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At least 19 recordsLinked to original sources
PubMedDate not supplied

[Characteristics of the cardiotropic effect of gutimine].

Experiments proved gutimine capable of intensify the collateral coronary circulation, intraventricular pressure and the rate of its accretion (dp/dt), the excitability and permeability of the heart, as well as to raise the cardiac contractility in dogs during an acute period of myocardial ischemia. In rats with pituitrin-isadrine induced cardiopathy the drug drastically depressed the permeability of the histohematogenous barriers of the myocardium and lengthened somewhat the life span of the animals. Parallel with is rising doses gutimine depressed the excitability threshold of the frog's heart "in situ" in a test with a liminal current producing extrasystole.

Amidines↗
PubMed1979

Myocardial anaerobic metabolism during isoprenaline infusion in a cyanotic animal model: possible cause of myocardial dysfunction in cyanotic congential heart disease.

Mongrel dogs were made acutely cyanotic by anastomosis of the inferior vena cava to the left atrium and measurements of high fidelity left ventricular pressure, arterial pressure, blood gases, and myocardial lactate arteriovenous differences were determined before pacing, with atrial pacing at a rate of approximately 240 per minute, and during an infusion of isoprenaline to increase myocardial oxygen demands. The animals were divided into two groups on the basis of the arterial PO2 during isoprenaline: acyanotic or control dogs (n = 4, PO2 greater than or equal to 6.7 kPa [50 mmHg], mean = 52) and cyanotic dogs (n = 5, PO2 less than or equal to 4.7 kPa (35 mmHg), mean = 32). Myocardial lactate arterio-venous difference showed no significant changes in the control dogs with pacing or isoprenaline, but myocardial lactate production occurred in all five cyanotic dogs with isoprenaline infusion. These studies demonstrate that myocardial anaerobic metabolism can be produced during times of stress with isoprenaline infusion in a cyanotic animal model at systemic oxygen levels that can occur clinically.

Anaerobiosis↗
PubMed1976

Heat illness. II. Pathogenesis.

The effects of elevated temperatures and the time-temperature combinations for irreversible damage are outlined. Coagulation abnormalities and the effects on the kidney, liver, heart, brain and serum enzymes, the role of electrolytes and water, including salt deficiency and the controversial question of salt supplements, potassium deficiency, changes in other electrolytes and sweat solutes, and rhabdomyolysis (including a discussion of experimental work on dogs) are reviewed. The section ends with a discussion of the effects of drugs and an account of a recent fatal case of heat stroke which may have been triggered by chlorpromazine therapy.

Adolescent↗
PubMed2026

A Combination of Alleles in LMOD2 and a lncRNA is Strongly Associated With Myxomatous Mitral Valve Disease in Cavalier King Charles Spaniels.

A previous genome-wide association study identified regions on canine chromosome (cfa) 13 and 14 associated with early onset myxomatous mitral valve disease (MMVD) in Cavalier King Charles Spaniels (CKCS). In the present study, whole genome sequencing (WGS) of 9 CKCS cases (mitral regurgitation (MR) before 4.5 years or congestive heart failure (CHF) at any age due to MMVD) and 10 CKCS controls (no or mild MR after 8 years of age) identified > 2000 genetic variants in the MMVD associated cfa13 and cfa14 regions. Ensembl Variant Effect Predictor (VEP) identified a possible functional impact of 18 variants. These were genotyped in 250 CKCS; 117 cases and 133 controls. The most significantly associated variants were a splice-site variant in a long noncoding RNA (lncRNA) on cfa13, a nonsynonymous variant in HYAL4, a 39 base-pair insertion in LMOD2 and a synonymous variant in ENSCAFG00000024436 (p-values from 2.03E-08 to 4.20E-06). Concomitant homozygosity for risk alleles in LMOD2 and the lncRNA gave an odds-ratio for MMVD of 52.5 compared to homozygosity for the nonrisk alleles (p = 0.00034, 95% CI: 8.8-1023.8). Upon validation of our results in an independent cohort, this gene variant combination in CKCS is expected to enable targeted breeding programs to reduce MMVD prevalence in CKCS.

Animals↗
PubMed1977

Cardiac lymphatic obstruction: ultrastructure of acute-phase myocardial injury in dogs.

Cardiac lymphatics exist as a network of intercommunicating channels in the myocardium and heart valves, and chronic obstruction of these vessels may result in endomyocardial fibrosis and mucoid degeneration of heart valves. The acute effects of experimental cardiac lymphatic obstruction were studied in the dog. Subendocardial edema and hemorrhage occurred within 150 minutes of the ligation of cardiac lymphatics. Ischemia-type myocardial injury was also observed. Attional changes detectable ultrastructurally included lymphangiectasia, myofibrillar degeneration, disruption of Z-band and intercalated disks, and various mitochondrial derangements. The spottiness of the changes was attributable to the known anatomic variability of lymphatic distribution in the heart. The findings reinforce the belief that greater attention should be focused on the role of cardiac lymphatics in the pathogenesis of a multitude of myocardial and vavular heart diseases.

Animals↗
PubMed1975

The effect of angiotensin on myocardial contractility.

Previous studies of the effect of angiotensin on myocardial contractility have yielded conflicting results. Possible reasons for the observed disparities include differences in techniques for measuring contractility, in species (dog, cat, and man), in myocardial state (normal or diseased), in preparation observed (heart-lung, isolated heart, papillary muscle, atrial myocardium, intact heart), and in dosage schedule. Moreover, there are no reported studies in the intact human heart, normal or diseased, in which contractility measurements are based on velocity-force relations. To resolve the conflict, left ventricular myocardial contractility was measured using the same expressions for the force-velocity relationship in all subjects. Studies were performed in five normal human subjects, six patients with cardiomyopathy, eight normal mongrel dogs, and six dogs with ischemic myocardial scarring, before and during angiotensin infusions in dosages producing 15--20-mm Hg increases of aortic diastolic pressure. Contractile element velocity at peak, dP/dt (Vce) and the Frank-Levinson contractility index (CyIx), which normalizes Vce for diastolic fiber length, decreased during angiotensin infusion in all groups. The mean decreases (11 to 19) per cent in Vce, 15 to 23 per cent in CyIx, SEM's 4-5 per cent) were significant (P values ranging from smaller than 0.05 to smaller 0.005) in the normal hearts of dogs and man and in the scarred canine hearts, in which preangiotensin Vce and CyIx were normal. In the cardiomyopathy group, in which contractility was depressed before angiotensin, the drug elicited a further decrease in Vce (mean fall 17 plus or minus 7 per cent, P smaller than 0.1) and CyIx (26 plus or minus 8 per cent, P smaller than 0.02). We conclude that, in the intact organism, with a normal myocardium or a diffuse or segmental myocardial disease, the administration of angiotensin results in a depression of contractility.

Alcoholism↗
PubMedDate not supplied

The effect of acute pulmonary edema on pulmonary vascular resistance: significance for the interpretation of dilated upper lobe vessels on chest radiographs.

Dilation of upper lobe pulmonary vessels is an important radiographic sign of acute, left heart failure. A prominent theory is that perivascular edema causes increased resistance at the lung bases and inverts the normal perfusion gradient such that upper lobe blood flow exceeds lower lobe flow. This theoretical increase in flow is thought to cause dilatation of upper lobe vessels. Previous experimental studies determined indirectly changes in resistance from changes in the perfusion gradient: Results were contradictory. We measured directly the effect of edema on resistance in isolated canine lungs. Resistance increased linearly with edema. The magnitude of increase was small, however, and insufficient to cause inversion of the perfusion gradient. Our data indicate that interstitial pulmonary edema does not cause significant redistribution of blood flow. We suggest that dilated upper lobe vessels are veins acting as pulmonary venous manometers, reflecting elevated left atrial pressure, not increased blood flow.

Acute Disease↗
PubMed1979

Respiratory and cardiac arrest under general anaesthesia: treatment by acupuncture of the nasal philtrum.

The philtrum point VG 26 (Jen Chung) was needled in 69 cases of respiratory depression or apnoea in dogs and cats during induction or maintenance of general anaesthesia. Respiration was restored to normal or near normal rates within 10 to 30 seconds of insertion of the needle in all the cases. In seven cases of anaesthetic apnoea with concurrent cardiac arrest and absence of vital signs, the revival rate was 43 per cent. Those which recovered required four to 10 minutes of acupuncture stimulation. In eight cases of collapse due to other causes, the revival rate was 25 per cent. The cases included five sheep in shock following liver biopsy, two cases of haemorrhagic shock (dog, cat) and one terminal collapse in chronic congestive heart failure (dog).

Acupuncture Therapy↗
PubMed1979

Hypertrophic cardiomyopathy in the dog.

Clinical and necropsy findings in 10 dogs with a spontaneous primary hypertrophic cardiomyopathy are described. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Septal:free wall thickness ratios in the 10 dogs ranged from 1.1 to 1.5; 6 had ratios greater than or equal to 1.3. However, marked cardiac muscle cell disorganization in the ventricular septum, characteristic of patients with hypertrophic cardiomyopathy, was present in only 2 of the 10 dogs. Death occurred most commonly while the dogs were under anesthesia during the course of operative procedures (5 dogs) or suddenly and unexpectedly in animals without previous symptomatic manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. In addition, 2 of these 4 dogs with heart failure and 1 dog without previous symptoms (that died during a noncardiac operation) manifested complete heart block. It is conceivable that dogs with spontaneous hypertrophic cardiomyopathy may prove useful in the future investigations of the clinical, hemodynamic, and pathologic features of this disease in humans.

Animals↗
PubMedDate not supplied

Cardiac function in the chronically volume-overloaded canine heart.

In the chronically volume-overloaded canine heart due to AV-block evaluations of cardiac function were performed during the development of hypertrophy and at stable hypertrophy. In an early stage (1 and 2 weeks of AV-block) when no or only a slight increase of cardiac muscle occurred, contractility measured from dP/dtmax at comparable load is elevated, while later (10 weeks of AV-block) when stable hypertrophy is present, contractility becomes again normal, In the hypertrophied heart a non-depressed cardiac performance and contractility and functional reserve was established from insitu experiments and from evaluations in the isolated heart.

Animals↗