scholarly journals CIRCULATORY EFFECTS OF PROSTAGLANDIN ENDOPEROXIDE ANALOGUES STUDIED IN THE DOG DURING LEFT VENTRICULAR BYPASS

1977 ◽  
Vol 61 (3) ◽  
pp. 395-398 ◽  
Author(s):  
I. ALTER ◽  
P.A. KOT ◽  
P.W. RAMWELL ◽  
J.C. ROSE ◽  
M.R. SHNIDER
Keyword(s):  
Left Ventricular ◽  
Prostaglandin Endoperoxide ◽  
Circulatory Effects

Responses to continuous negative-pressure breathing in man at rest and during exercise

1980 ◽  
Vol 48 (6) ◽  
pp. 977-981 ◽  
Author(s):  
H. Bjurstedt ◽  
G. Rosenhamer ◽  
C. M. Hesser ◽  
B. Lindborg
Keyword(s):  
Negative Pressure ◽  
Venous Pressure ◽  
Intrathoracic Pressure ◽  
Carbon Dioxide Tension ◽  
Minute Volume ◽  
Left Ventricular ◽  
Circulatory Effects ◽  
Ventricular Afterload ◽  
Negative Pressure Breathing ◽  
The Right

We studied the respiratory and circulatory effects in six healthy supine volunteers of continuous negative-pressure breathing (CNPB) at -15 and -30 cmH2O at rest and during dynamic leg exercies at 50% of individual working capacity. CNPB had no significant effects on respiratory minute volume, tidal volume, or arterial carbon dioxide tension. Mean arterial pressure remained essentially unchanged both at rest and during exercise, signifying that the reductions in intrathoracic pressure caused corresponding increases in left ventricular afterload. Nevertheless, cardiac output increased significantly in both conditions, causing reductions of mean central venous pressure that were considerably greater during exercise than at rest. These responses were reflected by increments in left ventricular work, amounting to 24 and 20% at rest and during exercise, respectively, at -30 cmH2O. We conclude that in CNPB at rest the increased activity of the left ventricle with associated juxtathoracic venous collapse protects the right heart and pulmonary circulation from congestion and that it does so even more effectively during exercise.

Nitric oxide synthase inhibition reduces venous return in porcine endotoxemia

1996 ◽  
Vol 271 (4) ◽  
pp. H1325-H1332 ◽  
Author(s):  
T. Saetre ◽  
O. A. Smiseth ◽  
T. Scholz ◽  
H. Carlsen ◽  
L. Nordsletten ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Return ◽  
Left Ventricular ◽  
Saline Infusion ◽  
Endotoxin Infusion ◽  
Circulatory Effects ◽  
Oxide Synthase

Mechanisms of circulatory effects induced by nitric oxide synthase inhibition in endotoxemia were investigated in 36 pigs randomized to 1) endotoxin infusion (1.7 micrograms.kg-1.h-1 iv) for 7 h and bolus NG-nitro-L-arginine methyl ester (L-NAME; 25 mg/kg iv) after 3 h; 2) endotoxin infusion for 7 h; 3) saline infusion for 7 h and L-NAME after 3 h; and 4) saline infusion for 7 h. Fifteen minutes after L-NAME injection during endotoxemia, reductions in cardiac output (41%, P < 0.05), portal venous flow (51%, P < 0.05), and hepatic artery flow (50%, P < 0.05) were observed. Systemic vascular resistance increased by 82% (P < 0.05), and the portocaval vascular resistance increased by 101% (P < 0.05). Despite marked vasoconstriction after L-NAME, left ventricular intracavitary filling pressure, central venous pressure, and arterial pressure remained unchanged. During endotoxemia, hematocrit increased from 38.4 +/- 1.4 to 41.9 +/- 1.2 after L-NAME, and blood volume (n = 3) was reduced by an average of 8.3 ml/kg body wt. These changes probably reflect transcapillary fluid loss as urine output was unchanged. In conclusion, L-NAME decreased intravascular blood volume and increased splanchnic venous resistance. These effects will tend to reduce venous return. Combined with a marked increase in left ventricular after-load, L-NAME may thus compromise cardiovascular function in endotoxemia.

Chronic arteriovenous shunt: evaluation of a model for heart failure in rat

1979 ◽  
Vol 236 (5) ◽  
pp. H698-H704 ◽  
Author(s):  
S. F. Flaim ◽  
W. J. Minteer ◽  
S. H. Nellis ◽  
D. P. Clark
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Plasma Catecholamine ◽  
Sprague Dawley ◽  
Blood Flows ◽  
Aortocaval Shunt ◽  
Circulatory Effects ◽  
High Output Heart Failure ◽  
Postsurgical Recovery

A model for high output heart failure (HCO) was developed in male, Sprague-Dawley rats using an abdominal aortocaval shunt equal to 50% of total cardiac output (CO) with 2 mo of postsurgical recovery. The model was evaluated by analysis of hemodynamics, peripheral blood flows (BF) (radioactive microspheres), and plasma catecholamine levels as well as mass and fluid content of organs. In HCO, CO and left ventricular end-diastolic pressure were increased with significant left and right ventricular hypertrophy. Mean blood pressure (BP) was unchanged, but pulse BP was increased in HCO. BF to skeletal muscle, cutaneous, and some splanchnic regions was reduced to HCO, whereas BF to the cerebral, coronary, and renal beds was protected. Plasma epinephrine and norepinephrine levels were significantly elevated in HCO suggesting enhanced sympathetic as well as adrenal catecholamine release. Tissue analysis indicated altered circulatory status secondary to HCO in liver, kidney, spleen, and lung. The results indicate that this model will be a relevant tool for studies of the circulatory effects of heart failure.

Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

1968 ◽  
Vol 26 ◽  
pp. 126-127
Author(s):  
George Hug ◽  
William K. Schubert
Keyword(s):  
Heart Failure ◽  
Biochemical Analysis ◽  
Left Ventricular ◽  
Size Number ◽  
Internal Structures ◽  
Left Ventricular Outflow ◽  
Chest X Ray ◽  
Myocardial Fibers ◽  
Muscle Biopsies ◽  
Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

Intracellular EDEMA does not adversely affect the ability to cryopreserve intact hearts

1993 ◽  
Vol 51 ◽  
pp. 278-279
Author(s):  
CL Hastings ◽  
RD Carlton ◽  
FG Lightfoot ◽  
AF Tryka
Keyword(s):  
Cell Injury ◽  
Median Sternotomy ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Hypoxic Cell ◽  
Free Wall ◽  
Sprague Dawley ◽  
Left Ventricular Free Wall ◽  
Sprague Dawley Rats

The earliest ultrastructural manifestation of hypoxic cell injury is the presence of intracellular edema. Does this intracellular edema affect the ability to cryopreserve intact myocardium? To answer this guestion, a model for anoxia induced intracellular edema (IE) was designed based on clinical intraoperative myocardial preservation protocol. The aortas of 250 gm male Sprague-Dawley rats were cannulated and a retrograde flush of Plegisol at 8°C was infused over 90 sec. The hearts were excised and placed in a 28°C bath of Lactated Ringers for 1 h. The left ventricular free wall was then sliced and the myocardium was slam frozen. Control rats (C) were anesthetized, the hearts approached by median sternotomy, and the left ventricular free wall frozen in situ immediately after slicing. The slam frozen samples were obtained utilizing the DDK PS1000, which was precooled to -185°C in liguid nitrogen. The tissue was in contact with the metal mirror for a dwell time of 20 sec, and stored in liguid nitrogen until freeze dry processing (Lightfoot, 1990).

Ultrastructural observations of the aorta of calves implanted with a mechanical left ventricular assist device

1990 ◽  
Vol 48 (3) ◽  
pp. 834-835
Author(s):  
J P Cassella ◽  
V Salih ◽  
T R Graham
Keyword(s):  
Left Ventricular Assist Device ◽  
Ventricular Assist Device ◽  
Left Ventricular ◽  
Aortic Tissue ◽  
Assist Device ◽  
Ventricular Assist ◽  
Transmission Electron ◽  
Left Ventricular Assist ◽  
Preliminary Study

Left ventricular assist systems are being developed for eventual long term or permanent implantation as an alternative to heart transplantation in patients unsuitable for or denied the transplant option. Evaluation of the effects of these devices upon normal physiology is required. A preliminary study was conducted to evaluate the morphology of aortic tissue from calves implanted with a pneumatic Left Ventricular Assist device-LVAD. Two 3 month old heifer calves (calf 1 and calf 2) were electively explanted after 128 days and 47 days respectively. Descending thoracic aortic tissue from both animals was removed immediately post mortem and placed into karnovsky’s fixative. The tissue was subsequently processed for transmission electron microscopy (TEM). Some aortic tissue was fixed in neutral buffered formalin and processed for routine light microscopy.

Left Ventricular Hypertrophy

2014 ◽  
Vol 19 (2) ◽  
pp. 11-15
Author(s):  
Steven L. Demeter
Keyword(s):  
Risk Factors ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Mass Index ◽  
Medical Science ◽  
Careful Analysis ◽  
Left Ventricular ◽  
Hypertensive Disease ◽  
Accurate Analysis ◽  
Clear Explanation

Abstract The fourth, fifth, and sixth editions of the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) use left ventricular hypertrophy (LVH) as a variable to determine impairment caused by hypertensive disease. The issue of LVH, as assessed echocardiographically, is a prime example of medical science being at odds with legal jurisprudence. Some legislatures have allowed any cause of LVH in a hypertensive individual to be an allowed manifestation of hypertensive changes. This situation has arisen because a physician can never say that no component of LVH was not caused by the hypertension, even in an individual with a cardiomyopathy or valvular disorder. This article recommends that evaluators consider three points: if the cause of the LVH is hypertension, is the examinee at maximum medical improvement; is the LVH caused by hypertension or another factor; and, if apportionment is allowed, then a careful analysis of the risk factors for other disorders associated with LVH is necessary. The left ventricular mass index should be present in the echocardiogram report and can guide the interpretation of the alleged LVH; if not present, it should be requested because it facilitates a more accurate analysis. Further, if the cause of the LVH is more likely independent of the hypertension, then careful reasoning and an explanation should be included in the impairment report. If hypertension is only a partial cause, a reasoned analysis and clear explanation of the apportionment are required.

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