Left ventricular assist device (LVAD) overpumping is associated with hemolysis, thrombus release, and tissue damage at the pump inlet. However, the impact of LVAD suction on pulmonary circulatory function remains unknown. We investigated LVAD suction as induced by pulmonary artery banding and overpumping in experimental animals and in a computer model. In six sheep, a rotary LVAD was implanted. Before inducing suction, partial support (40-60% of cardiac output) was established and characterized by measuring pressures and flows. In the animals, pulmonary artery occlusion (PAOC) elicited LVAD suction (left ventricular pressure was from -10 to -20 mm Hg) within 5-10 heartbeats. During suction, aortic pressure dropped to 50% and LVAD flow decreased significantly. After releasing the occlusion (20 s), the collapsed state persisted for another 20 s. A similar trend was obtained by simulating PAOC in the computer model. Additional simulations showed that pulmonary vascular resistance (PVR), volume status, and right ventricular (RV) contractility are exponentially related to the persistence of collapse after a suction event. Even modest increases in predisposing factors (elevated PVR, RV dysfunction, hypovolemia) caused sustained hemodynamic collapse lasting in excess of 15 min. Both in selected animals and the computer model, comparable suction-induced collapse was obtained by increasing LVAD speed by about 33%. Attempted compensation by simply decreasing speed was not effective, but temporarily shutting down the LVAD caused rapid reversal of collapse. In conclusion, rotary LVAD suction causes unfavorable conditions for effective unloading. The use of pump interventions appears a promising tool to detect suction and to avoid the associated hemodynamic depression.

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Laminitis, a highly debilitating disease of the foot in ungulates, is characterized by pathological changes of the complex lamellar structures that maintain the appendicular skeleton within the hoof. Laminitis is a multifactorial disease that involves perturbation of the vascular, hematological, and inflammatory homeostasis of the foot. Interestingly, the pathogenesis of the disease resembles what is observed in metabolic syndromes and sepsis-induced organ failure in humans and animals. We hypothesized that local administration of mesenchymal stem cells (MSCs) and platelet-rich plasma (PRP) might contribute to establishing an anti-inflammatory and pro-angiogenic environment, and could stimulate the injured tissue in order to restore its functional integrity. According to this assumption, an experimental protocol based on the local intravenous administration of adipose tissue-derived MSCs (aMSCs) in combination with PRP was developed for the treatment of horses affected by chronic laminitis. Nine horses with severely compromised venograms (showing grade III and IV laminitis) that had been unsuccessfully treated with conventional therapies were enrolled. aMSCs and PRP (15 × 106 cells resuspended in 15 mL of PRP) were injected into the lateral or medial digital vein three times, at one-month intervals. The first administration was performed with allogeneic aMSCs, while for the following administrations, autologous aMSCs were used. There was no adverse short-term reaction to the intravenous injection of aMSCs. In the long term, venograms outlined, in all subjects, a progressive amelioration of the vascularization of the foot. An improvement in the structure and function of the hoof was also observed. No adverse events were reported during the follow-up, and the horses returned to a comfortable quality of life. Although the number of animals enrolled in the study is limited, both clinical observations and venography demonstrated an enhancement in the condition of all horses, suggesting that the regenerative therapies in chronic laminitis could be useful, and are worthy of further investigation.

The aim of this retrospective, cross‐sectional, study was to evaluate clinical findings and outcomes for different ultrasonographic patterns of hepatic emphysema in dogs and cats. Dogs and cats with an ultrasonographic diagnosis of hepatic emphysema and a known outcome, from January 2010 to January 2018, were enrolled. The following data were recorded from medical and ultrasonographic records: ultrasonographic patterns of hepatic emphysema (parenchymal, portal venous, biliary), clinical signs, laboratory findings, and outcomes (favorable, poor). A total of 33 dogs and four cats met the inclusion criteria. Among these, 23 cases were classified as hepatic portal venous gas, 10 as parenchymal emphysema, and four as biliary emphysema. Clinical diagnosis categories were as follows: infection/sepsis (9), gastro‐intestinal disease (9), iatrogenic (9), trauma (5), and liver neoplasia (5). An increase in serum liver enzymes was significantly associated with parenchymal emphysema (P = .03). Other clinical and laboratory findings were not associated with the type of hepatic emphysema. Hepatic portal venous gas was mostly transient in patients with ultrasonographic follow‐up. The overall mortality was 40.5%. A significant difference was found between mortality by portal venous gas (21.7%) and mortality by parenchymal emphysema (90%) (P = .003). In conclusion, the ultrasonographic differentiation of hepatic emphysema between hepatic portal venous gas and parenchymal emphysema may be important for the prognosis of hepatic emphysema. The presence of parenchymal emphysema may be a poor prognostic indicator, while hepatic portal venous gas may be more benign. However, ultrasound findings should be carefully evaluated in the context of clinical findings.

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