bladder had regained its normal size and shape. Reimplantation of both the vessel and bladder catheters at this time allowed for an additional study of renal clearances within the same animals. Administration of the renin inhibitor CGP 29287 (1 mg/kg) to furosemide-pretreated conscious marmosets lowered blood pressure and increased renal blood flow. Glomerular filtration rate remained unchanged by CGP 29287, leading to a fall in the effective filtration fraction. Urinary volume and urinary sodium excretion also were unchanged by the renin inhibitor. We describe a novel method for the study of renal clearances in a small conscious primate and suggest that the renin-angiotensin system plays an important role in the control of renal function in the sodium-depleted marmoset.

Animals↗
PubMed1991

Renal blood flow response to angiotensin II infusions in conscious pregnant rabbits.

Renal blood flow (RBF) was measured in conscious rabbits while nonpregnant and during pregnancy using chronically implanted ultrasonic transit-time flow probes. The effects of the cyclooxygenase inhibitor meclofenamate (5 mg/kg) and the angiotensin-converting-enzyme inhibitor captopril (5 mg/kg) on basal RBF and on RBF responses to systemic angiotensin II infusions (2.5-80 ng.kg-1.min-1) were determined. Basal RBF declined (P less than 0.001 to P less than 0.005) with meclofenamate by 9-16% in pregnant (n = 7) and by 10% in nonpregnant (n = 7) rabbits. Captopril increased (P less than 0.05 to P less than 0.01) RBF by 9-11% in pregnant (n = 5) and by 12% in nonpregnant (n = 5) rabbits. There was no effect of the vehicle (normal saline) on RBF. The reduction in RBF (% from baseline) in response to infused angiotensin II was attenuated in pregnant compared with nonpregnant rabbits. Pretreatment with meclofenamate enhanced the renal vasoconstrictor action of angiotensin II in a similar fashion in both pregnant and nonpregnant rabbits. Captopril or saline did not alter the RBF responses to angiotensin II infusions. Mean arterial pressure was lower in pregnant (78 +/- 3 mmHg, n = 7) vs. nonpregnant (88 +/- 5 mmHg, n = 10) rabbits, suggesting lower total peripheral resistance. The data indicate 1) chronically implanted ultrasonic flow probes can be an effective tool for monitoring RBF in conscious rabbits, 2) prostaglandins and the renin-angiotensin system influence basal RBF in conscious rabbits, and 3) the renal vasoconstrictor effect of angiotensin II is blunted in pregnant rabbits and this attenuated response appears to be independent of prostaglandins.

Angiotensin II↗
PubMed1993

Assessment of changes in intrarenal blood flow in conscious rats using laser-Doppler flowmetry.

The present study was designed to develop, for the first time, a method that allows long-term repeated measurements of renal cortical blood flow (CBF) and medullary blood flow (MBF) in conscious unanesthetized rats. The use of fiber-optic probes (0.5 mm diam) for the chronic measurement of renal CBF and MBF was evaluated. Basal renal cortical and medullary laser-Doppler flow (LDF) signals and the responses to intravenous bolus injections of angiotensin II (ANG II, 12.5 ng) were determined every other day for 11 days in conscious Sprague-Dawley rats (n = 9). A recovery period of 5-7 days after surgery was required before stable signals were obtained from the implanted probes. Thereafter, the fiber-optic probes gave reproducible laser-Doppler measurements of CBF and MBF for 11 days. The CBF and MBF responses to intravenous bolus injections of ANG II (12.5 ng) were also constant during this period. Chronic implantation of the fiber-optic probes caused minimal tissue damage and did not significantly alter urine concentrating ability or renal function. These findings suggest that LDF technique with chronically implanted optical fibers provides a new tool for the continuous long-term monitoring of regional blood flow in the kidney of conscious rats.

Angiotensin II↗
PubMed1986

Pulmonary vascular responses to angiotensin II and captopril in conscious dogs.

Our objectives were to investigate the extent to which angiotensin II (ANG II) and converting-enzyme inhibition (CEI) exert a direct vasoactive influence on the pulmonary circulation of conscious dogs. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were constructed during normoxia in conscious dogs by stepwise constriction of the thoracic inferior vena cava to reduce Q. The effects of ANG II infusion (60 ng X kg-1 X min-1, iv) and CEI with captopril (1 mg/kg plus 1 mg X kg-1 X h-1, iv) on pulmonary vascular P/Q plots were assessed first with the conscious dogs intact and again after combined administration of pharmacological antagonists to block sympathetic alpha- and beta-adrenergic, cholinergic, and arginine vasopressin receptors. In intact dogs, ANG II increased (P less than 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure, PAP-PCWP) over the entire range of Q studied (60-120 ml X min-1 X kg-1). Conversely, CEI decreased (P less than 0.05) PAP-PCWP at each level of Q. After administration of the autonomic nervous system and arginine vasopressin receptor antagonists, ANG II again increased (P less than 0.01) and CEI decreased (P less than 0.01) PAP-PCWP over the entire range of Q studied. Thus exogenous administration of ANG II results in active, nonflow-dependent constriction of the pulmonary circulation, and this effect is not dependent on the autonomic nervous system or increased circulating levels of arginine vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1988

Absence of neural modulation of hypoxic pulmonary vasoconstriction in conscious dogs.

Our objectives were 1) to quantify the magnitude of the hypoxic pulmonary vasoconstrictor (HPV) response in conscious dogs by utilizing pulmonary vascular pressure-cardiac index (P/Q) plots and 2) to assess the extent to which the autonomic nervous system (ANS) modulates the HPV response. Multipoint P/Q plots were constructed in conscious dogs during normoxia and during bilateral alveolar hypoxia by stepwise constriction of the thoracic inferior vena cava to reduce Q. With the ANS intact, the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure) increased (P less than 0.01) approximately twofold during hypoxia over a broad range of Q. The absolute magnitude of the HPV response was related (P less than 0.01) to the level of Q. We hypothesized that if ANS activation reduces the magnitude of HPV in intact dogs, then we would expect the magnitude of HPV to be increased both after combined sympathetic alpha-(phentolamine) and beta-(propranolol) adrenergic block and after total autonomic ganglionic block (hexamethonium). A marked HPV response (P less than 0.01) was observed after both combined sympathetic block and ganglionic block over a broad range of Q during alveolar hypoxia. The magnitude of the HPV response with the ANS intact, however, was not significantly different from the magnitude of HPV after combined sympathetic block (P = 0.45) or after ganglionic block (P = 0.64) at any level of Q. Thus, during bilateral alveolar hypoxia, the ANS does not appear to attenuate the HPV response of intact conscious dogs.

Animals↗
PubMed1993

Lymphatic drainage of hypertonic solution from peritoneal cavity of anesthetized and conscious sheep.

Lymphatic drainage of the peritoneal cavity may reduce ultrafiltration in continuous ambulatory peritoneal dialysis. We assessed lymphatic drainage of the peritoneal cavity in sheep under dialysis conditions by cannulation of the relevant lymphatic vessels and compared lymphatic drainage in anesthetized and conscious animals. Lymph was collected from the caudal mediastinal lymph node and the thoracic duct, both of which are involved in the lymphatic drainage of the ovine peritoneal cavity. Volumes of a hypertonic dialysis solution (50 ml/kg 4.25% Dianeal) containing 25 microCi 125I-human serum albumin were instilled into the peritoneal cavity, and lymph flows and the appearance of labeled protein in the lymphatic and vascular compartments were monitored for 6 h. Intraperitoneal pressures increased 4-5 cmH2O above resting levels after infusion of dialysate. On the basis of the appearance of tracer in the lymph, drainage of peritoneal fluid into the caudal lymphatic was calculated to be 3.09 +/- 0.69 and 14.14 +/- 2.86 ml/h in anesthetized and conscious sheep, respectively. Drainage of peritoneal fluid into the thoracic duct preparations was calculated to be 1.32 +/- 0.33 and 14.69 +/- 5.73 ml/h in anesthetized and conscious sheep, respectively. Significant radioactivity was found in the bloodstream, and at least a portion of this was likely contributed by the right lymph duct, which was not cannulated in our experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1993

Pulmonary vascular beta-adrenoreceptor activity in conscious dogs after left lung autotransplantation.

Our objective was to determine whether chronic denervation associated with left lung autotransplantation (LLA) results in an alteration in sympathetic beta-adrenoreceptor regulation of the pulmonary circulation in conscious dogs. Continuous left pulmonary vascular pressure-flow (LPQ) plots were generated in conscious dogs 2-4 wk post-LLA and in sham-operated control conscious dogs. We tested the hypothesis that endogenous sympathetic beta-adrenoreceptor activation via circulating catecholamines acted to attenuate the chronic increase in pulmonary vascular resistance post-LLA. Administration of the sympathetic beta-adrenoreceptor antagonist propranolol had no significant effect on the LPQ relationship post-LLA. We also tested the hypothesis that pulmonary vascular reactivity to sympathetic beta-adrenoreceptor activation would be increased post-LLA. The thromboxane analogue U-46619 was used to acutely preconstrict (P < 0.01) the pulmonary circulation in control dogs; this preconstriction shifted the LPQ relationship to the same position measured post-LLA. Under these conditions, cumulative doses of the beta-adrenoreceptor agonist isoproterenol caused pulmonary vasodilation (P < 0.01) in the control group but had no effect post-LLA. However, after acute preconstriction with U-46619, the pulmonary vasodilator response (P < 0.01) to isoproterenol post-LLA was not significantly different from that in the control group. These differential responses to isoproterenol with and without acute preconstriction indicate that a significant component of the chronic increase in pulmonary vascular resistance post-LLA is mediated by passive nonvasoactive mechanisms. Moreover, sympathetic beta-adrenoreceptor reactivity of the pulmonary circulation is not enhanced by chronic denervation resulting from the LLA procedure.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Neurohumoral regulation of the pulmonary circulation during circulatory hypotension in conscious dogs.

We investigated the effects of circulatory hypotension (HYPO) on the left pulmonary vascular pressure-flow relationship in chronically instrumented conscious dogs and the role of five neurohumoral mechanisms in either mediating or modulating the response to this stimulus. HYPO was induced by acute (approximately 15-min) inflation of a hydraulic occluder implanted around the thoracic inferior vena cava, which decreased systemic arterial pressure to approximately 55 mmHg. HYPO resulted in active pulmonary vasoconstriction (53-66%; P < 0.01) in intact conscious dogs. Sympathetic alpha 1-adrenoreceptor block reduced (P < 0.01) the magnitude of HYPO-induced pulmonary vasoconstriction by 91-99%. Neither sympathetic beta-adrenoreceptor block nor cholinergic muscarinic receptor block had any significant effect on the magnitude of HYPO-induced pulmonary vasoconstriction. Surprisingly, angiotensin II receptor block increased (P < 0.05) HYPO-induced pulmonary vasoconstriction by 69-91%. In contrast, arginine vasopressin V1-receptor block reduced (P < 0.05) HYPO-induced pulmonary vasoconstriction by 34-41%. These results indicate that the pulmonary circulation of intact conscious dogs is actively regulated by three distinct neurohumoral mechanisms during HYPO. Sympathetic alpha 1-adrenoreceptor activation is the primary mediator of HYPO-induced pulmonary vasoconstriction. Angiotensin II and arginine vasopressin exert opposing pulmonary vasodilator and vasoconstrictor effects during HYPO, whereas sympathetic beta-adrenoreceptor and cholinergic muscarinic receptor activation do not appear to modulate the pulmonary vascular response to HYPO.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1994

Humoral pulmonary vasoregulation in conscious dogs after left lung autotransplantation.

We investigated the roles of cyclooxygenase metabolites, arginine vasopressin (AVP) and angiotensin II (ANG II), as mediators of the chronic increase in pulmonary vascular resistance associated with left lung autotransplantation (LLA) in conscious dogs. Continuous left pulmonary vascular pressure-flow (LP-Q) plots were generated in conscious dogs 2- to 5-wk post-LLA and in sham-operated control conscious dogs. LLA resulted in a marked shift (P < 0.01) in the LP-Q relationship as reflected by an approximate doubling of the pulmonary vascular pressure gradient at each common value of left pulmonary blood flow compared with the control group. Cyclooxygenase pathway inhibition (indomethacin) and AVP V1-receptor block had no effect on the LP-Q relationship post-LLA. Angiotensin-converting enzyme inhibition (captopril) also failed to reverse the increase in pulmonary vascular resistance post-LLA. Because captopril has the dual effect of inhibiting the production of ANG II and the degradation of bradykinin, additional studies utilizing a selective ANG II receptor antagonist were performed. ANG II receptor block (saralasin) significantly altered the LP-Q relationship post-LLA to cause active pulmonary vasodilation (P < 0.01). Thus, the chronic increase in pulmonary vascular resistance post-LLA is not mediated by metabolites of the cyclooxygenase pathway or AVP V1-receptor activation. A significant component of the increase in pulmonary vascular resistance resulting from LLA is mediated by ANG II. The differential responses to captopril and saralasin may imply a pulmonary vasoregulatory role for bradykinin post-LLA.

Animals↗
PubMed1986

Characteristics of the receptors which mediate the stimulation of ACTH secretion by vasopressin in conscious dogs.

In order to characterize the receptors which mediate the adrenocorticotropic hormone (ACTH) response to vasopressin in conscious animals, plasma 11-hydroxycorticosteroid concentration was measured in conscious dogs during the infusion of vasopressin or structural analogs of vasopressin which exhibit selective antidiuretic or vasoconstrictor activity. Vasopressin (1.0 ng/kg/min for 60 min) increased mean arterial pressure, decreased heart rate and increased plasma corticosteroid concentration from 1.0 +/- 0.2 to 2.2 +/- 0.2 micrograms/dl (p less than 0.001). A specific antagonist of the vasoconstrictor activity of vasopressin, d(CH2)5MeTyrAVP (10 micrograms/kg), completely blocked the cardiovascular and corticosteroid responses to vasopressin. A selective vasoconstrictor (V1) agonist, PheOrnOT (1.0 ng/kg/min), which produced the same cardiovascular responses as vasopressin, increased plasma corticosteroid concentration from 1.1 +/- 0.1 to 2.9 +/- 0.9 micrograms/dl (p less than 0.005). In marked contrast, a selective antidiuretic (V2) agonist, dDAVP (1.0 ng/kg/min) had no effect on blood pressure, heart rate or plasma corticosteroid concentration. These results indicate that the stimulation of ACTH release by vasopressin in conscious dogs is mediated by receptors which resemble vasoconstrictor-type (V1) receptors rather than antidiuretic-type (V2) receptors.

Adrenal Cortex Hormones↗
PubMed1995

Selective impairment of vagally mediated, nitric oxide-dependent coronary vasodilation in conscious dogs after pacing-induced heart failure.

BACKGROUND: Activation in conscious dogs of the carotid chemoreflex or cardiac receptors results in coronary vasodilation that is mediated by a vagal cholinergic mechanism. Our previous study showed that the coronary vasodilation following activation of carotid chemoreflex is also mediated by nitric oxide (NO). In addition, NO production is depressed after the development of heart failure. Therefore, we hypothesized that the coronary vasodilation after activation of reflexes that elicit efferent vagal coronary vasodilation would be blunted in conscious dogs after pacing-induced heart failure due to the disappearance of NO. METHODS AND RESULTS: Mongrel dogs were chronically instrumented using sterile techniques for measurements of systemic hemodynamics and left circumflex coronary blood flow (CBF). Without the heart rate controlled, intra-atrial injection of veratrine (4 micrograms/kg) caused bradycardia (-36 +/- 3 beats per minute). With the heart rate controlled, veratrine increased CBF in a dose-dependent manner: for example, 4 micrograms/kg of veratrine increased CBF by 54 +/- 5% from 38 +/- 4.9 mL/min (P < .05). The increases in CBF induced by veratrine were markedly blunted by nitro-L-arginine (NLA). Activation of carotid chemoreflex by nicotine increased CBF by 121 +/- 9% from 32 +/- 4 mL++/min (P < .05) with the heart rate controlled and caused bradycardia (-32 +/- 5 beats per minute) without the heart rate controlled. After the development of heart failure, in response to activation of carotid chemoreflex or cardiac receptors the coronary vasodilation was almost abolished (CBF increased by only 23 +/- 8% or 11 +/- 3%, P < .05 compared with control). There still was a marked bradycardia after injections of nicotine or veratrine (-50 +/- 11 or -48 +/- 7 beats per minute). CONCLUSIONS: Our results indicate that vagally mediated coronary vasodilation is selectively attenuated in conscious dogs after pacing-induced heart failure, whereas the vagally mediated bradycardia is preserved. Since muscarinic receptor-induced coronary vasodilation is mediated by NO, the disappearance of NO from blood vessels leads to a defect in the integrated neural regulation of coronary blood flow and myocardial function during heart failure.

Acetylcholine↗
PubMed1997

Long-term follow-up of cardioverter-defibrillator implanted under conscious sedation in prepectoral subfascial position.

BACKGROUND: Implantable cardioverter-defibrillators (ICDs) with intravenous electrode systems and downsized generators can be implanted by use of operative techniques similar to those employed for the insertion of permanent pacemakers. However, the safety, efficacy, and long-term follow-up of simplified implantation procedures remain to be evaluated. This report is a prospective long-term evaluation of nonselected patients receiving ICDs in the prepectoral subfascial position under conscious sedation. METHODS AND RESULTS: Clinical characteristics of the 231 consecutive patients included a mean age of 63 years, a male-to-female ratio of 6.4, a left ventricular ejection fraction of 0.34, a mild-to-moderate heart failure in 91%, coronary artery disease in 84%, and a history of aborted sudden cardiac death or refractory ventricular tachyarrhythmias. Insertion of transvenous leads and prepectoral subfascial ICD implantation were performed in electrophysiology laboratories under local anesthesia and conscious sedation with intravenous midazolam and propofol. Successful implantation in all patients (operation time, 80 +/- 32 minutes, mean +/- SD) irrespective of body size and skin thickness was free of major complications, including need for emergency intubation. After surgery, 1 pocket hematoma, 1 seroma, and 1 pneumothorax required treatment. There was no operative or first-month mortality. During long-term follow-up averaging 453 +/- 296 days, six leads required repositioning, but pocket erosions or infections did not occur. First-year total survival was 97%. CONCLUSIONS: Implantation under conscious sedation of ICDs in the prepectoral subfascial position is a safe and effective procedure with low operative and postoperative morbidity and favorable long-term outcome.

Adolescent↗
PubMedDate not supplied

Blood pressure responses of conscious normotensive and spontaneously hypertensive rats to intracerebroventricular and peripheral administration of captopril.

In conscious spontaneously hypertensive rats, intraxerebroventricular injection of captopril (2 mg/kg) resulted in a rapid hypotensive response that lasted several hours. The same dose given by intracerebroventricular injection had no significant effect on blood pressure (BP) of normotensive Wistar-Kyoto (WK) rats over 7 hours. There was no significant change in BP of conscious spontaneously hpertensive rats (SHR) in response to intracerebroventricular injection of vehicle and only a transitory fall in BP in response to intravenous injection of captopril (2 mg/kg). There was no significant differences between plasma renin activity (PRA) of conscious normotensive WKY rats and the PRA of SHR. These results suggest biochemical differences between the brains of SHR and normotensive WKY control rats. These differences could involve the brain renin-angiotensin system or other neuropeptides.

Animals↗
PubMedDate not supplied

Direct versus indirect pressor and vasoconstrictor actions of angiotensin in conscious dogs.

To determine the importance of the direct and the indirect pressor and vasoconstrictor actions of angiotensin II (ANG II), experiments were conducted in conscious dogs 2 to 8 weeks after instrumentation with aortic catheters and aortic electromagnetic flow probes to measure arterial pressure and cardiac output. Total peripheral resistance was calculated by an on-line digital computer. Pretreatment with propranolol eliminated complicating inotropic effects of norepinephrine, released by the indirect actions of ANG II. The pressor and vasoconstrictor responses after ganglionic blockade, in either the presence or absence of arterial baroreceptor nerves, were considered to be the direct effects of ANG II. In conscious dogs, systemically administered ANG II (32 ng/kg bolus) increased mean arterial pressure by 38 +/- 3 mm Hg, total peripheral resistance by 37 +/- 2 mm Hg/L/minute, and decreased heart rate by 15 +/- 2 beats/minute. After arterial baroreceptor denervation, administration of ANG II increased mean arterial pressure by 88 +/- 7 mm Hg, total peripheral resistance by 54 +/- 4 mm Hg/L/minute, and heart rate by 12 +/- 2 beats/minute. After arterial baroreceptor denervation and ganglionic blockade with hexamethonium, administration of ANG II increased mean arterial pressure by 53 +/- 8 mm Hg, total peripheral resistance by 27 +/- 3 mm Hg/L/minute, and left heart rate unchanged. These results indicate that in the conscious dog without baroreflex buffering nearly one-half of the pressor and vasoconstrictor actions of angiotensin are not direct, but are mediated by the autonomic nervous system.

Angiotensin II↗
PubMed1975

Reduced baroreflex sensitivity with volume loading in conscious dogs.

The Bainbridge reflex, i.e., the effect of rapid saline infusion (1.1 +/- 0.1 liters) on heart rate and arterial and atrial blood pressures, was examined in 12 intact conscious dogs; mean arterial blood pressure rose by 33 +/- 3 (SE) mm Hg, mean atrial pressure by 14 +/- 1 mm Hg, and heart rate by 75 +/- 9 beats/min. After beta-receptor blockade, heart rate rose slightly less (+49 +/- 5 beats/min, P = 0.05). Cholinergic blockade, combined cholinergic and beta-receptor, or beta-receptor blockade after vagotomy blocked the heart rate response to the infusion. The rise in heart rate in the face of an increase in arterial blood pressure with volume loading suggested that the arterial baroreceptor reflex was not responding appropriately to the increase in arterial blood pressure. In conscious dogs after denervation of the arterial baroreceptors, the increase in heart rate with volume loading was no greater than that in those dogs with their arterial baroreceptors intact, suggesting that the baroreceptor reflex was not restraining heart rate in the normal response to volume loading. The relationship between the pulse interval (PI) and the systolic arterial blood pressure (SAP) following an intravenous injection of methoxamine was used to evaluate the sensitivity of the baroreceptor reflex in intact conscious dogs. After a mild amount of volume loading, when atrial pressure was 8 +/- 2 mm Hg, the PI/SAP slope was significantly depressed from normal. When atrial pressure was elevated further to 28 +/- 1 mm Hg by volume loading, the slope was further depressed. Thus, arterial baroreflex sensitivity is reduced progressively as atrial pressure is raised by volume loading, an observation that explains how heart rate can rise strikingly in the face of an elevated arterial blood pressure.

Animals↗
PubMed1976

Regional myocardial blood flow during acute myocardial infarction in the conscious dog.

Regional myocardial blood flow was studied in the conscious dog at periods of 5 minutes to 4 days after occlusion of a major branch of the left coronary artery. Dogs were instrumented with aortic electromagnetic flow probes, occlusive cuffs on either the anterior descending or circumflex branch of the left coronary artery, and a left atrial Silastic catheter for injection of microspheres (15 +/- 5 mum) labeled with either 85Sr, 141Ce, or 51Cr. Microspheres were injected into 25 fully conscious dogs during three of the following time periods: control preocclusion and 0.1, 2, 6, 24, or 96 hours postocclusion. In the conscious dog, before occlusion, the endocardial half of the left ventricular myocardium received 28% more blood flow than the epicardial half. After sudden occlusion of a coronary artery branch, there was a marked reduction in blood flow as well as an alteration in distribution of blood flow within the ischemic tissue; blood flow was most severly reduced in the subendocardial center of the ischemic region, less so in the epicardial ischemic region, and least reduced in the marginal region of the infarct. Blood flow was increased to the nonischemic tissue. There was no change in this pattern of reduced blood flow by 6 hours postocclusion, but by 24 hours, flow was moderately increased to all areas except the central subendocardial core, and was further increased at 96 hours. Blood flow to the endocardial half of the left ventricular myocardium averaged 63 ml/100 g per min during the control period, was reduced to 12-18 ml/100 g per min at 0.1-6 hours in the ischemic region, increased to 29 ml/100 g per min at 24 hours, and to 48 ml/100 g per min by 96 hours. These findings indicate that there is a reversal of the flow ratio within ischemic myocardium with relative under-perfusion of the endocardial half of the wall, which is not corrected by 4 days. There is a modest increase of collateral blood flow to ischemic tissue by 24 hours and this increase is considerably augmented by 96 hours, apparently as a result of the growth and enlargement of collateral vessels.

Acute Disease↗
PubMed1976

The three-dimensional dynamic geometry of the left ventricle in the conscious dog.

The dynamic geometry of the left ventricle was assessed with the use of chronically implanted pulse-transit ultrasonic dimension transducers. The orientation of the transducers allowed the measurement of left ventricular minor and major axis diameters and equatorial wall thickness in the conscious dog. The left ventricle was modeled as a three-dimensional, prolate ellipsoidal shell. Left ventricular and pleural pressures were measured with high fidelity micromanometers. Aortic blood flow was obtained with electromagnetic flow probes. To test the assumptions inherent in this technique, left ventricular mass, internal volume, stroke volume, and peak aortic flow were computed from the dimension data and compared to directly measured values. Correlation coefficients of 0.95 or greater were obtained for each of these comparisons. In addition, the calculated left ventricular mass was constant to within +/- 6% of the mean value throughout the cardiac cycle. We found that the dynamic contraction pattern of the left ventricle was dependent on the physiological state of the dog. Furthermore, in the conscious state, shortening of the minor axis diameter, lengthening of the major axis diameter, and slight thickening or thinning of the wall were noted during isovolumic contraction (isovolumic ellipticalization pattern). In the open-chested, anesthetized state, however, marked rearrangements in geometry were observed during isovolumic contraction manifested by lengthening of the minor axis diameter, and significant thickening of the wall (isovolumic sphericalization pattern). We also observed that left ventricular volume was significantly diminished in the open-chested state. The isovolumic contraction pattern in open-chested dogs could be changed from sphericalization to ellipticalization by increasing end-diastolic volume with the infusion of saline. During a vena caval occlusion in the conscious state, the contraction pattern changed from isovolumic ellipticalization to isovolumic sphericalization as the end-diastolic volume decreased. Thus, the exact pattern of left ventricular contraction was found to be a function of left ventricular volume.

Animals↗
PubMed1985

Failure of atriopeptin II to cause arterial vasodilation in the conscious rat.

The cardiovascular actions of the synthetic natriuretic peptide, atriopeptin II, were examined in conscious unrestrained spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. The animals were chronically instrumented with miniaturized pulsed Doppler flow probes to allow measurement of regional blood flow, or with an electromagnetic flow probe on the ascending aorta to facilitate the measurement of cardiac output in the conscious rat. Intravenous infusion of increasing doses of atriopeptin II (0.25-4 micrograms/kg per min) caused a dose-dependent fall in mean arterial pressure in the hypertensive and normotensive rats. Blood flow in the renal, mesenteric, and hindquarters vascular beds was markedly decreased during the infusion of atriopeptin II, and regional vascular resistance was significantly increased in both groups of rats. Heart rate was significantly elevated (47 +/- 14 beats/min) in the spontaneously hypertensive rats during atriopeptin II infusion, but no change in heart rate was observed in the Wistar rats. In the hypertensive rats, atriopeptin II caused a marked dose-dependent decrease in cardiac output (maximal decrease = -39 +/- 4%) and stroke volume (maximal decrease = -48 +/- 4%). Central venous pressure and left atrial pressure were also significantly reduced during atriopeptin II infusion. Total peripheral resistance was increased over the infusion protocol by 26 +/- 3%. These data suggest that atriopeptin II infusion markedly attenuated cardiac output in the conscious spontaneously hypertensive rats. Total and regional vascular resistances were increased, possibly through reflex compensatory mechanisms, to maintain arterial pressure in the face of decreased cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗